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An 18-year-old young man is seen in the dental clinic for a cleaning. The dentist calls to ask if the patient requires endocarditis prophylaxis.Which of the following conditions require endocarditis prophylaxis?A.Pulmonary atresia palliated with a Blalock Taussig shunt.B.Successful atrial septal defect closure at 2 years of age. C.End-to-end coarctation of the aorta repair at 6 months of age.D.Bicuspid aortic valve with moderate regurgitation.E.Small restrictive ventricular septal defect.The correct answer is A.? According to the guidelines for infective endocarditis, the indications for antibiotic prophylaxis infective endocarditis include patients with cyanotic heart disease, those within 6 months of surgery, and patients who have a residual patch leak near a patch of foreign material. Choice A describes a patient with cyanotic heart disease palliated with surgical shunting. The remainder of the choices are incorrect because they do not fit the current recommendations for endocarditis prophylaxis. The earlier guidelines included a large number of patients; the current guidelines are more limited. Included conditions are:Prosthetic heart valves, including bioprosthetic and homograft valves;A prior history of infective endocarditis;Unrepaired cyanotic congenital heart disease, including palliative shunts and conduits;Completely repaired congenital heart defects with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure;Repaired congenital heart disease with residual defects at the site or adjacent to the site of the prosthetic device; and Cardiac valvulopathy in a transplanted heart. A 68-year-old man presents to a clinic appointment with a chief complaint of “heart racing” and shortness of breath. The patient has a past medical history significant for ischemic cardiomyopathy with an echocardiogram performed 1 month prior showing an EF of 30% and paroxysmal atrial fibrillation of 2 years’ duration. The patient has been hospitalized twice in the previous 60 days with similar symptoms. His current medications include aspirin 81 mg daily, simvastatin 40 mg daily, warfarin 5 mg daily, lisinopril 10 mg daily, carvedilol 6.25 mg twice daily, furosemide 40 mg daily, and digoxin 0.25 mg daily.Laboratory data at this time include: a sodium of 135 mEq/L, potassium of 4.3 mEq/L, serum creatinine of 0.9 mg/dl, an INR of 2.4, and a digoxin concentration of 0.9 ng/ml. Vital signs include a blood pressure of 110/62 mm Hg and a heart rate of 124 bpm. The decision is made to attempt rhythm control with amiodarone at this time. Which of the following concomitant medication dosages should be reduced at the time amiodarone is initiated?A.Warfarin only.B.Digoxin only.C.Simvastatin only.D.Warfarin and digoxin only.E.Warfarin, digoxin, and simvastatin. The correct answer is E.? Amiodarone is an inhibitor of both hepatic CYP450 enzymes (including CYP2C9, CYP2D6, CYP3A4) and p-glycoprotein. Based on the ability to inhibit different enzyme/transport targets, the potential exists for a number of drug interactions when amiodarone is prescribed. Current recommendations exist for a dose reduction of warfarin, digoxin, and simvastatin combined with frequent monitoring when amiodarone is initiated. Amiodarone increases digoxin concentrations by inhibition of p-glycoprotein and reducing digoxin’s clearance. If digoxin therapy is to be continued, a dose reduction of approximately 50% has been recommended when initiating amiodarone. For patients taking concurrent warfarin, the addition of amiodarone leads to an increase in the INR. Empiric warfarin dose reductions of 25-50% at the time of amiodarone initiation should be considered. The Food and Drug Administration recently provided recommendations for simvastatin dosing in patients’ medications that have the potential to increase simvastatin levels and the risk of myopathy. For patients receiving concomitant amiodarone, the daily dose of simvastatin should not exceed 10 mg. Therefore, the correct answer for this question is that a dose reduction is indicated for digoxin, warfarin, and simvastatin at the time amiodarone is initiated. A 65-year-old woman with a past medical history of diabetes, hypertension, and hyperlipidemia presents to the emergency room complaining of acute substernal chest pain, which began when she was mowing her grass. She notes radiation to her left arm and jaw, and associated diaphoresis and nausea. A 12-lead ECG was notable for apparently new inferior ST elevation. She undergoes coronary angiography that demonstrates a thrombus in her proximal right coronary artery. PCI is performed and a bare-metal stent is placed, resulting in TIMI III flow, resolution of ST elevation and symptom relief. During the second day of her hospitalization, she notes recurrent chest pain, which is different in character than her initial discomfort on presentation. This pain is worse with a deep breath and improved with leaning forward. On physical exam, she was hemodynamically stable, with a new finding of a three-component pericardial friction rub. Laboratory testing includes blood urea nitrogen (BUN) 10 mg/dl, creatinine 1.0 mg/dl, and troponin 12 ng/ml. The 12-lead ECG is consistent with pericarditis. Based on this assessment, which of the following is the most appropriate initial treatment for this patient?A.Ibuprofen 200 mg every 6 hours.B.Prednisone 40 mg daily.C.Metoprolol 25 mg twice a day.D.Aspirin 650 mg every 6 hours.E.Isosorbide mononitrate 30 mg daily. The correct answer is D.? Peri-infarct pericarditis typically occurs within days of an MI, with a classic finding of friction rub and symptoms consistent with pericarditis. Based on the ACC/AHA guidelines for STEMI, high-dose aspirin therapy receives a Class I indication for treatment of pericarditis post-STEMI. Other anti-platelet agents should generally be continued as well. Corticosteroids receive a Class IIb indication, and may increase risk of infarct scar thinning and subsequent myocardial rupture. Ibuprofen has a level of evidence of Class III due to concern regarding excessive platelet inhibition, and the potentially negative effect on healing and coronary vascular resistance. Colchicine and acetominaphen are considered Class IIa agents in this situation and may also be considered.ReferencesAntman EM, Anbe DT, Armstrong PW, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). J Am Coll Cardiol 2004;44:E1-E211.A 65-year-old man presents to the emergency room with chest pain and is diagnosed with a non-STEMI (NSTEMI). He has a history of diabetes complicated by end-stage renal disease on dialysis, and weighs 110 kg. After further evaluation, a noninvasive strategy (no plans for immediate coronary angiography) is selected.When considering the use and dosing of anticoagulant therapies, which of the following is most appropriate for this patient?A.Initial unfractionated heparin bolus at a dose of 60 U/kg (60 U/kg x 110 kg) should be given.B.After an initial bolus, unfractionated heparin infusion should be started at 1000 U/hr.C.Fondaparinux 2.5 mg daily can be considered as an alternative to unfractionated heparin.D.Bivalirudin at 1 mg/kg/hr can be considered as an alternative to unfractionated heparin.E.Enoxaparin at 1 mg/kg daily can be considered as an alternative to unfractionated heparin. The correct answer is B.? This case focuses on the dosing of anticoagulant therapies for patients with non-STE ACS. Current ACC/AHA guidelines for the use of unfractionated heparin recommend an IV bolus of 60 U/kg with a maximum dose of 4000 U, and infusion dose of 12 U/kg/hr with a maximum dose of 1000 U/hr. Based on these recommendations, option A is incorrect in that it exceeds the maximum bolus dose, but option B is correct. Current ACC/AHA guidelines consider fondaparinux, bivalirudin, and enoxaparin as appropriate alternatives to unfractionated heparin among patients with non-STE ACS. However, fondaparinux is contraindicated among patients requiring dialysis, and the contemporary trials evaluating both fondaparinux (OASIS-5) and enoxaparin (SYNERGY and OASIS-5) in this clinical setting have excluded patients requiring renal dialysis. Thus, choices C and E are incorrect. While bivalirudin can be used among dialysis patients going for PCI, the ACUITY trial, which assessed bivalirudin as initial anticoagulant strategy in unstable angina (UA)/NSTEMI, was limited to patients assigned to an early invasive strategy. Additionally, patients with a creatinine clearance <30 ml/min were excluded from this trial. Current ACC/AHA UA/NSTEMI guidelines do not recommend bivalirudin as a treatment option for patients being managed with an initial conservative strategy. Therefore, choice D is incorrect. A 50 year old woman presents to the Emergency Department with palpitations. She has had similar symptoms over the past 30 years, wherein she typically will bend over to pick something up and then when she rises back up, her heart suddenly seems to pound out of her chest. In the past year these episodes have occurred at least weekly and usually last about 30 minutes, but this is the first time her symptoms have lasted for more than two hours. She takes (Figure 1) is obtained in the Emergency Department, and about 15 minutes later her heart rate abruptly drops to 80 bpm in sinus rhythm.The next step in management should be:A.Refer for ablation for AV reentrant tachycardia (AVRT).B.Refer for ablation for AV nodal reentrant tachycardia (AVNRT).C.Refer for ablation for atrial flutter.D.Increase metoprolol tartrate to 50mg bid and perform 30 day event monitoring.E.Initiate flecainide 100mg bid and perform 30 day event monitoring.The correct answer is A.? The above ECG shows SVT, and the most likely etiology is AV reentrant tachycardia, utilizing a bypass tract for the retrograde limb of the tachycardia. The retrograde P wave is best seen in the inferior leads as a notching within the ST-T wave segment. In AV nodal reentrant tachycardia the P wave is at the terminal portion of the QRS complex, not within the ST segment. Given the frequent episodes that she has had, in particular despite the administration of an AV nodal blocking medication, the next course of action should be catheter ablation for definitive treatment.A 19-year-old, chronically anticoagulated woman with unrepaired tetralogy of Fallot and pulmonary atresia is admitted from the emergency room for treatment of a community-acquired pneumonia. For the last 3 days, she has reported chills, productive cough, and increased dyspnea. She is currently afebrile. Her blood pressure is 132/70 mm Hg and heart rate is 82 bpm. Her resting oxygen saturation is unchanged from her usual of 86% on room air. Her complete blood cell count shows a white blood cell count of 13.6, a hematocrit of 55.5%, platelet count of 252,000, and international normalized ratio (INR) 3.2. Ten minutes after an IV infusion of ampicillin/sulbactam is started, the house physician is called urgently to the bedside for acute onset of aphasia and dense right-sided hemiparesis. Stat CT of the head reveals no hemorrhage or mass lesion. There is abnormal low attenuation in the left middle cerebral artery territory consistent with acute infarction. Which intervention, had it been initiated, would have most likely prevented this event?A.IV line filter.B.Lower extremity sequential compression devices.C.Vitamin K.D.Subcutaneous LMWH.E.Therapeutic phlebotomy. The correct answer is A.? Recognized mechanisms for cerebrovascular events in individuals with cyanotic congenital heart disease include hemorrhage, emboli, and cerebral abscesses. This patient’s physiology puts her at risk for any of the three. Chronically cyanotic individuals commonly exhibit mild increases in INR and partial thromboplastin time due to decreased levels of factors V, VII, VIII, and X. Thrombocytopenia and platelet dysfunction are also common. In this instance, an intracranial bleed was ruled out by noncontrast head CT immediately upon discovery of her neurologic deficit. In the absence of an acute bleed, a modestly elevated INR of 3.2 would not justify administration of vitamin K. In contrast to polycythemia vera, phlebotomy is rarely indicated in cyanotic patients with compensatory erythrocytosis. Indeed, blood loss related to excessive phlebotomy can lead to iron deficiency and reduced red blood cell deformability. Studies in adults with cyanotic congenital heart disease have not consistently demonstrated an association between red blood cell mass and stroke, whereas phlebotomy and iron deficiency appear to independently increase the risk. Lower extremity sequential compression devices or subcutaneous heparins for deep venous thrombosis prophylaxis are important considerations in any patient. In the presence of a right-to-left shunt, a deep venous thrombosis can result in paradoxical embolism and stroke. However, given this patient’s INR of 3.2, the added benefit of either intervention is unlikely to be significant. This patient’s therapeutic INR and the timing of the stroke shortly after starting an IV infusion is very suggestive of an air embolus. Intracranial air bubbles can sometimes be demonstrated on CT in such cases. The ACC/AHA 2008 Guidelines for the Management of Adults With Congenital Heart Disease recognize this risk and recommend the use of air filters on IV lines and meticulous attention to avoid the injection of air bubbles in patients with right-to-left intracardiac shunts. Hyperbaric oxygen therapy may be of benefit when instituted early after stroke in these patients, but its use specifically in patients with congenital heart disease is unproven. ReferencesHenriksson P, Varendh G, Lundstrom NR. Haemostatic defects in cyanotic congenital heart disease. Br Heart J 1979;41:23-27.Gross S, Keefer V, Liebman J. The platelets in cyanotic congenital heart disease. Pediatrics 1968;42:651-8.Ammash N, Warnes CA. Cerebrovascular events in adult patients with cyanotic congenital heart disease. J Am Coll Cardiol 1996;28:768-72.Warnes CA, Williams RG, Bashore TM, et al. ACC/AHA 2008 guidelines for the management of adults with congenital heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines on the Management of Adults With Congenital Heart Disease). Developed in Collaboration With the American Society of Echocardiography, Heart Rhythm Society, International Society for Adult Congenital Heart Disease, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2008;52:e1-121. A 72-year-old man returns to clinic for follow-up. He has previously been diagnosed with severe aortic stenosis and hypertension and has been asymptomatic in the past. An echocardiogram 6 months ago demonstrated moderate aortic valve leaflet thickening, reduced leaflet excursion, a mean aortic valve gradient of 45 mm Hg, and a calculated aortic valve area of 1.0 cm2. His LV systolic function was normal. Currently he reports 2 weeks of substernal chest tightness and reduction in exertional capacity. Exam reveals a late-peaking crescendo-decrescendo murmur at the right second intercostal space with no audible S2.In addition to a repeat transthoracic echocardiogram, which one of the following studies should be performed?A.Transesophageal echocardiography (TEE) to assess valvular structure and prepare for balloon valvuloplasty.B.Left heart catheterization to assess transaortic gradient using a dual-lumen pigtail catheter.C.Coronary angiography to assess for associated obstructive CAD. D.Cardiac magnetic resonance imaging (MRI) to assess for myocardial contractile reserve. The correct answer is C.? This patient has symptomatic severe aortic stenosis with clinical features that fit with the echocardiographic findings. In most patients, transthoracic echocardiography (TTE) is sufficient for assessing the severity of aortic stenosis. TEE is a reasonable modality to assess aortic valve area by planimetry if poor echocardiographic windows preclude accurate assessment by TTE; however, transvalvular velocities and gradients are generally better assessed by TTE rather than TEE. Balloon valvuloplasty for aortic stenosis generally produces only a modest improvement in aortic valve area or symptoms, is associated with poor long-term results owing to a very high 6-month restenosis rate, and is associated with a high rate of serious complications (~10%). Hence, aortic valvuloplasty is not an alternative to aortic valve replacement in adult patients who are candidates for surgery. Hemodynamic assessment of the aortic valve is only indicated when there is a discrepancy between the clinical and echocardiographic findings. There is no evidence of impaired myocardial function in this patient, and MRI is not indicated. Preoperative coronary angiography is prudent in a patient of this age to assess for concomitant CAD, which may require bypass grafting at the time of aortic valve replacement. ReferencesBonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol 2006;48:e1-148.Lieberman EB, Bashore TM, Hermiller JB, et al. Balloon aortic valvuloplasty in adults: failure of procedure to improve long-term survival. J Am Coll Cardiol 1995;26:1522-8. ? A 65-year-old man with stage 4 non?small cell lung carcinoma is admitted to the hospital for tumor resection. Three days after the operation, he develops swelling of his left lower extremity. He denies chest discomfort or shortness of breath. Examination shows a well healing surgical incision and pitting edema of the left lower leg up to the mid-calf. Laboratory studies are significant for mild anemia and thrombocytosis, and a serum creatinine level of 1.0 mg/dl. A duplex ultrasound examination shows hazy material within a noncompressible popliteal vein. Doppler flow is absent through this region.Which of the following is the most appropriate therapy for this patient?A.IV unfractionated heparin while hospitalized, followed by 6 months of anticoagulation with warfarin.B.IV unfractionated heparin while hospitalized, followed by anticoagulation with warfarin indefinitely.C.Subcutaneous low molecular weight heparin (LMWH) for 3 months, followed by 3 months of anticoagulation with warfarin.D.Subcutaneous LMWH for 3 months, followed by anticoagulation with warfarin indefinitely.E.Subcutaneous fondaparinux for 3 months. The correct answer is D.? This patient has developed an acute deep venous thrombosis (DVT) of the left popliteal vein, likely resulting from immobilization after surgery. Current guidelines for anticoagulation therapy in acute DVT recommend initiation of anticoagulation with LMWH over unfractionated heparin except in cases of severe renal failure, making choices A and B incorrect (Recommendation 1.4.1). While the DVT is likely related to the patient’s recent surgery, patients with malignancy are in a state of hypercoagulability and the risk of venous thromboembolism recurrence even with appropriate anticoagulation therapy is 3 times higher than in patients without malignancy. Therefore, current guidelines suggest use of LMWH for the first 3-6 months of long-term anticoagulation therapy, with subsequent anticoagulation with warfarin or LMWH indefinitely or until the cancer has resolved (Recommendation 2.1.3). Choices C and E are incorrect, leaving choice D as the correct answer. A 30-year-old woman was referred for cardiology consultation after presenting to her primary care physician’s office with multiple episodes of near syncope over the last 2 years. The patient’s older siblings have similar symptoms. On physical exam, the patient has a 2/6 systolic murmur loudest at the second intercostal space, to the left of the sternal border. The intensity of the murmur decreases to 1/6 when the patient squats and increases to 4/6 immediately upon standing from a squatted position. This maneuver is accompanied by transient light-headedness. An echocardiogram reveals hypertrophic obstructive cardiomyopathy with a resting gradient of 55 mm Hg. Seventy-two hours later the patient presents to the emergency department with a fever of 104°F, tachycardia, and hypotensive, with a blood pressure of 70/30 mm Hg. She has a white blood cell count of 30,000. Urinalysis demonstrates clumps of gram-positive bacteria. Broad spectrum antibiotics and IV normal saline are administered. Which of the following IV medications would be most appropriate to treat his hypotension?A.Phenylephrine.B.Norepinephrine.C.Epinephrine.D.Dopamine.E.Sodium nitroprusside. The correct answer is A.? The patient’s physical exam and echo/Doppler are consistent with a dynamic LV outflow tract obstruction, as observed with hypertrophic obstructive cardiomyopathy (HOCM). Siblings of affected patients may also have phenotypes consistent with HOCM. A dynamic LV outflow tract gradient will become greater if a medication that increases inotropy is administered. It will also become greater if a medication that decreases afterload is administered. Norepinephrine, epinephrine, and dopamine all increase inotropy. Sodium nitroprusside decreases afterload. Phenylephrine increases afterload and will therefore decrease the LV outflow tract gradient and increase systemic blood pressure. ReferencesHenry WL, Clark CE, Griffith JM, Epstein SE. Mechanism of left ventricular outflow obstruction in patients with obstructive asymmetric septal hypertrophy (idiopathic hypertrophic subaortic stenosis). Am J Cardiol 1975;35:337-45.De Backer D, Biston P, Devriendt J, et al, on behalf of the SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med 2010;362:779-89. A 77-year-old man undergoes percutaneous coronary intervention with a drug-eluting stent to his midleft anterior descending (LAD) after presenting with a non–ST-segment elevation myocardial infarction (NSTEMI). He is now 3 months postpercutaneous coronary intervention (PCI), has no cardiac symptoms, and is tolerating his medical therapy including low dose aspirin, clopidogrel, a statin, an angiotensin-converting enzyme inhibitor (ACEI), and a beta-blocker. You receive a call from his pharmacy after concerns were raised regarding a potential drug interaction with a proton pump inhibitor (PPI) recently prescribed for gastroesophageal reflux symptoms refractory to both nonpharmacologic measures and a H2-receptor antagonist. He has a history of a prior upper gastrointestinal (GI) bleed 2 years ago. Repeat endoscopy recently revealed esophagitis but no ulceration or erosions.Which of the following is the most appropriate management strategy for this patient?A.Continue both agents.B.Discontinue the PPI.C.Discontinue aspirin.D.Switch from clopidogrel to prasugrel.E.Switch from clopidogrel to cilostazol. The correct answer is A.? Option A is the correct response. The patient clearly requires dual antiplatelet therapy early after a drug-eluting stent for acute coronary syndrome (ACS). He is at high risk of bleeding with a prior upper GI bleed and advanced age. He also has ongoing GI symptoms despite appropriate therapy for reflux disease. Option B is incorrect because his risk of GI bleeding and refractory GI symptoms outweigh the potential risk of a drug-interaction and warrant continuation of a PPI. Option C is incorrect. Dual antiplatelet therapy, including aspirin, is recommended following ACS and PCI. He has no ulcer disease on endoscopy and his aspirin should be continued.Option D is incorrect. The patient is at increased risk of bleeding complications with prasugrel due to his age of >75 years and a history of a prior bleed. Option E is incorrect. The use of aspirin and cilostazol without the use of thienopyridines following PCI with stenting is not recommended, and there may be an increased risk of stent thrombosis with this regimen as compared with aspirin plus thienopyridines. This topic remains controversial with conflicting data but a recent consensus statement provides some guidance for clinical practice. Pharmacodynamic studies suggested that concomitant use of PPIs may competitively inhibit activation of clopidogrel by CYP2C19, thereby attenuating its antiplatelet effect. Observational studies showed conflicting results regarding the risk of adverse events. A post-hoc analysis of the TRITON-TIMI 38 (Trial to Assess Improvement in Therapeutic Outcomes by Optimizing Platelet Inhibition With Prasugrel–Thrombolysis In Myocardial Infarction 38) study suggested no increased risk of adverse cardiovascular (CV) events with dual use of PPIs and clopidogrel. The results of the randomized, double-blinded COGENT (Clopidogrel and the Optimization of Gastrointestinal Events Trial) also suggested no increased risk of CV events and reduced GI events with combination agents. In general, concomitant use of these agents should be avoided. In a patient such as this, the increased risk of adverse GI events outweighs the low risk of a clinically significant drug interaction and warrants continued use of both agents. ReferencesAbraham NS, Hlatky MA, Antman EM, et al. ACCF/ACG/AHA 2010 expert consensus document on the concomitant use of proton pump inhibitors and thienopyridines: a focused update of the ACCF/ACG/AHA 2008 expert consensus document on reducing the gastrointestinal risks of antiplatelet therapy and NSAID use. A Report of the American College of Cardiology Foundation Task Force on Expert Consensus Documents. J Am Coll Cardiol 2010;56:2051-66.U.S. Food and Drug Administration. Information for healthcare professionals: update to the labeling of clopidogrel bisulfate (marketed as Plavix) to alert healthcare professionals about a drug interaction with omeprazole (marketed as Prilosec and Prilosec OTC). Available at: Accessed January 31, 2012.O’Donoghue ML, Braunwald E, Antman EM, et al. Pharmacodynamic effect and clinical efficacy of clopidogrel and prasugrel with or without a proton-pump inhibitor: an analysis of two randomised trials. Lancet 2009;374:989-97.Bhatt DL, Cryer BL, Contant CF, et al. Clopidogrel with or without omeprazole in coronary artery disease. N Engl J Med 2010;363:1909-17.Biondi-Zoccai GG, Lotrionte M, Anselmino M, et al. Systematic review and meta-analysis of randomized clinical trials appraising the impact of cilostazol after percutaneous coronary intervention. Am Heart J 2008;155:1081-9 A 64-year-old man presents with a LVEF of 30% on an echocardiogram and no coronary artery disease on a angiography. He has new symptoms of heart failure with exertion. On examination, his BP is 152/85 mm Hg, HR is 78 bpm. Other than cardiomegaly, his exam is unremarkable without evidence of jugular venous distention, rales, S3 or S4 gallop, murmur, or edema. His ECG reveals normal sinus rhythm and left ventricular hypertrophy (LVH) and a QRS duration of 100 msec. He does not have history of diabetes, alcohol, or drug abuse. Current medications include metoprolol tartrate 50 mg twice a day, lisinopril 40 mg once a day, and chlorthalidone 25 mg once a day. Which of the following therapies would you recommend at this time?A.Digoxin.B.Angiotensin-receptor blocker.C.An aldosterone antagonist.? D. NitrateE. Biventricular pacemaker. The correct answer is C.? Treatment with spironolactone is recommended in heart failure patients with New York Heart Association (NYHA) class III or IV symptoms and is not recommended in stage B (asymptomatic LV systolic dysfunction) patients. In the recent EMPHASIS-HF trial, eplerenone, as compared with a placebo, reduced both the risk of death and the risk of hospitalization among patients with systolic heart failure and mild symptoms. The trial randomized patients >55 years of age who had NYHA functional class II symptoms, an ejection fraction of no more than 30% (or, if >30 to 35%, a QRS duration of >130 msec on ECG), and treatment with a beta-blocker and either an ACEI, oran angiotensin-receptor blocker (ARB), or both. ACEI are recommended, and beta-blockers should be considered for patients with LV systolic dysfunction. The patient is already on these agents. In angiotensin-converting enzyme (ACE)-intolerant patients, ARBs are recommended in post-MI patients with asymptomatic LV systolic dysfunction patients and can be beneficial in nonischemic patients with LV systolic dysfunction. The addition of an ARB to an ACEI resulted in an increase in adverse events in the VAL-HEFT trial and is not recommended in current guidelines. Thiazide diuretics can be considered for treatment of HTN in heart failure patients (JNC-7 trial). Resynchronization therapy with a biventricular pacemaker is reserved for patients with a LVEF <35%, who have class III or IV heart failure, a QRS >120 msec, and sinus rhythm (Class 1, Level of Evidence A). It can also be used in patients with a reduced LVEF >35%, class III or IV heart failure, and AF (Class IIa, Level of Evidence B). For someone with mild symptoms (FC II), a biventricular pacemaker is appropriate if the patient is receiving maximal medical therapy and a pacemaker or implantable cardioverter-defibrillator is being considered for other reasons (Class IIb, Level of Evidence C). ReferencesJessup M, Abraham WT, Casey DE, et al. 2009 focused update: ACCF/AHA Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009;119:1977-2016.Rales Trial Investigators, Pitt B, Zannad F, Remme WJ, Cody R, Castaigne A, Perez A, Palensky J, Wittes J. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999:341:709-17.Zannad F, McMurray JJ, Krum H, et al. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2011;364:11-21.The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003;289:2560-72.5.Chobanian AV, Bakris GL, Black HR, et al; National Heart, Lung, and Blood Institute Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure; National High Blood Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7). JAMA 2003;289:2560-72.Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol 2008;51:e1-52. During cardiology consult service, you receive a phone call from an orthopedic clinic regarding anticoagulation management. The patient is a 75-year-old woman who is being scheduled for hip surgery next week. She has a mechanical valve (bi-leaflet) in the mitral position that was placed 10 years ago and her most recent international normalized ratio (INR) was 2.7. In addition to warfarin, she takes low dose aspirin.Which of the following do you recommend to manage this patient’s anticoagulation prior to surgery?A.Stop warfarin and aspirin for 3 days prior to the operation.B.Stop warfarin 3 days prior to the operation but continue aspirin.C.Stop warfarin and aspirin and admit the patient once the INR <2 for IV unfractionated heparin. D.Do not stop warfarin or aspirin and infuse fresh frozen plasma (FFP) day of procedure. The correct answer is C.? A mechanical valve in the mitral valve position is considered a “high-risk” patient for thrombosis. This is in contrast to patients with a mechanical valve in the aortic position when additional risk factors are needed to be considered “high risk” (AF, previous thromboembolism, LV dysfunction, hypercoagulable condition, older generation thrombogenic valve, or more than one mechanical valve). High-risk patients require that warfarin be stopped in order to decrease bleeding risk, but full anticoagulation intiated once the INR is below 2.0. From the 2006 Guidelines: “In patients at high risk of thrombosis, defined as those with any mechanical MV replacement or a mechanical AVR with any risk factor, therapeutic doses of IV UFH should be started when the INR falls below 2.0.” FFP is generally reserved for an emergency surgery and is generally not advocated for elective surgery. The use of low molecular weight heparin in the setting of a mechanical mitral valve remains controversial. ReferencesBonow RO, Carabello BA, Chatterjee K, et al; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2008;52:e1-142. A 67-year-old male with ischemic cardiomyopathy presents with worsening heart failure symptoms. His vital signs on presentation are: BP 153/85 mm Hg, HR 64 bpm, respiration rate 28 breaths/minute, oxygen saturation 96% on room air. The patient is started on an infusion of nitroprusside.Which of the following changes in (Figure 1) best demonstrates the effect of nitroprusside? A.Line e to line f B.Point 3 to point 5? (Correct)C.Point 3 to point 6D.Point 1 to point 7E.Point 8 to Point 3 Figure 1The correct answer is B.? Nitroprusside is an arteriodilator and venodilator, and thus decreases preload and afterload. Afterload reduction results in reduction in LV end-systolic volume (point 3 to point 5) and increase in stroke volume (width of the pressure-volume loop), it does not alter contractility or the slope of line e. Option A (line e to line f) represents improvement in contractility resulting in the end-systolic pressure volume relation shifting upwards and to the left, thus it is not correct. Option C (point 3 to point 6) represents an increase in afterload/end-systolic pressure resulting in an increase in end-systolic volume and decrease in stroke volume. Nitroprusside does not increase afterload. Option D (point 1 to point 7) represents an increase in end-diastolic volume. Nitroprusside does not result in an increase in end-diastolic volume. Option E (point 8 to point 3) represents decline in contractility, resulting in the end-systolic pressure volume slope shifting downwards and to the right. Nitroprusside should not result in a decline in contractility. ReferencesMechanisms of cardiac contraction and relaxation. In: Braunwald’s Textbook of Heart Disease. 8th ed. Pages 533-4.??? ? A 65-year-old man presents to the clinic for a follow-up appointment. His medical history is significant for HTN, heart failure with LVEF of 35%, and chronic renal insufficiency with a stable serum Cr of 2.4 mg/dl (Cr clearance of 27 ml/min). Serum K is 4.6 mEq/L. Current medications include lisinopril 5 mg daily, which was initiated 4 weeks ago, furosemide 40 mg daily, and carvedilol 12.5 mg twice daily. He continues to have limitation of more than ordinary physical activity (for example, climbing more than one flight of stairs) due to shortness of breath.During physical examination he appears comfortable. BP is 128/72 mm Hg, HR is 81 bpm, JVP is normal, soft systolic murmur without S3, and trace peripheral edema. Which of the following would be most appropriate at this time?A.Add spironolactone 25 mg daily. B.Increase lisinopril to 10 mg daily. C.Add losartan 50 mg daily.D.Add hydralazine 25 mg and isosorbide dinitrate 10 mg three times daily.E.Add HCTZ 25 mg daily. The correct answer is B.? Option B is correct. The ACC/AHA Guidelines for Heart Failure recommend cautious use of ACEI for patients with a serum Cr greater than 3 mg/dl, with close monitoring of Cr and K levels. For lisinopril, the ACC/AHA guidelines recommend a daily dose of 20 to 40 mg. Given that the patient has been on ACEI for 4 weeks with stable Cr and K levels along with adequate BP, a trial of advancing lisinopril toward the target dose would be most appropriate. Options A and E are incorrect. While outcome data support the use of aldosterone antagonists in patients established on target (or maximum tolerated) doses of ACEI and beta-blockers in the setting of post-MI LV dysfunction (EPHESUS trial), NYHA class III to IV chronic systolic heart failure (RALES trial) and most recently NYHA class II systolic heart failure in selected patients (EMPHASIS trial), patients with severe renal insufficiency were excluded. These trials also excluded patients with serum Cr >2.5 mg/dl (or Cr clearance <30 ml/min/1.73m2) or serum K >5 mmol/L. These exclusion criteria are reflected in the guidelines which recommend not to use these agents in patients with a serum Cr greater than 2.5 mg/dl for men and 2.0 mg/dl for women or those with hyperkalemia defined as K >5 mEq/L. Option C is incorrect. The ACC/AHA guidelines give only a Class IIb recommendation for addition of an ARB to conventional therapy including an ACEI in selected symptomatic patients with reduced LVEF. Data from a trial of patients with LV dysfunction following MI showed that adding an ARB to an ACEI did not improve clinical outcomes and led to more side effects including hyperkalemia and worsening renal function. Option D is incorrect. The beneficial effect of hydralazine and isosorbide dinitrate when added to ACEI and/or beta-blocker in African-American heart failure patients was recently demonstrated. However, at this time, the data do not exist showing similar clinical benefits in other patients with heart failure. While the ACC/AHA guidelines provide a Class IIa recommendation for the addition of hydralazine and isosorbide dinitrate to ACEI and beta-blocker in patients who remain symptomatic, the guidelines also advise this combination not be substituted for ACEI in patients tolerating ACEI. Given the fact that the patient is currently tolerating the lisinopril, along with the lack of data for the use of hydralazine and isosorbide dinitrate in the patient, the most appropriate choice would be option B. ReferencesJessup M, Abraham WT, Casey DE Jr, et al. 2009 focused update incorporated into the ACCF/AHA 2005 guidelines for the diagnosis and management of chronic heart failure in adults with the 2008 focused update incorporated. J Am Coll Cardiol 2009;53:e1-90.Pitt B, Remme W, Zannad F, et al., for the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study Investigators. Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med 2003;348:1309-21.Pitt B, Zannad F, Remme WJ, et al, for the Randomized Aldactone Evaluation Study Investigators. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. N Engl J Med 1999;341:709-17.Zannad F, McMurray JJV, Krum H, et al, for the EMPHASIS-HF Study Group. Eplerenone in patients with systolic heart failure and mild symptoms. N Engl J Med 2011;364:11-21.Pfeffer MA, McMurray JJ, Velazquez EJ, et al. Valsartan, captopril, or both in myocardial infarction complicated by heart failure, left ventricular dysfunction, or both. N Engl J Med 2003;349:1893–906.Taylor AL, Ziesche S, Yancy C, et al. Combination of isosorbide dinitrate and hydralazine in blacks with heart failure. N Engl J Med 2004;351:2049-57. A 39-year-old man has presented to the emergency room (ER) with rapid palpitations three times over the last 5 months. His electrocardigram (ECG) during one of these episodes shows AF with wide QRS complex and rates from 150-250 bpm. These episodes terminate spontaneously after 1-2 hours. His follow-up ECG is shown (Figure 1).Which of the following would be the most appropriate therapy?A.Metoprolol. B.Catheter ablation at tricuspid annulus. C.Catheter ablation of his bypass tract. D.Catheter ablation to achieve pulmonary vein isolation.E.Flecainide. Figure 1The correct answer is C.? The ECG shows a delta wave indicating an accessory bypass tract at the mitral annulus, likely in a posterior-lateral location. For a patient with Wolff-Parkinson-White syndrome and AF, AF may initiate from supraventricular tachycardia and, therefore, ablation of the accessory pathway can be effective in not only eliminating the risk for sudden death but also AF.ReferencesBlomstr?m-Lundqvist C, Scheinman MM, Aliot EM, et al. ACC/AHA/ESC guidelines for the management of patients with supraventricular arrhythmias--executive summary. a report of the American college of cardiology/American heart association task force on practice guidelines and the European society of cardiology committee for practice guidelines (writing committee to develop guidelines for the management of patients with supraventricular arrhythmias) developed in collaboration with NASPE-Heart Rhythm Society. J Am Coll Cardiol 2003;42:1493-531.A 32-year-old woman presents with HTN. She reports taking hydrochlorothiazide 25 mg daily for the past 4 years. BP in her right arm is 152/96 mm Hg and in her left arm is 144/92 mm Hg. Her HR is 65 bpm. Her BMI is 25. There is a 1/6 systolic murmur at the second right intercostal space. There is no abdominal bruit and femoral pulses are brisk. Laboratory tests: Na 133 mEq/L, K of 4.0 mEq/L, and Cr 0.6 mg/dl.Which of the following is the next best diagnostic step in the evaluation of this patient?A.Magnetic resonance angiography of the renal arteries. puted tomography angiography of the cerebrovascular system. C.Plasma free metanephrines.D.Echocardiography.E. Polysomnography. The correct answer is A.? Early onset HTN in a young woman raises the possibility of fibromuscular dysplasia (FMD), a nonatherosclerotic, noninflammatory vascular disease that results in arterial narrowing and aneurysms of small- and medium-sized vessels. The absence of an abdominal bruit has a limited negative predictive value and further evaluation is necessary. Once the diagnosis of FMD has been established, it is important to interrogate the cerebrovascular system (option B) because carotid or vertebral arteries may be involved in 25%-30% of cases. Options C and E evaluate for pheochromocytoma and sleep apnea, respectively; these are reasonable considerations after excluding FMD. Examination does not suggest hemodynamically significant aortic coarctation given the brisk lower extremity pulses. When clinical suspicion for this entity exists, the diagnosis can be established with echocardiography using the suprasternal notch window (option D). Polysomnography (option E) is useful to evaluate for sleep apnea as cause of HTN in a patient at risk (obesity, snoring) or with resistant HTN. ReferencesElliott WJ. Renovascular hypertension: an update. J Clin Hypertens (Greenwich) 2008;10:522-33.Olin JW, Pierce M. Contemporary management of fibromuscular dysplasia. Curr Opin Cardiol 2008;23:527-36. ??? ??? A 75-year-old woman with a past medical history of hypertension, diabetes mellitus, chronic kidney disease, paroxysmal atrial fibrillation, and a transient ischemic attack (2 years ago) presents to an ambulatory cardiology clinic for evaluation of shortness of breath. Her symptoms began 8 weeks ago and have been slowly progressive. She denies orthopnea, paroxysmal nocturnal dyspnea, weight gain, or progressive swelling of the feet, ankles, or legs. Current medications include lisinopril 40 mg daily, HCTZ 25 mg daily, dronedarone 400 mg twice daily, and aspirin 325 mg daily. Physical examination vitals are: blood pressure 150/60 mm Hg; heart rate 134 bpm; respiration 20-22 per minute; temperature 37.0°C (oral); weight 60 kg; O2 saturation 94% (room air). Cardiovascular: irregularly irregular S1 and S2; II/VI systolic murmur along the left sternal border, radiating to the aortic area. Laboratory values and diagnostic tests are: sodium 131 mmol/L, potassium 3.6 mmol/L, chloride 102 mmol/L, CO2 24 mmol/L, blood urea nitrogen (BUN) 20 mg/dl, creatinine 2.2 mg/dl. Estimated creatinine clearance (CrCl) is 21 ml/min. An echocardiogram reveals mild LV hypertrophy, an estimated LVEF of 45%, normal LV end-diastolic dimensions, and thickening of the aortic valve. The left atrial size is 4.0 cm. Doppler evidence of a mean aortic valve gradient of 20 mm Hg is present. The ECG reveals atrial fibrillation with a rapid ventricular response and LV hypertrophy. Based on the patient’s clinical status and available evidence, which of the following is the optimal initial management of this patient?A.Immediate hospital admission, anticoagulation with low molecular weight heparin, and initiate amiodarone 600 mg daily.B.Initiate rate control therapy with a calcium channel blocker, anticoagulation with dabigatran at a dose of 150 mg twice daily, and elective cardioversion in 3 weeks.C.Initiate rate control therapy with digoxin, continue aspirin, and perform a cardioversion in several days.D.Increase the dose of dronedarone for rate control, continue aspirin, and schedule a TEE-cardioversion in 1 week.E.Initiate rate control therapy with a beta-blocker, anticoagulation with warfarin, titrated to a target international normalized ratio (INR) of 2.5 (range 2.0-3.0), and schedule a follow-up office visit within the next week. The correct answer is E.? Atrial fibrillation is the most common cardiac arrhythmia in the U, increasing steadily with age. The most feared and devastating complication of atrial fibrillation is cardioembolic stroke and, accordingly, anticoagulation represents a mainstay of treatment. The patient under consideration has developed atrial fibrillation with a rapid ventricular response and mild heart failure. Her CHADS2 score is high. Rate control is the most important first step in management with concomitant anticoagulant therapy. Although dabigatran is Food and Drug Administration (FDA) approved for atrial fibrillation, this patient has a CrCl below 30 ml/min and is also a receiving dronedarone, a P-glycoprotein antagonist that increases dabigatran area under the concentration (AUC) and the maximum plasma concentration (Cmax) by 100% and 70%, respectively. In addition, the current ACC/AHA/Heart Rhythm Society (HRS) guidelines acknowledge that dabigatran 75 mg twice daily was not tested in the RE-LY study. The patient’s clinical status does not warrant immediate hospitalization. Additional Amiodarone will not be beneficial. ReferencesWann LS, Curtis AB, January CT, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (Updating the 2006 Guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2011;57:223-42.Wann LS, Curtis AB, Ellenbogen KA, 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (update on dabigatran). A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2011;57:1330-7. A 28-year-old woman is evaluated in the cardiology clinic after presenting with a 5-month history of fatigue, subjective fevers, and night sweats. For the last 2 weeks, she has noticed weakness and an aching pain in her right arm while painting. The pain generally resolves within 5 minutes of rest. Carrying her 2-year-old son in her right arm produces similar symptoms. She has not had arm pain at rest and has noticed no joint redness or swelling, rash, or skin changes. On physical exam, her weight is 127 lbs, heart rate is 74 bpm, oxygen saturation is 99% on room air, and right and left arm blood pressures are 94/58 and 132/64 mm Hg, respectively. Right radial and brachial pulses are diminished. Exam is otherwise unremarkable, including normal oropharynx and skin, as well as joint exams of both upper extremities. Laboratory evaluation reveals a white blood cell count of 9200 cells/cm3, Hb 9.7 g/dl, platelets 335,000 cells/microL, creatinine 0.9 mg/dl, and erythrocyte sedimentation rate (ESR) is 84 mm.Which of the following is the most likely diagnosis?A.Coarctation of the aorta.B.Takayasu arteritis.C.Thoracic outlet syndrome.D.Beh?et disease.E.Polyarteritis nodosa. The correct answer is B.? Contrast CT of chest/abdomen/pelvis with upper and lower extremity runoff is obtained, which reveals severe stenosis of the right subclavian artery, with moderate bilateral renal artery stenosis. The vignette describes a young woman with Takayasu arteritis, a large vessel vasculitis involving the aorta and its major branches in adults in their second and third decades of life, affecting women up to 10 times more frequently than men. She initially experienced the classic constitutional symptoms indicative of the acute phase, followed by the claudication suggestive of stenosis in the chronic phase. The diagnosis may be made using the 1990 American College of Rheumatology criteria as follows:Age of onset <40 years oldIntermittent claudicationDiminished brachial artery pulseSubclavian artery or aortic bruitSystolic blood pressure variation of greater than 10 mm Hg between armsAngiographic (CT, MR) evidence of aorta or aortic branch vessel stenosisCoarctation of the aorta generally presents in infancy or childhood. Coarctation rarely presents in adulthood, and if so, one would expect greater perfusion in the upper than lower extremities. Thoracic outlet syndrome is a syndrome involving compression of a neurovascular bundle passing between the anterior and middle scalenes. The subclavian artery can be affected, but the compression is external/mechanical and stenosis would not be found in other areas of the vasculature. Beh?et disease is a small-vessel vasculitis, diagnosed by the presence of oral ulcers (aphthous stomatitis), in addition to two of the following three findings: recurrent genital ulceration, uveitis or retinal vasculitis, or skin lesions (such as erythema nodosum, pseudofolliculitis, or pathergy). Polyarteritis nodosa is a nongranulomatous disease of medium-size arteries. Deep skin inflammatory changes are often present and cardiac disease (congestive heart failure, MI, pericarditis), neuropathy (especially mononeuritis multiplex), renal infarction/insufficiency, hypertension, and segmental pulmonary infarctions can also be seen. ReferencesWeyand CM, Goronzy JJ. Medium- and large-vessel vasculitis. N Engl J Med 2003;349:160-9.Arend WP, Michel BA, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990;33:1129-34.Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the diagnosis and management of patients with thoracic aortic disease. A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Association for Thoracic Surgery, American College of Radiology, American Stroke Association, Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am Coll Cardiol 2010;55:e27-e129.Criteria for diagnosis of Behcet’s disease. International Study Group for Behcet’s Disease. Lancet 1990;335:1078-80. An 85-year-old-man is being evaluated in the clinic for hypertension. Serial blood pressure measurements over two clinic visits demonstrate a blood pressure of 163/85 mm Hg and pulse of 55 bpm. The patient is otherwise healthy without prior medical history. He is on no medications. Despite a trial of appropriate lifestyle modification, his blood pressure remains elevated. Diagnostic studies including urinalysis, ECG, and serum chemistries are unremarkable.Which of the following is the most appropriate next step in his medical management?A.A thiazide diuretic and ACE inhibitor.B.A thiazide diuretic and beta-blocker.C.A thiazide diuretic alone.D.A beta-blocker alone.E.An ACE inhibitor alone. The correct answer is A.? Though monotherapy is a consideration, the majority of patients with an index blood pressure >20/10 mm Hg above goal will require combination therapy. Furthermore, beta-blocker would not be an ideal medication given his resting bradycardia. A recent trial focused on blood pressure management in the elderly demonstrated a benefit from blood pressure reduction in this demographic. In the HYVET trial, 3,845 patients >80 yearrs of age with an index systolic blood pressure >160 were randomized to placebo or pharmacologic therapy. After 2 years, one-fourth remained on monothearpy (thiazide), whereas three-fourths required combination thiazide and ACE inhibitor. Patients in the pharmacologic arm demonstrated a reduction in stroke, heart failure, and cardiovascular events. Most impressive was a 21% reduction in all-cause death. Option A, the combination of a thiazide and ACE inhibitor, is therefore the most supported first choice for hypertension control in this age range. ReferencesBeckett NS, Peters R, Fletcher AE, et al. Treatment of hypertension in patients 80 years of age or older. N Engl J Med 2008;358:1887-98.??? A 38-year-old man is referred to cardiology clinic for burning chest pain that is substernal in nature without clear exacerbating or alleviating factors. He has a known history of hyperlipidemia and smokes a pack of cigarettes daily. He reports brisk walking for 30 minutes, 3 times per week. Physical examination reveals an obese male with a blood pressure of 130/76 mm Hg and heart rate of 74 bpm and is otherwise unremarkable. His ECG reveals nonspecific T-wave inversion in leads II and III.Which of the following is the most appropriate next diagnostic test?A.Dobutamine stress echocardiography.B.Exercise stress ECG.C.Exercise SPECT myocardial perfusion imaging.D.Coronary angiography.E.Transthoracic echocardiography. The correct answer is B.? This 38-year-old man has a low pretest likelihood of having coronary artery disease as the etiology of his chest pain by the Diamond and Forrester criteria. Although he is obese, he exercises regularly and should be able to undergo treadmill stress. His ECG is interpretable. The 2009 appropriateness criteria for radionuclide imaging state that exercise stress ECG should be the initial diagnostic test of choice in patients with low pretest likelihood of coronary artery disease and an interpretable ECG, who are able to exercise. Stress echocardiography and perfusion imaging are inappropriate in this clinical setting. Coronary angiography is not required and has additional risks. Transthoracic echocardiography will not effectively evaluate chest pain. ReferencesHendel RC, Berman DS, Di Carli MF, et al. ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging: A Report of the American College of Cardiology Foundation Appropriate Use Criteria Task Force, the American Society of Nuclear Cardiology, the American College of Radiology, the American Heart Association, the American Society of Echocardiography, the Society of Cardiovascular Computed Tomography, the Society for Cardiovascular Magnetic Resonance, and the Society of Nuclear Medicine. J Am Coll Cardiol 2009;53:2201-29.A 66-year-old with no prior history of heart disease is admitted to the coronary care unit after presenting to the emergency department with fleeting chest discomfort. She reported a prolonged episode of severe chest pain two days earlier. Her physical examination is unremarkable, and her ECG is notable for a prominent R wave in lead V1; Q waves with inverted T-waves in leads II, III and aVF; and no ST-segment deviation. Her troponin I is 15.6 ng/ml. Initial treatment includes aspirin, clopidogrel, unfractionated heparin, metoprolol, and intravenous nitroglycerin. Several hours later, she complains of sudden dyspnea. On repeat exam, she is tachypneic and pale. Her blood pressure is 74/50 mm Hg with a pulse of 115 bpm. Pulse oximetry saturation is 88%. Her jugular venous pressure is not well seen. There are bilateral pulmonary rales. The heart sounds are soft and muffled, with no audible murmurs. An ECG reveals sinus tachycardia, but is otherwise unchanged. A Swan-Ganz catheter is placed, demonstrating a right atrial pressure of 10 mm Hg, a RV pressure of 60/10 mm Hg, a pulmonary artery pressure of 59/41 mm Hg, and a mean pulmonary artery wedge pressure of 35 mm Hg with large v-waves. Which of the following is the most likely diagnosis?A.Acute ventricular septal rupture.B.Acute pulmonary embolism.C.Acute papillary muscle rupture. D.Cardiac tamponade. E. acute RV infarction The correct answer is C.? This patient presents 2 days after suffering an acute inferoposterior MI and has developed acute, severe MR. The mechanism of the MR is most likely rupture of the posteromedial papillary muscle, which has a single blood supply from the posterior descending coronary artery, although acute LV dilation with mitral valve leaflet tethering can also cause severe MR. Acute papillary muscle rupture is more common with inferoposterior than anterior MI. Patients suffering their first MI, over the age of 60, and receiving thrombolytic therapy late (>24 hours) after symptom onset are at higher risk for all forms of ventricular rupture. The patient with acute papillary muscle rupture usually presents with sudden pulmonary edema and/or hypotension, 3-5 days after an acute MI, although the median time to presentation in the SHOCK Trial Registry was 22 hours. On examination, findings of acute pulmonary edema are present. The heart sounds are soft, and there is usually a short, early systolic murmur heard at the lower left sternal border or apex, although a murmur may not be heard if hypotension is present and left atrial pressure is high. Bedside echocardiography can rapidly establish the diagnosis with identification of a mobile papillary muscle head or flail mitral leaflet. Pulmonary artery catheterization demonstrates large v-waves on pulmonary capillary wedge tracings with markedly elevated left-sided filling pressures. Medical therapy for acute papillary muscle rupture is not effective. Initiation of aortic balloon counterpulsation followed by emergent surgical repair is the treatment of choice. Patients with acute ventricular septal rupture present with shock, pulmonary edema, and severe right-sided heart failure, usually with a palpable systolic thrill at the mid or lower left sternal border, an oxygen step-up from the vena cava to the pulmonary artery, and color flow Doppler evidence of a left-to-right shunt at the ventricular level. Acute pulmonary embolism may present with hypotension, but is not associated with pulmonary edema and left heart failure. In cardiac tamponade, pulmonary edema is absent and there is equalization of diastolic filling pressures. ReferencesHochman JS, Sleeper LA, Webb JG, et al. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock? N Engl J Med 1999;341:625-34.Brilakis ES, Reeder GS, Gersh BJ. Modern management of acute myocardial infarction. Curr Probl Cardiol 2003;28:7-127. ? ?A 48-year-old man with no significant past medical history presents to the emergency department with 3 days of progressive chest pain. His discomfort is located in the middle of the chest, and the patient feels worse when lying down and with taking deep breaths. His father has a history of MI at age 64. Your hospital does not have a cardiac catheterization laboratory and the nearest tertiary care center is approximately 120 minutes away. On physical exam, he appears uncomfortable. His temperature is 99.8°F, heart rate is 95 bpm, and blood pressure is 125/80 mm Hg. Jugular venous pressure is normal. His heart sounds are regular, with a normal S1 and S2. A 2/6 mid-systolic murmur is heard best at the right upper sternal border. He has no lower extremity edema. His ECG is shown. Which of the following is the most appropriate next step in his care?A.Primary percutaneous coronary intervention (PCI).B.Tenecteplase (TNK-tPA).C.Two liters of intravenous fluids.D.Metoprolol tartrate 50 mg po.E.Ibuprofen 400 mg po. Figure 1The correct answer is E.? This patient most likely has pericarditis, given the progressive chest pain that is pleuritic and positional. His ECG shows typical diffuse ST elevations. He does not have a friction rub on exam, which can often be absent in acute pericarditis. Choices A and B are incorrect because they imply that the patient is having an ST-segment elevation MI. Choice D is incorrect because there is no indication for a beta-blocker, since the patient does not have acute coronary syndrome. Choice C is incorrect; although intravenous fluids are unlikely to harm the patient, there is no clear indication for them. Choice E is correct because nonsteroidal anti-inflammatory drugs are appropriate treatment for pericarditis. ReferencesTroughton RW, Asher CR, Klein AL. Pericarditis. Lancet 2004;363:717-27.Oh J, Talreja D, Nishimura R, Murphy J. Mayo Clinic Cardiology Concise Textbook. Rochester, MN: Mayo Clinic Scientific Press and Informa Healthcare USA, Inc.; 2007. ?? A 55-year-old asymptomatic, active man presents to you with a heart murmur and no other medical problems. On examination, his blood pressure is 120/75 mm Hg, his carotid has a delayed upstroke, his lungs are clear, and he has a 3/6 mid-peaking systolic ejection murmur at the right upper sternal border, and a single second heart sound. Echocardiography reveals normal LV size with an EF of 45, and a calcified aortic valve with a mean gradient of 50 mm Hg.Which of the following is the most appropriate next step for this patient?A.Treadmill exercise test.B.Right and left heart catheterization.C.Coronary angiogram followed by aortic valve replacement.D. Trans-esophageal echocardiogramE. Medical follow-up. The correct answer is C.? Patients with severe aortic stenosis should undergo aortic valve replacement for symptom development, in the context of surgery performed for another reason (e.g., CABG) or in the asymptomatic patient with LV dysfunction. It is not necessary to perform a hemodynamic catheterization; the diagnosis of “severe” aortic stenosis has already been made based on the physical examination and a mean gradient by Doppler echocardiography >40 mm Hg. Thus, coronary angiography should be performed to rule out concomitant coronary disease, and the patient should then undergo aortic valve replacement.ReferencesBonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease).A 61-year-old man without significant past medical history presents to the emergency department following a syncopal episode that occurred while operating heavy machinery. A review of systems is normal, aside from one episode of emesis that occurred just prior to his syncopal episode. He takes no prescription or over-the-counter medications. He has a history of tobacco use. On arrival in the emergency department, the patient was afebrile, supine blood pressure was 99/65 mm Hg in the left arm and 75/60 mm Hg in the right arm with a pulsus paradoxus of 8 mm Hg, heart rate 100 bpm, respiration 16 breaths/minute, and oxygen saturation was 99% by pulse oximetry with 10 liters of supplemental oxygen via nasal cannula. As noted by the emergency medical system, he was cyanotic from the clavicles to the top of his head, but neck veins were normal. The heart sounds were distant. Abdominal exam was normal. There was no edema. A chest X-ray demonstrated clear lung fields with normal mediastinal and cardiac silhouettes. A 12-lead ECG revealed sinus tachycardia with right-axis deviation and nonspecific ST-segment abnormalities. Which of the following laboratory tests has been found to be useful in establishing the diagnosis of an aortic dissection?A.Serum troponin. B.Serum B-type natriuretic peptide.C.Serum D-dimer. D.Serum creatinine kinase. E. CRPThe correct answer is C.? D-dimer is a useful diagnostic marker in evaluation of suspected aortic dissection. Numerous studies have examined whether plasma D-dimer can be used to identify patients with acute aortic dissection. A value of 500 ng/ml was defined as the threshold for a positive plasma D-dimer finding because it is widely used for excluding pulmonary emboli. When data were pooled across studies, sensitivity (0.97; 95% confidence interval [CI], 0.94-0.99) and negative predictive value (0.96; 95% CI, 0.93-0.98) were high. Specificity (0.56; 95% CI, 0.51-0.60) and positive predictive value (0.60; 95% CI, 0.55-0.66) were low. Negative likelihood rations (LR) showed an excellent discriminative ability (0.06; 95% CI, 0.03-0.12), whereas positive LR did not (2.43; 95% CI, 1.89-3.12). In conclusion, this meta-analysis suggests that plasma D-dimer <500 ng/ml is a useful screening tool to identify patients who do NOT have aortic dissection. Plasma D-dimer may thus be used to identify subjects who are unlikely to benefit from further aortic imaging. ReferencesShimony A, Filion KB, Mottillo S, Dourian T, Eisenberg MJ. Meta-analysis of usefulness of D-dimer to diagnose acute aortic dissection. Am J Cardiol 2011;107:1227-34. ?? A 40-year-old man is referred to you for evaluation of syncope. While at work at his desk 2 weeks ago, he abruptly felt lightheaded and then found himself slumped over his desk. He is not sure how long he was out, but does not think it was more than several seconds. Two years ago, he had a similar event. He has no known medical problems and does not take any medications; he does not smoke and only rarely consumes alcohol. His father died in his 40s after a “massive heart attack,” where he collapsed on his way home from work and there was no autopsy. His referring physician performed a stress echo, with normal echocardiographic findings and no inducible ischemia. His ECG (leads V1 and V2) is shownWhich of the following should be the next step in management of this patient?A.Initiation of metoprolol.B.Initiation of quinidine.C.Electrophysiologic study.D.Implantation of an ICD.E.Genetic testing. The correct answer is D.? The V1 lead shows coved ST-segment elevation, diagnostic of Brugada syndrome in a patient with syncope. Therapy at this point should proceed with implantation of an ICD to prevent sudden cardiac death. There is no known medical therapy to prevent sudden death in Brugada syndrome patients, although quinidine may help suppress ventricular tachyarrhythmias. Genetic testing has low yield to identify a mutation in Brugada syndrome patients.ReferencesZipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006;48:e247-346.?A 52-year-old man is seen as a new patient in your clinic. He reports a history of type 2 diabetes, coronary artery disease with an MI 8 years ago, and a kidney transplant 5 years ago. His current medications include metoprolol, ramipril, aspirin, cyclosporine, and metformin. He has no prior history of smoking, and exercises regularly. His blood pressure is 130/80 mm Hg, BMI is 25 kg/m2, and waist circumference is 32 inches. He has no family history of premature heart disease. His labs are as follows: Total cholesterol 210 mg/dl Triglycerides 225 mg/dl HDL-C 35 mg/dl LDL-C 130 mg/dl HbA1c 7.5% In addition to therapeutic lifestyle changes and diet, which of the following additional therapies would you recommend for this patient?A.Simvastatin 20 mg/day and gemfibrozil 600 mg twice per day.B.Simvastatin 40 mg/day. C.Pravastatin 40 mg/day and gemfibrozil 600 mg twice per day.D.Pravastatin 40 mg/day. E. Simvastatin 80 mg/ dayThe correct answer is D.? This patient is taking cyclosporine, which increases his risk for myositis, particularly in combination with statins, which are metabolized by CYP3A4 such as lovastatin and simvastatin. Pravastatin (as well as fluvastatin and rosuvastatin) are not extensively metabolized by CYP3A4, and thus, levels of these statins do not significantly increase when used in patients taking cyclosporine. Several studies have observed less muscle toxicity in transplant patients taking pravastatin, as compared to other statins such as simvastatin. Pravastatin is approved by the FDA for use in patients taking cyclosporine; thus, it would be recommended over simvastatin. This patient should be counseled to maintain a therapeutic lifestyle change diet, which may significantly improve his elevated triglycerides, HDL-C and glucose control. This patient has a history of coronary artery disease, along with risk factors including diabetes mellitus; thus, a goal LDL-C of <70 mg/dl is a reasonable. His baseline LDL-C is 130 mg/dl. A 30-40% reduction in LDL-C, obtained with a standard dose of pravastatin 40 mg/day, would bring his level down below 100 mg/dl. It is likely that this patient will require /day of pravastatin. Rosuvastatin would be an acceptable alternative to obtain an LDL-C target of <70 mg/dl. The non-HDL-C level in this patient is 175, and his goal non-HDL is <100 to 130. Combination therapy with a statin and either a fibrate or nicotinic acid would improve his triglyceride and HDL-C, leading to an improvement in his non-HDL. However, the risk for muscle toxicity increases with combination therapy. A combination of statins and gemfibrozil can increase the risk of myositis from 1% to 5%. In this patient who is taking cyclosporine, the risk is likely to be even higher. Fenofibrate appears to have a better safety profile then gemfibrozil when used in combination with a statin. For this patient, initiation with a pravastatin as monotherapy is recommended. A 57-year-old woman presents to the emergency department with recurrent atrial fibrillation. These episodes occur 4-6 times per month and last 3-4 days. They are associated with dyspnea but no syncope, and they terminate spontaneously. Her resting electrocardiogram (ECG) after termination of one of these episodes shows normal sinus rhythm at a rate of 70 bpm and normal intervals. Her past medical history includes rheumatic heart disease with mitral stenosis and systemic hypertension. Her current medications include aspirin 325 mg daily, metoprolol 25 mg twice daily, and hydrochlorothiazide 25 mg daily. Her echocardiogram shows moderate mitral stenosis, mild mitral insufficiency, and a left atrial size of 50 mm.Which of the following is the most appropriate therapy for prevention of stroke?A.Initiate clopidogrel 75 mg qd.B.Continue aspirin 325 mg daily. C.Anticoagulation with warfarin. D.Left atrial appendage occlusion.E.Anticoagulation with dabigatran. The correct answer is C.? Patients with rheumatic valvular heart disease and atrial fibrillation are at increased risk for stroke, and anticoagulation with warfarin is indicated. The history of hypertension adds further risk. Dabigatran was studied in the RE-LY trial in patients with nonvalvular atrial fibrillation, and therefore, no recommendation can be made for this medication for valvular atrial fibrillation.ReferencesFuster V, Ryden LE, Cannom DS, et al. 2011 ACCF/AHA/HRS Focused Updates Incorporated into the ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation: A report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in partnership with the European Society of Cardiology and in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. J Am Coll Cardiol 2011;57:e101-98. ? A 72-year-old retired cardiologist is admitted with a non-STEMI. He had 3 hours of substernal chest discomfort. His symptoms were finally relieved in the emergency department. He was given aspirin 325 mg, nitroglycerin, enoxaparin and clopidogrel 600 mg.An ECG showed diffuse and symmetric T-wave inversions across the anterior precordial leads. Cardiac catheterization was performed through the right radial artery and demonstrated a focal 95% stenosis in the proximal LAD coronary artery. A 3.5 x 18 mm DES was placed. He is doing well the next day and asks you about checking his CYP2C19 genotype or overall platelet function. Which of the following do you recommend?A.Checking his platelet reactivity, but not his CYP2C19 genotype.B.Checking his CYP2C19 genotype, but not his overall platelet function.C.Checking both CYP2C19 genotype and overall platelet function.D.Checking neither CYP2C19 genotype and overall platelet function.E. Checking bleeding time insteadThe correct answer is D.? This patient has a focal lesion treated with one stent. There is no indication to check his platelet reactivity or genotype. The ACCF/AHA Clopidogrel Clinical Alert expertly summarizes the issues surrounding clopidogrel and the use of genotype testing, as well as the potential for routine platelet function testing. There has been much interest in whether clinicians should perform routine testing in patients being treated with clopidogrel. The routine testing could be for genetic variants of the CYP2C19 allele and/or for overall effectiveness for inhibition of platelet activity. Commercially available genetic test kits are expensive and not routinely covered by most insurance policies. Additionally, no prospective studies demonstrate that the routine use of these tests, coupled with modification of antiplatelet therapy, improves clinical outcomes or reduces subsequent clinical events. On the basis of the current evidence, it is difficult to recommend genotype testing routinely in patients with acute coronary syndrome (ACS), but it might be considered on a case-by-case basis, especially in patients who experience recurrent ACS events despite ongoing therapy with clopidogrel. In addition, the availability of alternative P2Y12 inhibitors makes many of these issues moot. ReferencesHolmes DR Jr, Dehmer GJ, Kaul S, Leifer D, O'Gara PT, Stein CM. ACCF/AHA clopidogrel clinical alert: approaches to the FDA "boxed warning": a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents and the American Heart Association. Endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol 2010;56:321-41?? A 27-year-old woman is admitted to the intensive care unit with fevers, chills, shortness of breath, and chest pain. She has a history of lupus and takes cyclophosphamide. She was at her baseline state of health until 3 days ago when her symptoms appeared, and they have been progressive since then. Her temperature is 102.4°F, pulse is 120 bpm, and blood pressure 100/60 mm Hg. She appears acutely ill. Her exam reveals a normal JVP, tachycardia with a normal S1 and S2, and a harsh pericardial friction rub. A transthoracic echocardiogram is obtained for further evaluation of her borderline hypotension, and it demonstrates hyperdynamic ventricular function, no valvular disease, and a moderate circumferential pericardial effusion with visible stranding. A diagnostic pericardiocentesis is performed and 400 cc of fluid is removed. The sample was sent for further analysis, with the following results: Protein: 4.1 g/dl, glucose: 30 mg/dl, white blood cell count: 40,000/microL, 94% neutrophils, hematocrit: 1.4%. A 12-lead ECG prior to thoracentesis is shown. Which of the following is your recommendation?A.Ibuprofen 600 mg three times daily.B.Emergent cardiac surgery consult for treatment of RV perforation.C.IV methylprednisolone 80 mg daily.D.IV cefepime 2 g twice daily.? (Correct)E.No change in therapy; wait for further diagnostic testing.The correct answer is D.? Nonsteroidal anti-inflammatory drugs, salicylates, and/or colchicine would be appropriate for acute pericarditis, but based on the fluid analysis, she clearly has an exudative pericardial effusion with a very high white blood cell count, worrisome for bacterial or purulent pericarditis. The mortality approaches 100% if not treated with aggressive antibiotic therapy; thus, broad-spectrum IV antibiotics should be started while awaiting culture data. IV steroids would not be indicated in the setting of bacterial pericarditis, and lupus-associated serositis is unlikely in this scenario. There is no evidence of RV perforation from the pericardiocentesis as the hematocrit on the pericardial fluid is low, although surgical intervention may be indicated for pericardiectomy if antibiotics fail as first-line treatment. The ECG shows electrical alternans consistent with the heart swinging in the pericardial sac within a large pericardial effusion. References1. Sagrista-Sauleda J, Barrabes JA, Permanyer-Miralda G, Soler-Soler J. Purulent pericarditis: review of a 20-year experience in a general hospital. J Am Coll Cardiol 1993;22:1661-5. Leoncini, L. Iurilli, A. Queirolo, and G. Catrambone. Primary and secondary purulent pericarditis in otherwise healthy adults. Interact Cardiovasc Thorac Surg 2006;5:652-4. ?A 30-year-old man is referred for evaluation of a diastolic heart murmur. He has no significant medical history, is not taking any medication, and is asymptomatic. On examination, he is 70 inches, 185 lbs, blood pressure is 155/65 mm Hg, and heart rate is 78 and regular. Prominent carotid pulsations are noted. Jugular venous pulsations are noted at the level of the sternal notch. Lungs are clear. Apical impulse is enlarged and laterally displaced. Auscultation reveals normal S1, soft S2, and S3 is present. There is an early-systolic click that does not change with inspiration, a soft crescendo-decrescendo systolic murmur, and a decrescendo diastolic murmur along the left sternal border.The patient likely has which of the following valve abnormalities?A.Pulmonic valve stenosis with regurgitation.B.Degenerative aortic stenosis with regurgitation.C.Bicuspid aortic valve with regurgitation.D.Rheumatic mitral stenosis and regurgitation.E.Patent ductus arteriosus.The correct answer is C.? Pulmonic valve stenosis is unlikely, since the ejection click does not decrease with respiration, the JVP is normal, and the LV is enlarged on examination. Degenerative aortic stenosis is not associated with a systolic click. Rheumatic mitral stenosis may be associated with a diastolic opening snap, not systolic click, and the associated diastolic murmur is low pitched and rumbling. Patent ductus arteriosus produces a continuous “machinery” murmur and is not associated with a click. Bicuspid aortic valves can cause sudden cessation of valve opening (which creates a systolic click), and are often associated with significant regurgitation. Findings of chronic aortic regurgitation with LV volume overload include an enlarged and laterally displaced LV apical beat, wide pulse pressure, and an S3.ReferencesBonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2008;52:e1-142.A 46-year-old man presents to the cardiovascular clinic with 2 months of stable exertional chest pain. He has a known history of hypertension and tobacco abuse. His ECG reveals normal sinus rhythm without ST or T changes, and his physical examination is unrevealing. He undergoes an ECG exercise stress test using a Bruce protocol and he exercises for 9 minutes. He reaches 100% of his maximum age-predicted heart rate without electrocardiographic evidence of ischemia.Which of the following is the closest approximation of his risk of cardiac death or MI over the next year?A.<1.0%. B.5%.C.15%.D.20%.E. 30%The correct answer is A.? This patient presents with stable chest pain and undergoes a normal and adequate stress ECG. He has no high-risk findings on his stress ECG. The exercise ECG is a well-established, inexpensive procedure that is appropriate for screening patients with suspected coronary artery disease when there are no baseline abnormalities on the resting ECG. Patient gender, age, coronary risk factors, and type of chest pain help determine the pretest probability of disease and the diagnostic accuracy. Some data regarding prognosis can also be obtained. One method uses the Duke exercise treadmill score. It is a number derived from the exercise time (in minutes on a Bruce protocol) minus (5 x the maximal ST depression in mm) minus (4 x the exercise angina score [0 = none, 1 = nonlimiting, 2 = limiting]). Low risk is exemplified by a score ≥5, moderate risk by a score of -10 to +4, and high risk ≤ -11). In this situation, the score is 9 and his prognosis is excellent. The addition of exercise SPECT or echocardiography has been shown to help further refine the prognostic value, but is not necessary in this situation. ReferencesHachamovitch R, Berman DS, Shaw LJ, et al. Incremental prognostic value of myocardial perfusion single photon emission computed tomography for the prediction of cardiac death. Circulation 1998;97:535-43. Mark DB, Shaw LJ, Harrell FE Jr, et al. Prognostic value of a treadmill score in outpatients with suspected coronary artery disease. N Engl J Med 1991;325:849-53. ? A 75-year-old woman presents for preoperative cardiac evaluation prior to undergoing a left knee replacement. She has a history of hypertension, adult-onset diabetes, and hyperlipidemia, and has degenerative arthritis of her left knee that has limited her ambulation. Over the past several months, she has noted dyspnea on exertion that now occurs after walking short distances in her house, and has developed mild pedal edema. Her medications include hydrochlorothiazide and metformin. Her blood pressure is 142/90 mm Hg, heart rate is 88 bpm, and oxygen saturation is 96% on room air. Her JVP is 8 cm H2O. Lungs are clear aside from faint bibasilar crackles. Her point of maximal impulse is in the sixth intercostal space at the anterior axillary line. There is a faint holosystolic murmur at the apex, and a soft S4 is appreciated. There is 2+ bipedal edema. Labs are notable for hemoglobin of 12 g/dl and a creatinine of 1.7 mg/dl. Her ECG reveals normal sinus rhythm, left-axis deviation, left atrial enlargement, and LV hypertrophy voltage. Which of the following is the best management strategy for this patient?A.Start beta-blocker and proceed with knee surgery.B.Start ACE-I and proceed with knee surgery.C.Insert a pulmonary arterial catheter and proceed with knee surgery.D.Cancel surgery to determine etiology and treatment of heart failure. E. nitroglycerine? patch & proceed with surgery The correct answer is D.? This patient has evidence of new-onset heart failure, and elective surgery should be cancelled until the mechanism of heart failure is defined and the condition is treated and stabilized. She has features that could be consistent with either systolic dysfunction (i.e., point of maximal impulse is displaced, soft mitral regurgitation murmur is present) or diastolic dysfunction (elderly female with hypertension, diabetes, and an S4 gallop), and clarification of her LV function with echocardiography is indicated. Institution of beta-blocker and/or ACE-I may eventually be indicated; however, these agents need to be started carefully in patients with new-onset congestive heart failure, and renal insufficiency and clinical parameters (i.e., blood pressure, congestive heart failure, renal function) monitored. Stress testing is reasonable in patients with ischemic symptoms, but is not the primary testing modality in patients with new congestive heart failure. ?? A 70-year-old man presents to the emergency department after experiencing several shocks from his ICD. He had just come home from a brisk evening walk, as he usually does for exercise, when he noticed his heart seemed to be faster than usual, and then he suddenly experienced an abrupt “kick,” which he realized was his defibrillator firing. Six other shocks then occurred in rapid succession. He did not lose consciousness and he called 911 immediately. His past history includes coronary artery disease with an anterior wall MI 5 years ago, resulting in systolic heart failure with an LVEF of 30%. A dual-chamber ICD was implanted 2 years ago for primary prevention of sudden cardiac death, and his last device check was 2 months ago, where he was told “everything was fine.” He had a shock last year from his device. His other medical history includes hypertension and type 2 diabetes. His medications include aspirin 81 mg daily, clopidogrel 75 mg daily, carvedilol 25 mg twice daily, lisinopril 20 mg daily, and glyburide 5 mg daily. On examination, his blood pressure is 130/60 mm Hg and heart rate is 135 bpm. His jugular venous pulse is modestly elevated at 8 cm H20, his lung sounds are clear, and heart sounds show a single S1, a paradoxically split S2 without murmur. The device is well healed in the left chest. An ECG is shown (Figure 1). While speaking with him, you see him jerk again with an ICD shock apparent on the telemetry monitor, which results in about 2 beats of sinus rhythm, and then tachycardia resumes. He is alert throughout and anxious.Which of the following should be your next course of action?A.Sedate and externally cardiovert.B.Place a magnet over the defibrillator. C.Initiate IV esmolol.D.Call for device interrogation and reprogramming.E. oral Cordarone The correct answer is B.? This patient presents with ventricular tachycardia that is hemodynamically tolerated. He is being shocked multiple times by his ICD and the first course of action should be to stop the device from delivering shocks, which is done by placing a magnet. A magnet will suspend detection, and thus, the delivery of therapies from an ICD. If ventricular tachycardia suddenly becomes hemodynamically compromising, the magnet can be removed. The next steps in treatment after the magnet is placed should be focused on suppressing the re-initiation of ventricular tachycardia, which can include administration of amiodarone, beta-blockade, and ablation. The device could be reprogrammed as well, to fire at a faster tachycardia rate. External cardioversion is of no benefit, as the problem is that ventricular tachycardia continues to reinitiate after successful cardioversion from the device. ReferencesZipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol 2006;48:e247-346.A 31-year-old woman is 6 days postpartum and evaluated in the emergency department for a complaint of severe anterior chest pain. She appears anxious and complains of chest discomfort that began the previous hour, which is associated with nausea. She denies shortness of breath. Her right upper extremity and left upper extremity blood pressure is 150/65 and 161/67 mm Hg, respectively. The patient’s ECG reveals 2 mm ST-segment elevation in leads II, III, and aVF and is otherwise significant for sinus tachycardia at a rate of 115 bpm. Plain roentgenogram reveals mild cardiomegaly without evidence of mediastinal widening or pulmonary edema.Which of the following is the next most appropriate step in the patient’s management?A.Initiate therapy with IV esmolol titrated to a heart rate of 60 bpm and request an emergency contrast CT scan of the chest and abdomen. B.Initiate therapy with IV unfractionated heparin, including a loading bolus, and perform an emergency transthoracic echocardiogram to assess right ventricular function.C.Initiate therapy with IV unfractionated heparin, including a loading bolus, aspirin 325 mg by mouth, 0.5 mg nitroglycerin tablet sublingual, and activate the cardiac catheterization laboratory.D.Prepare for emergency pericardiocentesis.The correct answer is A.? Option A is the correct answer because the clinical information provided is most consistent with acute aortic dissection. Although acute aortic dissection is overall uncommon as a complication of pregnancy, nearly 50% of all dissections in women younger than 40 years of age occur in the peripartum time period. Therefore, a low clinical index of suspicion for aortic dissection is necessary in the management of any woman in the peripartum period presenting with symptoms or clinical signs that may be consistent with aortic dissection (such as severe chest pain in this patient). The initial clinical management of suspected aortic dissection involves short-acting IV β-adrenergic receptor antagonist therapy and a diagnostic imaging study, such as a CT scan of the chest and abdomen. Options B and C describe the appropriate management for pulmonary embolism and spontaneous coronary dissection, respectively. Despite the association of pulmonary embolism with pregnancy, in the absence of shortness of breath, hemodynamically significant pulmonary embolism is unlikely and may be evaluated further, if necessary, pending exclusion of aortic dissection. Cardiac catheterization to evaluate for acute coronary syndrome or spontaneous aortic dissection may be tempting given the presence of chest pain and ST-segment elevations on ECG. However, type A aortic dissection can involve the right coronary artery to produce signs of inferior myocardial ischemia. Owing to the potentially catastrophic consequences of anticoagulation and instrumentation of the aorta in patients with aortic dissection, it is critical to consider the possibility that aortic dissection is present even in the presence of electrocardiographic features of myocardial injury. In this patient, hypertension (rather than hypotension), severe chest pain, and blood pressure dissymmetry between the upper extremities suggests aortic dissection. Option D is incorrect because there is no clinical evidence to support the presence of cardiac tamponade. Furthermore, hemopericardium due to acute, proximal aortic dissection requires surgical treatment. ReferencesAziz F, Penupolu S, Alok A, Doddi S, Abed M. Peripartum acute aortic dissection: a case report and review of the literature. J Thorac Dis 2011;3:65-67. Braverman AC. Acute aortic dissection: clinician update. Circulation 2010;122:184-8. ?A 72-year-old man presents to the cardiology clinic for evaluation of a cardiac murmur. He has a history of AS, with echocardiography 1 year ago showing an aortic velocity of 3.7 m/s, mean gradient of 33 mm Hg, and valve area 1.1 cm2. He currently denies cardiac symptoms, but has cut back on his activities due to “getting older.” His past medical history is also positive for hypertension and hypercholesterolemia.Current medications include a beta-blocker and a statin. Physical examination shows a blood pressure of 142/86 mm Hg and pulse of 68 bpm. There is a 4/6 systolic ejection-type murmur at the base with radiation to the carotids. Repeat echocardiography shows an aortic velocity of 4.3 m/s, mean gradient of 44 mm Hg, and valve area 0.8 cm2.Which of the following is the most appropriate next step in management?A.Start an angiotensin-converting enzyme inhibitor.B.Perform an exercise stress test.? (Incorrect)C.Obtain a serum BNP level.D.Schedule an annual follow-up echocardiogram.E.Refer for AVR. The correct answer is E.? This patient has severe symptomatic AS, so prompt AVR is indicated. Although he denies overt symptoms of angina, HF, or syncope, he does endorse decreased exercise tolerance, which is the typical early symptom of AS. This meets a Class I indication for AVR. He also has evidence of rapid hemodynamic progression compared with the typical progression rates of an increase in aortic velocity of 0.3 m/s per year and a decrease in valve area of 0.1 cm2 per year. Severe AS with evidence of rapid progression is a Class IIb indication for AVR. Additional medical therapy for hypertension would be appropriate if he were asymptomatic, although a low starting dose and slow upward titration is critical when AS is present to avoid excessive vasodilation and hypotension. An exercise stress test or a serum BNP level might be helpful if symptom status were unclear, but stress testing is hazardous once symptoms are present, as in this patient. In addition, given his history, the findings on stress testing or the BNP level would not alter management at this point. Reassurance with annual follow-up is reasonable with asymptomatic AS, even when severe, but the frequency of follow-up should reflect both disease severity and the rate of progression, so a shorter interval would be appropriate if this patient were asymptomatic.ReferencesBonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol 2006;48:e1-148.Vahanian A, Baumgartner H, Bax J, et al. Guidelines on the management of valvular heart disease: The Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology. Eur Heart J 2007;28:230-68.A 50-year-old asymptomatic woman is evaluated for a history of heart murmur detected on annual physical examination. She has a long history of heart murmur, but has not experienced shortness of breath, chest discomfort, or palpitations with normal activities. Blood pressure is 125/75 mm Hg, pulse rate is 78 bpm and regular, and respiration rate is 14 breaths/minute. Lungs are clear to auscultation bilaterally. Her cardiac examination shows normal jugular venous pressure. There is a regular rhythm and a grade 3/6 holosystolic murmur at the apex that radiates to the axilla.Electrocardiography shows sinus rhythm with left-axis deviation. Transthoracic echocardiography shows normal wall thickness of the left ventricle with an ejection fraction of 65%. The left ventricular end-diastolic diameter is 55 mm and end-systolic diameter is 36 mm. There is posterior mitral valve prolapse with severe MR present. The mitral leaflets are not calcified. The left atrium is moderately dilated with area of 28 mm2. The right ventricle is mildly enlarged with normal contractility. There is mild tricuspid regurgitation with an estimated right ventricular systolic pressure of 64 mm Hg.Which of the following is the appropriate treatment for this patient?A.Begin enalapril.B.Begin sildenifil.C.Mitral valve replacement surgery.D.Mitral valve repair surgery.E. Mitral Valve Clip Procedure The correct answer is D.? This patient should undergo mitral valve repair surgery. Although she has severe asymptomatic MR with normal left ventricular systolic function, there is evidence of pulmonary hypertension. Indications for surgical intervention for MR include: 1) left ventricular ejection fraction below 60%, 2) left ventricular end-systolic diameter >40 mm, 3) severe pulmonary hypertension at rest (pulmonary artery systolic pressure >50 mm Hg) or during exercise (>60 mm Hg), or 4) new onset of atrial fibrillation.Enalapril or other vasodilators theoretically will reduce left ventricular afterload and regurgitant volume, and may improve acute hemodynamic status in patients with acute, severe MR. However, oral vasodilator treatment has not been shown to reduce progression of chronic MR or cardiac events.Although the patient has pulmonary hypertension, the presence of left-sided heart disease with elevated left atrial pressure is the likely cause, rather than idiopathic pulmonary arterial hypertension. Treatment with a pulmonary vasodilator, such as sildenifil, may worsen heart failure symptoms by increasing pulmonary blood flow with fixed, elevated pulmonary venous pressure.Mitral valve repair rather than replacement has clinical benefits, including higher left ventricular ejection fraction after surgery and better long-term survival. In addition, repair will not require long-term anticoagulation and its associated risks compared with mechanical valve replacement, which is commonly performed for the mitral location because of its longer durability. The likelihood of successful repair is dependent on the mitral valve anatomy as well as surgical operator and center experience.ReferencesBonow RO, Carabello BA, Chatterjee K, et al. 2008 focused update incorporated into the ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to revise the 1998 guidelines for the management of patients with valvular heart disease). Endorsed by the Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. J Am Coll Cardiol 2008;52:e1-e142.?? A 52-year-old woman presents with fever and malaise. She has no significant medical history and lives alone. She reports feeling well until 3 weeks ago, when she began to notice night sweats, diffuse muscle aches, and anorexia. She denies having any recent surgeries or dental procedures. A transthoracic echocardiogram demonstrates mild aortic valve regurgitation with an 8 mm mobile mass attached to the ventricular surface of a bicuspid aortic valve.She is admitted to the hospital and empiric IV antibiotic therapy is started. Blood cultures reveal S epidermidis in three of four culture bottles collected over a 2-hour period. Her fever resolves on hospital day 4; however, she begins to complain of severe dyspnea. A repeat echocardiogram demonstrates that the mobile mass is smaller, but there is now moderate-to-severe AR with diastolic preclosure of the mitral valve.Besides continuing IV antibiotics, which of the following is the appropriate treatment strategy for this patient at this time?A.Add IV diuretics, and continue to monitor in hospital.B.Add beta-blocker therapy and continue to monitor in hospital.C.Arrange to implant an intra-aortic balloon pump to alleviate her heart failure symptoms.D.Refer for surgical replacement of the aortic valve. E. Add ACE-I to the regimen The correct answer is D.? This patient has developed moderate-to-severe aortic valve regurgitation due to native valve endocarditis. Her symptoms and echocardiogram are consistent with acute decompensated heart failure with elevated LV diastolic pressures. This prematurely closes the mitral valve before systole (before the QRS interval on the ECG) and is referred to as preclosure. This is an ACC/AHA Class I1 indication for surgical intervention to replace her aortic valve.Diuretics would offer only brief symptomatic relief. Beta-blocker therapy has not been shown to improve outcomes in patients with acute significant AR, and a slowing of the heart rate might increase the degree of AR per beat. An intra-aortic balloon pump is contraindicated in the setting of significant aortic valve regurgitation.ReferencesBonow RO, Carabello BA, Chatterjee K, et al. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing Committee to Revise the 1998 guidelines for the management of patients with valvular heart disease) developed in collaboration with the Society of Cardiovascular Anesthesiologists endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons. J Am Coll Cardiol 2006;48:e1-148.??? Which of the following patients with an LVEF of 25% would be most appropriate to refer for a pulmonary artery catheterization (Swan-Ganz)?A.A 60-year-old man with an LVEF of 25% is admitted with shortness of breath and is found to have blood pressure 130/80 mm Hg, pulse 90 bpm, and JVP of 14 cm with 2+ leg edema and warm extremities, with creatinine 1.2.B.A 20-year-old man is referred for cardiac transplantation due to his low LVEF despite 6 months of beta-blocker therapy. He reports mild fatigue while playing racquetball and his examination shows blood pressure 120/80 mm Hg, pulse 72 bpm, JVP <8 with no hepatojugular reflux, and there is no S3. Extremities are warm to touch, with no edema.C.A 30-year-old woman is admitted to the hospital with shortness of breath and a blood pressure of 90/70 mm Hg. Following 2 days of intravenous diuretics, her examination is notable for JVP of 16 cm and 2+ leg edema, with a systolic blood pressure of 78 mm Hg. Her creatinine has increased from 1.6 to 2.5, with diuresis. D.A 40-year-old woman with asthma and heart failure is admitted to the hospital. Her examination is notable for blood pressure 150/80 mm Hg; pulse 110 bpm and regular; lungs with diffuse expiratory wheezes; JVP <8 cm with no hepatojugular reflux; cardiac auscultation with S12 and no S3; legs with no edema and are warm to touch.E.An 85-year-old man with a 30-year history of diabetes previously received laser photocoagulation therapy of diabetic retinopathy, and has ongoing leg pain from neuropathy. He now presents with shortness of breath, has a blood pressure of 200/100 mm Hg, anasarca, and a creatinine of 10.The correct answer is C.? The ACCF/AHA 2009 Focused Update of the 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults state that “invasive hemodynamic monitoring should be performed to guide therapy in patients who are in respiratory distress or with clinical evidence of impaired perfusion in whom the adequacy or excess of intracardiac filing pressures cannot be determined from clinical assessment.” Although the patient has evidence of elevated JVP and leg edema, she has developed systemic hypotension and worsening renal function. At this point, it will be important to determine with certainty whether her LV filling pressures are elevated or not (i.e., whether she is one of the ~20% of subjects where the right-sided filling pressures are not concordant with the LV filling pressures). Patient A has a hemodynamic profile consistent with volume overload and adequate perfusion, and a right heart catheterization is not indicated at this point. Patient B, although referred for cardiac transplantation, has a high exercise capacity and a normal examination; there is no indication for right heart catheterization. Patient D has an examination suggesting absence of congestion and adequate perfusion, and likely has an asthma exacerbation. Patient E presents with renal failure likely on the basis of progressive diabetic nephropathy. In both cases, invasive measurement of hemodynamics would not be warranted at this point.ReferencesHunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. J Am Coll Cardiol 2009;53:e1-e90.? A 65-year-old man with a longstanding ischemic cardiomyopathy and LVEF 20% by an echocardiogram obtained 1 month ago, was admitted to the hospital yesterday for increased shortness of breath over the last 3 weeks. You are evaluating him in consultation with his internist. Overnight he had made 1 liter of urine in response to diuretic therapy. On examination, you find him to be in no acute distress at rest, blood pressure 110/70 mm Hg, pulse 96 bpm and regular, and his BMI is 38 kg/m2. He reports persistent shortness of breath when ambulating in the corridors or in the supine position, the latter requiring two pillows to allow him to breathe comfortably. The remainder of his examination is notable for JVP estimated to be 14 cm, S12 with no S3 or murmur, a benign abdomen with no hepatomegaly, and extremities which are entirely free of edema and are warm to touch. His mental status is normal. Laboratory studies today include: sodium 140, blood urea nitrogen 55, creatinine 1.9 (stable from admission), and hematocrit 34. Admission BNP was 75. A chest X-ray shows cardiomegaly with no evidence of pulmonary edema, pleural effusions, or infiltrates.At this point, which of the following is the most appropriate therapy to recommend?A.Administration of normal saline at 75 cc/hour for possible volume depletion.B.Administration of IV Lasix 80 mg bid for presumed acute on chronic systolic heart failure. C.Administration of IV Lasix 80 mg bid plus an infusion of dobutamine 2.5 mcg/kg/min to provide inotropic support for treatment of acute on chronic systolic heart failure complicated by renal insufficiency.D.Order an echocardiogram and base further therapeutic decisions about the need for diuretics or saline administration on the E/e’ ratio.E.Schedule for a right heart catheterization and adjust therapy based on invasively measured hemodynamics.The correct answer is B.? The patient presents with volume overload confirmed by the finding of elevated JVP and orthopnea. Although he has evidence of renal insufficiency, the finding of elevated JVP and orthopnea strongly suggests volume overload, not volume depletion. Thus, a normal saline infusion is not appropriate. Elevated central venous pressures have been associated with the cardiorenal syndrome. By examination, the patient would be classified as Stevenson profile B (“warm and wet”). In such cases, there would be no need to include inotropic therapy in the initial treatment strategy, as the cardiac index is likely normal. Evidence of adequate perfusion includes a normal pulse pressure and that his extremities are warm, not cold, to touch. Recent data have suggested that the E/e’ may not be a reliable method to assess filling pressures in advanced systolic heart failure. Finally, right heart catheterization would not be warranted at this point, as his hemodynamic status can be assessed reliably with the available noninvasive methods, and the ESCAPE trial demonstrated no benefit of therapy tailored to hemodynamic goals. The ACC/AHA 2009 heart failure guidelines gave a Class III recommendation for routine right heart catheterization in normotensive subjects who are responding to diuretic therapy.ReferencesHunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. J Am Coll Cardiol 2009;53:e1-e90.Drazner MH, Hellkamp AS, Leier CV, et al. Value of clinician assessment of hemodynamics in advanced heart failure: the ESCAPE trial. Circ Heart Fail 2008;1:170-7.Nohria A, Lewis E, Stevenson LW. Medical management of advanced heart failure. JAMA 2002;287:628-40.Mullens W, Borowski AG, Curtin RJ, Thomas JD, Tang WH. Tissue Doppler imaging in the estimation of intracardiac filling pressure in decompensated patients with advanced systolic heart failure. Circulation 2009;119:62-70.??? HEart Failure prognosis correlates MOST STRONGLY with which of the following?A.Impaired renal function. B.Resting EF.C.NYHA class.? D.Genetic predisposition.E.Diastolic dysfunction.The correct answer is A.? Hillege et al reported on 1,906 patients with advanced HF in the PRIME II (Second Prospective Randomized Study of Ibopamine on Mortality and Efficacy in Heart Failure) study.1 Their data demonstrated that impaired renal function, as determined by the calculated glomerular filtration rate, was a stronger predictor of mortality in this cohort than reduced ejection fraction and NYHA class. Impaired renal function was furthermore associated with increased levels of N-terminal atrial natriuretic peptide, a well-known risk factor for cardiovascular disease. Patients with a glomerular filtration rate <44 ml/min had approximately three times the mortality risk (relative risk, 2.85; p < 0.0001) compared to those with a glomerular filtration rate >76 ml/min. Importantly, low glomerular filtration rates predicted HF mortality independent of decreased EF and NYHA class.Data linking genetic abnormalities to HF mortality are preliminary and require further investigation and validation, thus choice D is incorrect. Patients with isolated diastolic dysfunction may have similar or lower mortality than patients with systolic dysfunction. Given that renal dysfunction confers higher mortality risk than systolic function, as reported by Hillege et al., diastolic dysfunction would not correlate with higher HF mortality, and thus option E is incorrect.ReferencesHillege HL, Girbes AR, de Kam PJ, et al. Renal function, neurohormonal activation, and survival in patients with chronic heart failure. Circulation 2000;102:203-10.?? A 73-year-old woman with hypertension, diabetes, and HF with preserved EF presents to the emergency department with a 2-week history of progressive dyspnea on exertion, weight gain, and lower extremity edema. A diagnostic cardiac catheterization 1 year earlier demonstrated normal coronary arteries. Her outpatient medications include lisinopril 5 mg once daily, metoprolol succinate 100 mg once daily, furosemide 40 mg once daily, and metformin 500 mg twice daily.Her physical examination is notable for a jugular venous pressure of 14 cm of water, bibasilar inspiratory rales, and 2+ lower extremity edema to the knees bilaterally. Her chest X-ray shows mild cardiomegaly with pulmonary vascular redistribution and a small left pleural effusion. She is admitted to the hospital service with a diagnosis of ADHF.Risk stratification during a HF hospitalization helps to predict acuity of illness and to plan for discharge. Which of the following two clinical and/or laboratory parameters obtained at the time of admission would place this patient at the highest risk of inpatient mortality?A.Systolic blood pressure 160 mm Hg and oxygen saturation <92% on room air.B.Systolic blood pressure 100 mm Hg and hematocrit 32%.C.Systolic blood pressure 100 mm Hg and serum creatinine 2.2 mg/dl.? D.Heart rate 100 bpm and serum sodium 132 mg/dl.E.Heart rate 100 bpm and blood urea nitrogen 40 mg/dl.The correct answer is C.? Clinical information obtained at the time of admission can help to predict outcomes during the hospitalization and following discharge. The ADHERE registry1 found that the single best predictor for mortality was an elevated blood urea nitrogen (≥43 mg/dl), followed by low systolic blood pressure (<115 mm Hg) and high serum creatinine (≥2.75 mg/dl). A more recent model from the OPTIMIZE-HF registry2 also found systolic blood pressure (≥100 mm Hg) and serum creatinine (≥2.0 mg/dl) to be powerful predictors of in-hospital mortality (Figure 1).Hypertension (option A) is associated with improved outcomes. Anemia (option B) and hyponatremia (option D) are common in patients with advanced HF, and predict adverse long-term outcomes. Tachycardia (options D and E) has not been shown to predict either in-hospital or post-discharge mortality in patients with ADHF.ReferencesFonarow GC, Adams KF, Jr., Abraham WT, Yancy CW, Boscardin WJ. Risk stratification for in-hospital mortality in acutely decompensated heart failure: classification and regression tree analysis. JAMA 2005;293:572-80.Abraham WT, Fonarow GC, Albert NM, et al. Predictors of in-hospital mortality in patients hospitalized for heart failure: insights from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF). J Am Coll Cardiol 2008;52:347-56.A 68-year-old woman presents to the emergency room with severe orthopnea for the past 12 hours. She has a history of hypertension, osteoarthritis, and borderline diabetes mellitus. Exam revealed irregular rate and rhythm with heart rate 115 bpm, blood pressure 190/100 mm Hg, jugular pressure 14 cm, and body mass index 38 kg/m2. Chest auscultation showed bilateral rales, while precordial exam revealed an irregular and rapid heart rate with distant heart sounds and no discernible gallop. The patient is given intravenous furosemide, diltiazem, and nitroglycerin infusions, with prompt improvement in symptoms.Forty-eight hours later, she is now on oral losartan, diltiazem, aspirin, and furosemide. Her heart rate is now irregular at 70 bpm, blood pressure is 130/65 mm Hg, venous pressure is normal, but she still complains of moderate dyspnea on exertion.Which of the following would you recommend?A.Transesophageal echocardiogram-guided cardioversion. B.Switch diltiazem to atenolol.C.Switch losartan to lisinopril.D.Nocturnal supplemental oxygen.E.Recommend bariatric surgery.The correct answer is A.? This is a typical presentation of acute hypertensive pulmonary edema in a woman with HFpEF. She presented in rapid atrial fibrillation, which may have precipitated the decompensation. These patients typically respond fairly quickly with good control of blood pressure and ventricular response. Atrial fibrillation is extremely common in HFpEF, noted in 30-40% of patients. In contrast to HFrEF, there are no trials comparing rate versus rhythm control in HFpEF, but because there is potential for increased reliance on atrial systole in the setting of diastolic dysfunction, ACCF/AHA guidelines recommend strong consideration of cardioversion for atrial fibrillation (Class IIb, Level of Evidence C). Because this is the first episode, the likelihood to have a durable restoration of sinus rhythm is enhanced. There is no evidence to support atenolol over diltiazem or lisinopril over losartan in HFpEF, as no treatments have been prospectively shown to be effective in large randomized trials. The patient’s body habitus and atrial fibrillation increase the risk of sleep disordered breathing, and this should be evaluated, but she should not be started on oxygen in the absence of a diagnosis, particularly if obstructive sleep apnea is present. There is hope that weight loss with interventions such as bariatric surgery may improve cardiovascular function, but there are not conclusive data at this point, and certainly other lifestyle interventions should be exhausted first.ReferencesHunt SA, Abraham WT, Chin MH, et al. 2009 focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. J Am Coll Cardiol 2009;53:e1-e90.From AM, Borlaug BA. Heart failure with preserved ejection fraction: pathophysiology and emerging therapies. Cardiovasc Ther 2011;29:e6-e21.Gandhi SK, Powers JC, Nomeir AM, et al. The pathogenesis of acute pulmonary edema associated with hypertension. N Engl J Med 2001;344:17-22.A 30-year-old male exercises daily. Recently, he has noted episodes of rapid and irregular heart palpitations shortly after finishing a workout. His exercise program consists of aerobics and weight lifting that lasts for more than 1 hour every day.Diagnostics and physical exam: Patient is in excellent health; physical exam including blood pressure is normal. Holter monitor recording reveals several short bursts of AF at 160 bpm; the longest bout lasts for 15 seconds. Resting electrocardiogram (ECG) and echocardiographic examination are normal. Patient does not have a history of AF.Which of the following anticoagulation protocols should a patient with a CHADS2 score of zero receive?A.No anticoagulation.? B.Aspirin 325 mg/day.C.Aspirin 162 mg/day.D.Warfarin at international normalized ratio (INR) 1.6-2.0.E.Warfarin at INR 2.0-3.0.The correct answer is A.? A patient with a CHADS2 score of 0 does not need anticoagulation or at most low-dose aspirin might be prescribed.ReferencesFuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol 2006;48:854-906.= Required for completion= CompleteBACKNEXTPROGRESSAn 81-year-old man was admitted to the hospital for laparoscopic cholecystectomy. His past medical history includes high blood pressure and hypercholesterolemia. Postoperatively, the patient was noted to have been in normal sinus rhythm, with a heart rate of 35 bpm while sleeping. He denies any symptoms and shows a rise in heart rate to 70-80 bpm while walking in the hospital. His current medications include aspirin 325 mg/day, metoprolol tartrate 25 mg twice a day, and simvastatin 20 mg a day.Which of the following is the most appropriate course of treatment for this patient’s bradycardia?A.Discontinue metoprolol.B.Continue current medications.C.Implant a dual-chamber pacemaker.D.Implant a single-chamber pacemaker.E.Perform an electrophysiologic study.The correct answer is B.? Based on current guidelines for treatment of sinus node dysfunction, it is a Class III indication to implant a permanent pacemaker for sinus node dysfunction in asymptomatic patients, especially for patients also receiving a rate slowing medication. This patient has sinus bradycardia and is on metoprolol while sleeping, which is not causing symptoms and does not require specific treatment or change in current medications. There is no need for further evaluation.?A 65-year-old politician male presents to the emergency room after a fall with significant head trauma. Head computed tomography (CT) demonstrates a moderate-sized subdural hematoma. He undergoes surgery for evacuation of the bleed due to concerns for increased intracranial pressure. On the third hospital day, he complains of difficulty breathing as well as left lower extremity pain and swelling. His blood pressure is 120/75 mm Hg. Heart rate is 97 bpm. Oxygen saturation is 94% on 2 liters of oxygen via nasal cannula. Examination is remarkable for unchanged neurologic exam with tenderness in the left calf. Doppler imaging reveals a left common femoral vein thrombus, and a chest CT demonstrates a right upper pulmonary artery thrombus. Which of the following is the most appropriate therapy for this patient?A.Inferior vena cava filter placement. B.Pulmonary embolectomy.C.Unfractionated heparin (UFH).D.Warfarin.E.Tissue plasminogen activator (t-PA)The correct answer is A.? Systemic anticoagulation (choices C, D, and E) is contraindicated in this patient because she has an intracranial bleed. No trials to date have studied dabigatran specifically for treatment of acute pulmonary embolism, and therefore, it is not currently approved for this indication. Current guidelines recommend use of inferior vena cava filters only for patients with a contraindication to anticoagulation (Recommendation 4.6.2; evidence grade 1C) or for patients undergoing pulmonary thromboembolectomy for chronic thromboembolic pulmonary hypertension (Recommendation 6.1.3; evidence grade 2C).1 Due to the significant risks of anticoagulation in this patient, placement of an inferior vena cava filter (choice A) is the most appropriate therapy. Pulmonary embolectomy (choice B) for initial treatment of acute pulmonary embolism should be reserved for select critically ill patients.1 ReferencesKearon C, Kahn SR, Agnelli G, Goldhaber S, Raskob GE, Comerota AJ. Antithrombotic therapy for venous thromboembolic disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest 2008;133:454S-545S.?? A 52-year-old woman with hypertension presents to the emergency department with the acute onset of chest pain and markedly elevated blood pressure. You discover that she is not having an acute ST elevation myocardial infarction, but are concerned she may be having an aortic dissection.Based on the results of the imaging study (Figure 1), which of the following do you recommend as the next best step in management of this patient?A.Medical therapy to reduce her blood pressure and repeat imaging in 1 week.B.Medical therapy to reduce her blood pressure and immediate surgical repair. C.Medical therapy to reduce her blood pressure and surgical repair once her hypertension is under control.D.Medical therapy to reduce her blood pressure and endovascular stent placement.E.Medical therapy alone.Figure 1The correct answer is B.? The image shows a Stanford type A or DeBakey type I aortic dissection. Therapy for this type of dissection is immediate surgical repair, because mortality increases with time; therefore, options A, C, D, and E are incorrect.The patient is a 58-year-old male with witnessed sudden collapse in Suvarnbhumi airport. A bystander performed CPR and an automated external defibrillator (AED) was obtained and applied. EMS was simultaneously alarmed. The AED detected a shockable rhythm and a single shock was performed. The AED detected a nonshockable rhythm and additional chest compressions were begun. EMS arrived and detected a pulse. Chest compressions were halted and a pulse of 110 with a blood pressure (BP) of 150/90 was documented. However, the patient remained unresponsive. He is transported to the nearest hospital. The ECG in the ED shows only sinus tachycardia.Which of the following is the optimal post-resuscitation care?A.Begin therapeutic hypothermia in the ED with rapid iced-saline infusion (1-2 liters), admit to ICU and continue therapeutic hypothermia with a commercial mechanical surface cooling system to a goal of 33°C for 24 hours. Rewarm slowly (0.3-0.5°C/h) after 24 hours.B.Provide comfort care and prepare the family for an inevitable poor outcome (i.e., either death or significant and incapacitating anoxic brain injury).C.Call the catheterization laboratory for emergency coronary angiography and potential PCI. Afterwards admit the patient to the ICU for consideration of therapeutic hypothermia induction.D.Begin therapeutic hypothermia in the ED while simultaneously calling the catheterization laboratory for emergency coronary angiography. Attempt PCI for any acute coronary occlusion or unstable, high grade presumed culprit lesion thought responsible for the cardiac arrest. Continue hypothermia in the catheterization laboratory and later in the ICU, to a goal of 33°C for 24 hours. Rewarm slowly (0.3-0.5 °C/h) after 24 hours. The correct answer is D.? This patient is ideal for aggressive post-resuscitation care. He had a witnessed VFCA, received immediate bystander CPR, and received early defibrillation with an AED. His time to ROSC was short and he was hemodynamically stable upon arrival at the ED. He remained comatose upon presentation and hence was a good candidate for therapeutic hypothermia to preserve central nervous system function and improve his chance for meaningful long-term survival. Such hypothermia should be begun immediately upon his arrival and continued for 24 hours, with a goal of 33°C.His etiology of circulatory collapse is almost certainly cardiac, as manifested by its sudden, unexpected occurrence. He deserves a careful search for an acute coronary ischemic event as the precipitating cause of this cardiac arrest. This is best accomplished by emergency coronary angiography even though his post-resuscitation ECG does not show ST elevation. One in four of such patients are identified as having an acutely occluded or culprit coronary lesion that is responsible for their cardiac arrest, which can be treated with emergent coronary angiography and PCI.Question18of 25A previously healthy 30-year-old man presents to the emergency department with 2 days of fever, and chest pain with radiation to his left jaw, left arm, and back. He remembers having a sore throat several days prior to his presentation. He also has shortness of breath due to splinting. The pain is worse when lying on his back. He has taken ibuprofen and acetaminophen at home with minimal impact on his symptoms. His vitals on admission include a blood pressure of 125/85 mm Hg, pulse of 105 bpm, temperature of 101.2 degrees Fahrenheit, and a respiratory rate of 22 breaths/minute. His admission labs are significant for a white blood cell count of 30,000 with 29% bands, a creatinine of 1.5 mg/dl, and a troponin of 1.3 ng/ml. Broad spectrum antibiotics are begun. His admission chest X-ray, chest CT, 12-lead ECG, and a parasternal long-axis image from his transthoracic echocardiogram are shown (Figures 1, 2, 3, 4). Which of the following is the next best step in his management? A.Left heart catheterization.B.IV diuretics.C.IV steroids.D.Pericardiocentesis.E.Thoracic surgery consultation. Figure 1Figure 2Figure 3Figure 4The correct answer is E.? This patient presents with bacterial pericarditis, likely due to anaerobic organisms, which have spread from an infection in his neck. His ECG shows changes consistent with pericarditis. His chest X-ray shows a widened mediastinum and his chest CT shows mediastinal air in addition to mediastinitis. There is no obvious fluid collection to drain on his echocardiogram; thus, the next best step in his management would be a surgical consultation for debridement/evacuation of his mediastinum.ReferencesBonow RO, Mann DL, Zipes DP, Libby P. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia: Saunders; 2011.Maisch B, Risti? AD. Practical aspects of the management of pericardial disease. Heart 2003;89:1096-103. ?? A 75-year-old woman is hospitalized for shortness of breath with chest pain. A pulmonary embolism is diagnosed and she is initiated on heparin. Several hours later, she becomes hypotensive and does not respond to a fluid bolus. One hour later, she collapses on the way to the bathroom and a code arrest is called. The monitor shows a slow, wide, complex rhythm at 35 bpm, without a pulse, and chest compressions are started. External pacing through the defibrillator patches is attempted, but there is no ventricular capture. Chest compressions have been ongoing for 4 minutes.Which of the following is the next step that should be taken?A.Administration of atropine 1 mg IV.B.Placement of a transvenous temporary pacing wire.C.Endotracheal intubation.D.Administration of epinephrine 1 mg IV. E.Thrombolytic therapy.The correct answer is D.? In PEA, the first administered drug is epinephrine. Vasopressin can be substituted for the first or second dose of epinephrine. A transvenous pacing wire would require undue interruptions in chest compressions, and should not be attempted prior to administration of a vasopressor agent, epinephrine. Atropine can be considered after epinephrine is given, but is unlikely to be of benefit.ReferencesNeumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation 2010;122:S729-67.??? A 48-year-old man presents to the emergency department with 3 hours of profound dyspnea and lightheadedness and 2 days of right leg pain and swelling. He has a history of diabetes and coronary artery disease status/post large anterior MI with a left ventricular ejection fraction of 30%. He is afebrile, but has a blood pressure of 70/30 mm Hg and an oxygen saturation of 84% on room air. His ECG demonstrates sinus tachycardia at 120 bpm and no other changes compared with a prior tracing. Chemistry panel, complete blood count, and coagulation tests are normal. Cardiac troponin T is 2 ng/ml (normal <0.2 ng/ml). His chest X-ray demonstrates cardiomegaly with clear lung fields. Contrast-enhanced chest CT demonstrates large bilateral main pulmonary emboli. He is immediately started on intravenous unfractionated heparin as a bolus followed by infusion.Based on the presentation and initial assessment, which of the following is the most appropriate next step in the management of this PE patient?A.Refer the patient for catheter-based embolectomy.B.Insert an IVC filter.C.Administer recombinant tissue-plasminogen activator 100 mg over 2 hours via a peripheral intravenous line. D.Refer the patient for open surgical pulmonary embolectomy. E.Continue systemic anticoagulation with unfractionated heparin.The correct answer is C.? Answer C is correct because the patient has suffered massive PE and is at increased risk of death from RV failure if reperfusion therapy is not instituted. He has no evidence of active bleeding, thrombocytopenia, or other contraindication to fibrinolytic therapy.Answers A and D are incorrect because the patient does not have any contraindications to fibrinolytic therapy. Catheter-based and surgical pulmonary embolectomy are generally reserved for patients with contraindications to fibrinolytic therapy or catheter-based techniques. Answer B is incorrect because IVC filter placement will not reverse the RV pressure overload that is resulting in RV failure and hypotension. Answer E is incorrect because systemic anticoagulation alone will not improve RV failure rapidly enough to avert further hemodynamic collapse and possibly death.ReferencesPiazza G, Goldhaber SZ. Fibrinolysis for acute pulmonary embolism. Vasc Med 2010;15:419-28.Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation 2011;123:1788-830.Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: Antithrombotic therapy and prevention thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012;141:e419s-94s.A 30-year-old man with known HCM and an implantable cardioverter-defibrillator (ICD) comes to your office because he wishes to run a marathon. He has no symptoms, and has not had any shocks since the ICD was implanted 5 years ago. Family history is negative for SCD, septal thickness by echo is 2.1 cm, and there is no LV outflow obstruction.Which of the following would be the proper recommendation according to the 36th Bethesda Conference recommendations?A.Since he is in a low-risk category, allow him to participate in the marathon.B.Because he has an ICD, allow him to participate in the marathon.C.Running a marathon is not recommended.D.No sports are allowed, even low-dynamic, low-static sports.E.All sports are allowed, provided genetic testing reveals a low-risk gene.The correct answer is C.? The 36th Bethesda Conference recommendations for participation in sports provide recommendations as to whether play is allowable for an athlete with a cardiac condition. The underlying cardiac pathology, and the physiology of the sport should be taken into consideration. As marathon running is a high dynamic sport (Class IC), the athlete would be at high risk for a cardiac event during this activity. Thus, it would not be allowed. In contrast, golf is considered low dynamic, and low static (Class IA), and would be allowed.Option A is not correct: An athlete with HCM would not be considered “low risk,” as the underlying substrate is arrhythmogenic, regardless of pharmacologic therapy or corrective surgery. The presence of an ICD has not yet been shown to protect against SCd under the conditions of athletic participation. Thus, option B is not correct. There is reason to believe that ICDs may not be effective under the conditions of a rigorous sport, where there are fluid and electrolyte shifts, and abnormally high levels of catecholamines. Option D is incorrect because Class IA sports like golf are allowed. The Bethesda Conference recommendations do not make a distinction between those HCM athletes who are genetically positive and those who are not. Thus, option E is not correct.ReferencesMaron BJ, Ackerman MJ, Nishimura RA, Pyeritz RE, Towbin JA, Udelson JE. Task Force 4: HCM and other cardiomyopathies, mitral valve prolapse, myocarditis, and Marfan syndrome. J Am Coll Cardiol 2005;45:1340-5.Lawless CE. Implantable cardioverter defibrillators in athletes: rationale for use and issues surrounding return to play. Curr Sports Med Rep 2008;7:86-92.Lawless CE. Return-to-play decisions in athletes with cardiac conditions: guidelines and considerations. In: Lawless CE, ed. Sports Cardiology Essentials: Evaluation, Management and Case Studies. 1st ed. New York: Springer Science+Business Media; 2010:387-401.????? A 25-year-old man is seen in your office for evaluation of a heart murmur. He notes that he has had a murmur for the past several years, and that his prior physician had told him that he had a “leaky valve” in his heart. He has not had an echocardiogram in years. He takes no medications other than antibiotics at the time of dental work. On physical examination, the patient is a well-appearing young man. He is tall in stature, at 6 feet 5 inches tall. He weighs 190 lbs. Blood pressure in both arms is 120/80 mm Hg, and his heart rate is 76 bpm. Oropharyngeal exam demonstrates slight arching of the palate. His lungs are clear to auscultation. Chest examination demonstrates a mild pectus excavatum. His point of maximal cardiac impulse is displaced slightly. He is in a regular rate and rhythm, with a normal first and second heart sound. He has a soft mid-systolic heart sound. With hand-grip, the sound moves earlier in systole; in addition, he has a grade 1 murmur, which peaks earlier in systole with hand-grip. You also appreciate an early diastolic murmur, which does not change with dynamic auscultation. The abdominal examination is normal. His extremities demonstrate increased span from fingertip to fingertip, and modest hypermobility of the thumbs, relative to the palms. The patient is referred for same-day echocardiography, which demonstrates mild bileaflet prolapse of the mitral valve, associated with mild mitral regurgitation. In addition, there is dilation of the aortic root, with effacement of the sinuses of Valsalva; the aortic root measures 50 mm at the level of the sinuses, and there is mild aortic regurgitation associated with a normal trileaflet aortic valve. The patient is started on a beta-adrenergic blocker. Which of the following is the most appropriate next step in the patient’s management? A.Referral to a cardiac surgeon for valve-sparing root and ascending aortic replacement.? B.Slow titration of beta-blocker, with the addition of an angiotensin-receptor blocker.C.Immediate hospitalization for management of acute aortic dissection.D.Initiation of steroids for management of acute aortitis.The correct answer is A.? Commentary: Referral to a cardiac surgeon for valve-sparing root and ascending aortic surgery is recommended given the root size of 50 mm. The patient has several criteria for Marfan syndrome. The major threat to patients with the Marfan syndrome is acute aortic dissection, the risk for which relates to numerous factors, including aortic size, as well as history of dissection in similarly affected family members. For those with the Marfan syndrome, it is recommended that prophylactic repair of proximal aortic dilation be performed when the aortic root size exceeds 45 mm. Option B is not correct: The patient has criteria for the diagnosis of Marfan syndrome. As such, with annuloaortic ectasia, cystic medial degeneration, and dilation of the aorta at 50 mm, consideration should be given for immediate referral for replacement of the ascending aorta to reduce the risk for dissection and/or rupture. Option C is not correct: While the patient is at higher risk for aortic dissection, there is nothing in the history to suggest acute dissection. The mechanism of aortic regurgitation is related to incomplete aortic leaflet closure from dilation of the sinotubular apparatus and stretching of the aortic leaflet support. Aortitis is not pertinent to his clinical scenario. ??? = Required for completion= CompleteBACKNEXTPROGRESSA 35-year-old woman is seen for consultation prior to a planned second pregnancy. She has been told of a heart murmur since childhood, but does not recall the diagnosis; she uses antibiotic prophylaxis for dental procedures. Her first pregnancy and delivery 5 years ago were uncomplicated. She has no symptoms. Exam reveals blood pressure 110/68 mm Hg, and heart rate 72 bpm and regular. Oxygen saturation is 98%. JVP is estimated 6 cm H2O ; normal carotid arterial pulses. Normal LV impulse, no palpable RV. Normal S1 and S2. Systolic thrill at left mid sternal border. 4/6 high-pitched holosystolic murmur along left sternal border, loudest at the third left intercostal space, radiating toward the apex. There is no respiratory variation of the murmur, and no change with physiological maneuvers (standing-squatting, handgrip) or positional changes. No extra sounds, gallops, or other murmurs are heard. ECG and chest X-ray are normal. An echocardiogram is pending insurance approval. Based on these findings, which of the following is your initial clinical diagnosis?A.Bicuspid aortic stenosis.B.Discrete membranous subaortic stenosis.C.Subpulmonary ventricular septal defect (VSD), large.D.Perimembranous VSD, small.E.Ebstein anomaly with severe tricuspid regurgitation.The correct answer is D.? A holosystolic murmur and thrill at that site could be a small VSD in the mid or anterior muscular position, perimembranous location (most common type), or even outlet subpulmonic position (though those are usually not small). A large VSD would have no VSD murmur (except for rare cases, e.g., double outlet RV, outside the scope of this discussion), but at this age, would have the features of Eisenmenger syndrome. Bicuspid aortic stenosis would not have a holosystolic murmur, but would have a crescendo-decrescendo murmur with radiation to the right base and to the apex, usually with an associated ejection sound. Discrete subaortic stenosis would have the same type of crescendo-decrescendo murmur, but without the ejection sound, and usually only radiating to the left base. Although some types of mitral regurgitation (posterior leaflet prolapse, for example) may radiate anteriorly, the thrill, if present (as with flail mitral valve at times) is still usually at the apex. High-pressure tricuspid regurgitation may have this type of murmur, often distinguished by some respiratory variation, provided the RA pressure is not exceedingly high (not evident in this instance). ??? A 50-year-old man presents with months of fatigue, orthopnea, and dyspnea. He has been hospitalized three times in the last 9 months. He has a 5-year history of a dilated cardiomyopathy and hypertension. Medications include captopril 12.5 tid, carvedilol 12.5 bid, digoxin 0.125 qd, spironolactone 25 qd, and furosemide 80 mg daily. On exam, His blood pressure is 150/100 mm Hg, and heart rate is 100 bpm. Venous pressure is visible above the clavicle seated. Lungs are clear. Slight RV heave with a third heart sound is audible. Murmurs of mitral and tricuspid regurgitation are present. Liver is not palpable. There is trace edema and the extremities are cool. ECG shows sinus tachycardia; QRS 110 msec. Echocardiogram shows EF of 20%, end-diastolic dimension 7.0 cm, moderate-severe mitral regurgitation, and normal RV function. Sodium 136, potassium 4.5, blood urea nitrogen (BUN) 40, creatinine 1.5. Which of the following is the most appropriate intervention?A.Start dobutamine.B.Increase captopril. C.Increase digoxin.D.Increase carvedilol.The correct answer is B.? This patient has acute decompensated HF. He appears to be both congested (i.e., high venous pressures, orthopnea) and low flow (i.e., fatigue, azotemia, cool extremities). He presents hypertensive on only a modest dose of captopril. Increasing the dose of an ACE inhibitor will help to hemodynamically unload the vasoconstricted state and provide increased neurohormonal blockade. Beta-blockers should generally not be increased in the face of decompensated HF because it will exacerbate a low flow state and congestion. There is no evidence to support increasing digoxin levels in acute decompensated HF. The routine use of intravenous inotropes is generally discouraged due to the concerns of increasing mortality.??? A 26-year-old bus driver comes to you because of decreasing exercise tolerance during his daily runs. Fingertip oximetry reveals oxygen saturation 95%. Blood pressure is 110/68 mm Hg. His JVP is 8 cm H2O above the mean RA with a prominent increased A wave. You note a palpable RV impulse along the LSB with an early systolic click noted to decrease during inspiration and increase with expiration, plus a 4/6 long harsh crescendo-decrescendo systolic murmur loudest at the third left intercostal space with radiation throughout the precordium and to the neck. The S2 has increased splitting with a soft pulmonary closure component. No diastolic murmur. An S4 gallop is heard over the LLSB.Based upon these findings, which of the following is your working diagnosis?A.Primary pulmonary hypertension.B.Small perimembranous VSD.C.Subaortic stenosis.D.Ebstein anomaly.E.Valvular pulmonic stenosis.? The correct answer is E.? This young man presents with the classic findings of valvular pulmonary stenosis. Though a pulmonary ejection sound may be heard with pulmonary hypertension (from the dilated pulmonary trunk), it is less likely to vary with respiration, and this type of murmur would not be heard in that setting. The combination of an ejection sound decreasing with inspiration and this crescendo-decrescendo systolic murmur along the LSB is classic for mobile, usually bicuspid, pulmonic stenosis. An uncomplicated isolated small restrictive perimembranous VSD will have a loud holosystolic murmur and no ejection sound. A crescendo-decrescendo systolic murmur along the LSB can be due to subaortic stenosis, but there is no ejection sound with subaortic stenosis, and the RV would not be palpable nor would the JVP show an increased A wave. Ebstein anomaly would show none of these exam or auscultatory features.A 25-year-old woman with trisomy 21 (Down) syndrome and an unrepaired atrioventricular septal defect is referred for consultation by her internist because of increased fatigue and headaches. She lives with her mother. Mild glucose intolerance is controlled with diet. There is a history of heavy irregular menstrual periods. Exam shows Brushfield spots, prominent epicanthal folds, and palmar creases. Blood pressure is 120/70 mm Hg, no brachial-femoral delay, symmetric central (oral) and digital cyanosis and clubbing, oxygen saturation (fingertip pulse oximetry) 70%, JVP 9 cm H2O with equal A and V waves, palpable ventricle along LSB, normal S1 followed by a systolic ejection sound without respiratory variation along the LSB, a 2/6 holosystolic murmur at LSB and apex, loud single S2 with palpable closure sound at left upper sternal border followed by a high-pitched early diastolic murmur along the mid LSB. ECG shows right superior QRS axis (+150 degrees) and RV hypertrophy. Chest X-ray shows RV hypertrophy or enlargement with prominent main pulmonary artery and proximal branches with prompt tapering of the mid-lung field vasculature; RA silhouette appears large. Hematocrit 58%, MCV 78 fL, white blood cell count 6500, and platelet count 80,000.Given these data, which of the following do you recommend?A.Phlebotomy to hematocrit <55%.B.Surgical repair.C.Balloon valvuloplasty.D.Oral iron supplementation.? E.Home Oxygen therapy The correct answer is D.? This long complicated story encompasses a classic Down patient with an unoperated atrioventricular septal defect with pulmonary hypertension due to pulmonary vascular disease. The physical features are typical. The central issue here is management of cyanotic Eisenmenger patients. In Down syndrome adults, diabetes is more frequent. In females with cyanotic heart disease, menstrual abnormalities are common, here resulting in signs of iron deficiency with a relatively low hematocrit for the degree of desaturation, partially confirmed by the low MCV. Most patients with an oxygen saturation in the 70s will have a hematocrit of approximately 65%.This “relative iron deficiency anemia” causes decreased tissue oxygen delivery (decreased hemoglobin per cell, and abnormal microspherocytes, which have abnormal rheology being less deformable in the microcirculation) and consequently her symptoms. This is actually “excessive erythrocytosis” due to cyanosis, not “polycythemia,” given that the white blood cell count is normal and the platelet count, incidentally, is commonly low in this scenario. The management then is careful iron repletion, with caution not to do so too quickly. One must overcome the outdated tendency to prescribe “therapeutic phlebotomy” for “polycythemia,” which in fact will aggravate the situation in the long run. The other answers are inappropriate for this syndrome.A 60-year-old businessman has history of obesity, with a body mass index (BMI) of 32. His history includes prior cigarette smoking, hypertension, and hyperlipidemia. Six months ago, he decided to start climbing three flights of stairs to his office each morning. When performing this activity, he notes a pressure sensation localized to his substernal region that resolves within 2-3 minutes once he sits down at his desk. He describes this symptom to his physician, who orders an ETT. The results are as follows: exercise duration 8 minutes of the Bruce protocol; the patient requests to stop because of his chest pressure; exercise ECG is negative for ischemia.Which of the following statements is TRUE?A.The post-test probability of CAD is >90%.? B.The post-test probability of CAD is <20%.C.The post-test probability of severe (i.e., left main or three-vessel) CAD is <1%.D.The annual risk of cardiac death is <1%.E. can not calculate pretest likelihood from the dataThe correct answer is A.? A 60-year-old man with typical angina has a pretest probability of CAD that is >90%. According to Bayes Theorem, a negative exercise ECG shifts this probability very little, and the posttest probability of CAD remains >90%. Even for patients who can exercise into the third stage of the Bruce protocol with a negative exercise ECG, the probability of left main or three-vessel CAD is approximately 10%. This patient’s Duke treadmill score can be calculated as 0: 8 minutes Bruce protocol – 0 (for no ST-segment depression) – 8 (4 x 2, for test limiting angina). A Duke treadmill score of zero places a patient into the intermediate-risk category for cardiac death, where annual cardiac mortality ranges between 1-3%.?? A 35-year-old man is referred for evaluation after a heart murmur was noted at his employment physical. He has a history of asthma and has been treated with inhalers, although his pulmonary function tests and methacholine challenge were recently normal. He reports mild dyspnea on climbing hills, but is otherwise asymptomatic. On examination, he has a fixed split S2 and soft systolic ejection murmur over the left upper sternal border. His lungs are clear, the jugular venous pressure is not elevated, and the pulses are normal.All of the following are likely to be present on diagnostic studies EXCEPT:A.Mild pulmonary hypertension on echocardiography.B.Borderline right heart enlargement on echocardiography.C.Decreased pulmonary vascularity on chest X-ray. D.An incomplete bundle branch block on electrocardiogram.E.Right-to-left shunt by bubble study on echocardiography.The correct answer is C.? The lung X-ray in this case would be expected to demonstrate increased lung vascularity. The patient described in this case has an atrial septal defect (ASD), most likely a secundum type. The characteristic physical examination findings are the pulmonic outflow murmur resulting from increased pulmonary blood flow due to left-to-right shunting and the fixed split S2. If sufficiently large, ASDs lead to right heart enlargement and an incomplete right bundle branch block pattern on electrocardiography. Pulmonary hypertension can result from increased blood flow, and up to 10% may develop Eisenmenger's physiology if uncorrected. As with any atrial flow communication, a bubble study on echocardiography would be expected to be positive, providing the right atrial pressure can be made to exceed the left atrial pressure (such as following a Valsalva's maneuver).??? A 25-year-old woman presents with a 1-year history of worsening dyspnea. Currently she is characterized as New York Heart Association functional class II. She also complains of atypical chest pain. Her past medical history is significant for two episodes of pneumonia as a child.Her physical examination reveals a prominent RV impulse with a palpable pulmonary artery. On auscultation she has a normal S1, a loud pulmonic component to her second heart sound with fixed splitting, and a systolic ejection murmur at the left upper sternal border. The remainder of her physical examination is unremarkable.An echocardiogram demonstrates mild right-sided chamber enlargement, mild pulmonary hypertension, and is suggestive of a shunt at the intra-atrial level.Cardiac catheterization is performed and hemodynamics and saturations are recorded as follows:PA (mm Hg)?35/15?mean 23RA (mm Hg)?6?PCW (mm Hg)?10?PA saturation (%)?88?SVC saturation (%)?66?IVC saturation (%)?71?PV saturation (%)?99?AO saturation (%)?97?Which of the following is the most effective management approach?A.Warfarin anticoagulation.B.Oral calcium channel blockers.C.Closure of the defect.? D.No therapy at this time.The correct answer is C.? This patient has an atrial septal defect with exclusively left-to-right shunting and very mild pulmonary hypertension. Because she has not yet developed Eisenmenger physiology, she is a candidate for surgical correction.??? You see a 24-year-old HIV-infected woman in your office. At her last HIV clinic appointment, she had a CD4 cell count of 557 cells/mm3 and an undetectable viral load. She tells you that she is taking a PI. On routine laboratory tests, you find that she has an LDL of 163 mg/dl, HDL of 44 mg/dl, and TG of 279 mm/dl.Which of the following is the best management for this patient?A.Start atorvastatinB.Change her PI to another antiretroviral class. C.Start simvastatin.D.Stop her ART.E.Start fish oil.The correct answer is A.? This woman’s main issue is her elevated LDL. Studies have demonstrated that initiating a lipid-lowering medication is likely a better option than switching her antiretrovirals. Also, the newer PIs have fewer associated lipoprotein abnormalities than the older ones, and the scenario does not indicate which specific PI she is currently taking. Statins show good results for lowering LDL in HIV-infected individuals, but some have interactions with antiretrovirals.? Pravastatin, fluvastatin, or atorvastatin are the preferred statins, while lovastatin and simvastatin generally should be avoided. ART interruption to improve lipids results in increases in inflammation and decreases in HDL, and generally should be avoided.ReferencesMallolas J, Podzamczer D, Milinkovic A, et al. Efficacy and safety of switching from boosted lopinavir to boosted atazanavir in patients with virological suppression receiving a LPV/r-containing HAART: The ATAZIP study. J Acquir Immune Defic Syndr 2009;51:29-36.Fichtenbaum CJ, Gerber JG, Rosenkranz SL, et al. Pharmacokinetic interactions between protease inhibitors and statins in HIV seronegative volunteers: ACTG Study A5047. AIDS 2002;16:569-77.Tebas P, Henry WK, Matining R, et al. Metabolic and immune activation effects of treatment interruption in chronic HIV-1 infection: implications for cardiovascular risk. PLoS One 2008;3:e2021.??? A 50-year-old man with diabetes mellitus and a history of cigarette smoking underwent PCI of his mid left anterior descending artery 2 months ago. At the time of his procedure, he was noted to have a total cholesterol of 350 mg/dl, LDL-C of 180 mg/dl, HDL-C of 20 mg/dl, and triglycerides of 280 mg/dl. He was placed on atorvastatin, 40 mg daily, and repeat laboratory tests obtained today show a total cholesterol of 200 mg/dl, LDL-C of 98 mg/dl, HDL-C of 23 mg/dl, and triglycerides of 250 mg/dl.Which of the following is the most appropriate next step?A.Increase atorvastatin dose to 80 mg daily. B.Initiate probucol therapy.C.Instruct the patient to take gemfibrozil and atorvastatin.D.Prescribe a long-acting preparation of niacin in addition to atorvastatin.E.Stop the statin and initiate therapy with a bile acid sequestrant.The correct answer is A.? For individuals with established CAD and diabetes, an LDL-C goal of <70 mg/dl is a reasonable therapeutic strategy. Although administration of a statin reduced the patient's LDL-C, since it is not at goal, the statin dose should be increased. Probucol would be a poor choice, as it lowers HDL-C. Gemfibrozil is used primarily to treat hypertriglyceridemia, and an increased incidence of myositis is observed when it is used concomitantly with a statin. The addition of niacin to a statin is attractive because it may further increase HDL and reduce triglycerides, but it has not been shown to reduce CV events. Bile acid sequestrants would not be prescribed, as they have little effect on HDL-C.???? A 48-year-old woman is admitted with progressive dyspnea. She has noted abdominal swelling and her physical examination shows her jugular venous pressure is elevated and she has bilateral lower extremity edema. She is anxious and is somewhat tachypneic at rest (respiratory rate, 20). Her blood pressure is 120/60 mm Hg; heart rate is 90 bpm and regular. The central venous pressure tracing is shown in Figure 1.Based on these data, your recommendation should be which of the following?A.Reassure the patient and her medical team that the patient’s problem is noncardiac.B.Emergency pericardiocentesis.C.Emergency cardiac surgery consultation for open surgical pericardiectomy.D.Detailed hemodynamic evaluation with right- and left-heart catheterization.? E.Administer thrombolytic therapy for pulmonary emboli.Figure 1The correct answer is D.? The best recommendation based on this initial data is to get detailed hemodynamic data with right- and left-heart catheterization. The central venous pressure is markedly elevated and further evaluation as to its cause is needed. Such elevation could be from right-heart failure, such as is seen with pulmonary hypertension, or it may be due to myocardial or pericardial disease. When the the right and left heart filling pressures are elevated and similar in magnitude, this study needs to include measurement of simultaneous RV and LV pressure to distinguish patients with restrictive cardiomyopathy from those with constrictive pericarditis.This patient clearly has elevated right-sided filling pressures by physical examination and direct pressure measurement, making cardiac diseases the likely cause of her symptoms. The patient does not have pericardial tamponade based on the central venous pressure tracing shown in this patient, which reveals prominent X and Y descents. These descents are blunted in patients with compressive pericardial fluid. Treatments such as pericardiectomy or thrombolytic therapy should not be recommended until the cause of the right-heart failure is defined.??? A 45-year-old, postmenopausal school teacher reports periods of heart palpitations that last for many minutes throughout the day. Palpitations are associated with fatigue, but not dyspnea or chest discomfort. The patient has lost 10 pounds during the last 6 months and notes that her hair is thinning.Diagnostics and physical exam: Prominent eyes, tremor, and smooth skin on elbows. Holter monitor reveals five episodes of rapid AF at a rate of 145 bpm; heart rate in sinus rhythm = 80-101 bpm. The longest episode lasts 24 minutes.Laboratory exam: Thyroid stimulating hormone (TSH) = 0.03 ng/mlWhich of the following anticoagulation protocols should this patient receive?A.No anticoagulation.B.Aspirin 325 mg/day.C.Aspirin 162 mg/day.D.Warfarin at INR 1.6-2.0.E.Warfarin at INR 2.0-3.0. The correct answer is E.? Patients with AF secondary to hyperthyroidism are at risk for AF-related arterial embolism and should be anticoagulated with warfarin at an INR of 2.0-3.0. An alternative medication would be dabigatran.ReferencesFuster V, Ryden LE, Cannom DS, et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). J Am Coll Cardiol 2006;48:854-906. ................
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