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Comprehensive Clinical Case StudyLeah FiteWright State University-Miami ValleyCollege of Nursing and HealthComprehensive Clinical Case StudyHistory and PhysicalPatient InformationName: V.C., Age: 65, Race: Caucasian, Gender: MaleSourcePatient and wife, both reliable sourcesChief Complaint“My husband awoke not knowing who I was and was unable to speak. He started hyperventilating and fell to his knees with nausea. So I called the squad.”History of Present IllnessV.C. is a 65 year old male who presented to the emergency department after he experienced what his wife described as an “amnesiac moment.” He was unable to speak and did not recognize her. He then became dyspneic and nauseous. The patient has no recollection of the event up until arriving in the emergency department. He does report that he experienced a similar event about a year ago while vacuuming the floor. He knew the names of his wife and children, but didn’t remember who they were. At that point he lied down for a nap, and when he awoke, he felt better. He went to the emergency department at that time, where they told him he had a moment of amnesia, and no further testing was done. Both episodes have been unrelated to time or activity. He complains of increasing fatigue over the past two years, but remains active, walking two miles daily. He denies chest pain, palpitations, swelling of the feet, or any other associated symptoms other than dyspnea and nausea with both episodes. The patient feels that this episode was more “severe” than the last. Medical HistoryHypertensionSurgical HistoryRight knee ACL repair x3Bilateral lasik surgeryFamily HistoryMaternal grandmother “died” of diabetes. Father with positive history of throat cancer, mother with history of multiple myeloma, and brother died at 58 from lung cancer. No other significant family history.Social HistoryPatient is married with two children; one grown and one still in grade school. He is a previous smoker, with a 30 pack year history, who quit 30 years ago. He denies illicit drug use, but admits to drinking one fifth of alcohol weekly. He also drinks one pot of coffee per day. He engages in regular physical activity, walking two miles daily with no associated shortness of breath, chest pain, or claudication. He is up to date on all vaccines and wears his seatbelt regularly.AllergiesAspirin-rash/hivesHome MedicationsLosartan/HCTZ 50/12.5mg dailyMultivitaminCurrent MedicationsLosartan 50mg dailyHydrochlorothiazide 12.5mg dailyColace 100mg dailyReview of SystemsGeneral: Denies fever, weight gain/loss. Admits to increased fatigue over the past 2 yearsSkin/Hair/Nails:Admits history of benign skin cancer which he had removed. Denies dermatitis, rash/itching, non-healing wounds, sores, or abcess.HEENT:Denies loss of hearing, tinnitus/vertigo, earaches, sinus problems, nose bleeds, blurred vision, double vision, light sensitivity, glaucoma, or cataractsNeck:Denies swollen glands, difficulty swallowing, or neck painChest:Admits shortness of breath with these episodes, and sleep apnea. Denies shortness of breath with regular activity, frequent/chronic cough, asthma, COPD, wheezing, tuberculosisCV:Denies chest pain, palpitations, syncope, or feet swellingGI:Admits to intense nausea associated with these episodes. Has occasional heart burn. Denies abdominal pain, vomiting, diarrhea, blood in stool, or difficulty swallowingGU:Denies urinary incontinence, urinary frequency or hesitancy, denies kidney stones, prostate problems, blood in urine, or bladder infectionsM/S:Admits to arthritis in R hand. Denies joint pain or swelling, gait problemsNeuro:Admits to episodes of confusion and amnesia with these episodes. Admits to problems with speech during episodes. Denies headache, weakness, numbness, seizures, lightheadedness, falling, prior stroke or head injuryPsychosocial:Denies depression, anxiety, or panic attacksPhysical ExamVitals:BP 117/78 mmHg; HR 78 bpm; RR 18bpm; Temp 97.9 F; SpO2 99% on room airGeneral:No apparent distress. Appears stated age. Pleasant and cooperativeSkin/Hair/Nails:Pink and warm; appropriate for ethnicity. No rashes, lesions, or scars. Nails smooth without clubbing or cyanosis. Hair thinning with normal age progression.HEENT:Head normocephalic; EOMI; No nystagmus. Pupils 3mm, equally round and reactive to light. Nasal mucosa pink and moist, no exudates. Throat without lesions. Oral mucosa pink and moist without errythema. Good dentitionNeck:Neck supple, trachea midline. No palpable lymphadenophathy. No rigidity. Brisk upstroke on bilateral carotid pulsesChest:Normal respiratory effort, symmetric without use of accessory muscles. Lungs CTA bilaterally; no rhonchi, wheezes, or crackles. Resonant percussion in all lung fields. No tactile fremitus noted. Cardiac:Regular rate. PMI at 5th ICS, MCL. Grade III systolic murmur at right sternal border, which radiates to the carotids. S1 with no audible S2. No thrills, heaves or lifts. No JVD. No peripheral edema noted. 2+ palpable pulses noted bilateral radial, femoral, dorsalis pedis; 1+ bilateral posterior tibial pulses.Breasts:N/AGI:Abdomen soft, rounded, nontender. Bowel sounds heard equally x4 quadrants. Tympanic percussion over epigastrum. No hepatosplenomegaly. No palpable massesGU/Rectal:Voiding per urinal; clear, yellow urineMusculoskeletal:Strength 5/5 throughout with good muscle tone in all extremities. No tenderness or erythema noted on hands, elbows, knees, ankles. Neuro:Alert and oriented x4. Appropriate speech and good memory recall other than the events of the episode. Laboratory FindingsTable 1. Complete Blood Count and Renal PanelComplete Blood Count (CBC)ResultsNormal ValuesRenal PanelResultsNormal ValuesWBC9.1K cells/mL3.6-10.5K cells/mLSodium140 mEq/L135-145 mEq/LRBC5.51M cells/mL4.4-5.8M cells/mLPotassium3.4 mEq/L3.6-5.1 mEq/LHemoglobin15.4 g/dL13.5-16.5 g/dLChloride102 mEq/L101-111 mEq/LHematocrit46%40-50%Carbon Dioxide23 mEq/L24-36 mEq/LMCV84 fL82-97 fLBUN17 mg/dL8-26 mg/dLMCH28 pg27-33 pgCreatinine1.0 mg/dL0.5-1.2 mg/dLMCHC3332-36 g/dLGlucose154 mg/dL74-99 mg/dLRDW13.6%<15.3%Anion Gap20 mEq/L6-18 mEq/LPlatelet246 K/uL140-375 K/uLTable 2. PT/INR and Cardiac EnzymesPT/INRResultsNormal ValuesCardiac EnzymesResultsNormal ValuesPT12.2 seconds9.0-11.4 secondsCPK134 IU/L0-200 IU/LINR1.20.8-1.2CK-MB2.7 ng/mL<6.1 ng/mLPTT26.4 seconds23-32.5 secondsTroponin0.01 ng/mL<0.05 ng/mLOther laboratory studies performed on this patient include ethanol level, drug toxicology screen, and urinalysis. No ethanol or illicit drugs were detected. Urinalysis was clear, and negative for abnormal findings, with a urine specific gravity of 1.013.Diagnostic Findings12 lead electrocardiogram (ECG) shows left axis deviation and left ventricular hypertrophy as evidenced by deep S wave in V1, and tall R wave in V6. Chest radiography (CXR) shows no acute cardiopulmonary findings, with no evidence of cardiomegaly. Computed tomography (CT) of the head is negative for any signs of bleeding or mass. MRI of the head is negative for ischemia. Electroencephalography illustrates dysrhythmic grade I slowing consistent with normal age related changes. Carotid Doppler study shows mild bilateral stenosis, less than 50%. Differential DiagnosisMr. C presents with an amnesiac episode unrelated to activity with associated dyspnea. Transient global amnesia is an event usually seen in people over the age of 50, which is characterized by acute memory deficit, often in the setting of physical exertion or emotional stress, in which the person is alert but confused (Seeley & Miller, 2012). Differential diagnoses to rule out for these symptoms include transient ischemic attack, stroke, and seizure disorder. The presence of a murmur leads to further differential diagnoses including coarctation of the aorta and aortic stenosis.Transient ischemic attack (TIA) is a cessation of blood flow causing neurologic symptoms mimicking stroke that typically last less than one hour (Smith, English, & Johnston, 2012). Symptoms vary among patients, but may include hemiparesis of the face, arms, or legs, dysarthria, and weakness. Several etiologies contribute to TIA but most often are related to the heart, and include atrial fibrillation, rheumatic heart disease, mitral valve disease, infective endocarditis, or atrial septal defect (Smith et al., 2012). Atherosclerosis of the carotid arteries or aortic arch, arterial inflammatory disorders, and hypotension may also contribute to the development of TIA. The history of hypertension in this patient can lead to a likelihood of this diagnosis. He reports no history of palpitations or abnormal cardiac rhythms and denies history of rheumatic fever. He is currently afebrile, which would likely rule out the diagnosis of infective endocarditis contributing to TIA. Echocardiogram needs to be performed to evaluate valve function. Carotid ultrasound shows no significant blockage, and MRI is negative for areas of ischemia, likely ruling out this diagnosis.Hemorrhagic or ischemic stroke may be a cause of the amnesiac moments the patient is experiencing, although this is highly unlikely. Ischemic infarct may be caused by uncontrolled hypertension or diabetes, or thrombotic or embolic occlusion of major vessels, while intracerebral hemorrhage causes include poorly controlled hypertension, bleeding or hematologic disorders, high alcohol intake, or brain tumor (Aminoff & Kerchner, 2013). While symptoms vary according to location of the stroke, and whether it is hemorrhagic or ischemic, rarely does a patient present with only amnesiac moments. Symptoms may include hemiplegia or unilateral weakness of the arm or leg, frank confusion, visual loss, vertigo, urinary incontinence, ataxia, global aphasia, and drowsiness leading to stupor or coma (Aminoff & Kerchner, 2013). Negative carotid ultrasound and MRI can rule out ischemic stroke as a cause for symptoms. Hemorrhagic stroke is unlikely due to resolution of symptoms and negative head CT. Seizures can be related to a variety of causes, and can be described as abnormal neuronal firing within the brain causing transient interruption in normal cerebral function (Aminoff & Kerchner, 2013). Causes of seizure include genetics; structural, related to tumor or space occupying lesion; metabolic due to drug or alcohol withdrawal, uremia, or hypoglycemia; or unknown causes (Aminoff & Kerchner, 2013). Seizures are typically evidenced by convulsive jerking or loss of postural tone with urinary incontinence, however, some seizures may be manifested as dysphagia and amnesiac symptoms such as déjà vu (Aminoff & Kerchner, 2013). The possibility that this patient presents with seizures related to alcohol withdraw due to his drinking history is unlikely, as the patient openly discusses his drinking habits with the provider and his wife, explaining that he has cut back on his drinking over the last few weeks. Space occupying lesion can be ruled out due the negative head CT. Blood glucose is normal. Focal seizure may be possible due to the presentation of symptoms, however, EEG is negative for activity that would alert the provider to this diagnosis.Coarctation of the aorta may be causing the current symptoms the patient is experiencing, and is associated with a heart murmur. A narrowing of the aortic arch occurs in coarctation of the aorta as a result of hypertension, with greater than 50% of cases having bicuspid aortic valve (Bashore et al., 2012). Hypertension is usually greater in the upper extremities than the lower extremities, with decreased femoral pulsations, and midsystolic murmur heart over the left interscapular area, with left ventricular hypertrophy evident on ECG (Child & Aboulhosn, 2012). Dilated ascending aorta and left subclavian artery on the left mediastinal border is evident on CXR, while echocardiogram can identify the area of coarctation and should be obtained. Although this diagnosis may be present in adulthood, it is usually detected and repaired in childhood. Ruling out this diagnosis warrants echocardiography studies, but is doubtful based on clinical and diagnostic findings.Clinical findings of decreased S2 and systolic murmur which radiates to the carotids, along with ECG suggesting left ventricular hypertrophy, are highly suggestive of aortic stenosis in this patient. Systolic murmur with radiation to the carotids has a sensitivity of 73% and specificity of 91% for accurately detecting aortic stenosis with bedside assessment (Etchells et al., 1998). The amnesiac moments the patient has experienced could be related to bradycardia, or maneuvers that increase afterload, which decrease volume and contribute to decreased cerebral blood flow. Calcification of the valve secondary to vascular atherosclerosis or congenital heart disease such as bicuspid aortic valve is the primary cause of aortic stenosis, and is associated with increased risk of MI and death in patients greater than 65 years of age (O’Gara & Loscalzo, 2012). Echocardiogram is needed for definitive diagnosis in this patient, but aortic stenosis is highly probable. Diagnosis of severe aortic stenosis is made when the patient is symptomatic and the echocardiogram reveals an aortic valve area (AVA) of less than one cm2, the aortic peak velocity of greater than four m/s, and a mean flow gradient greater than forty mmHg (Nishimura et al., 2014).Diagnostic Tests/RationaleElectrocardiogram (ECG)ECG is an inexpensive, non-invasive test that can assess the electrical activity within the heart, presence of coronary ischemia, and cardiac chamber enlargement that can be a useful tool in the evaluation of patients with murmur. Absence of arrhythmias, prior myocardial infarction (MI), active ischemia, ventricular hypertrophy, or atrial enlargement can provide exclusion criteria for diagnosis. The incidence of prior MI or left ventricular hypertrophy should prompt further testing for definitive diagnosis. Left ventricular hypertrophy and existence of a murmur is indicative of valvular disease, however, there are no ECG findings that are specific or sensitive for diagnosis of exact valve disease. Chest Radiography (CXR)CXR can provide information regarding the location, shape, and size of the heart, but is generally nonspecific when identifying valve disease. Aortic stenosis may cause hypertrophy which may be seen on the frontal view as a rounding of the apex, or a dilated ascending aorta may also be seen (O’Gara & Loscalzo, 2012). Calcification of the aortic valve may be seen on lateral view CXR, but the degree of calcification cannot be determined, and warrants further testing (O’Gara & Loscalzo, 2012). Dual Source Computed Tomography (DSCT)DSCT is a noninvasive test that can provide high quality images within the cardiac structure (Li et al., 2009). Accurate evaluation of ejection fraction, AVA, and aortic root dimensions can be accomplished through DSCT. DSCT also evaluates valve anatomy for severity of stenosis, and can identify other valvular lesions or masses. This test is costly, and not available in many facilities, therefore rarely used for the assessment and diagnosis of aortic stenosis. DSCT has a 91% sensitivity and 100% specificity for correctly identifying patients with aortic stenosis (Li et al., 2009). Echocardiography The gold standard diagnostic tool for the evaluation of aortic stenosis is echocardiography. Not only can echocardiography assess left ventricular dysfunction and wall thickness, but also the degree of valve calcification and the presence of other associated valve diseases (Bashore et al., 2013). Two-dimensional doppler transthoracic echocardiogram (2D echo) is favorable for its capability to estimate aortic valve gradient, and the severity of stenosis. 2D echo has a sensitivity of 74% and specificity of 67% to accurately predict AVA for severe aortic stenosis (Kupfahl et al., 2004). Echocardiography is a portable, reliable, cost-effective test used for the accurate diagnosis of valvular disease. To establish etiology, confirm diagnosis, and determine severity, prognosis, and timing of intervention, echocardiogram should be completed with the initial assessment, and is a class Ia ACC/AHA recommendation (Nishimura et al., 2014). This patient did undergo echocardiogram revealing severe concentric left ventricular hypertrophy with normal wall motion, and an ejection fraction of 55%. The left atrium is mildly dilated. Mild mitral calcification with trace mitral regurgitation. The aortic valve is severely calcified and appears bicuspid. The AVA is 0.9 cm2; peak aortic velocity is 4.3 m/s; mean gradient is 55 mmHg. The aortic root is not well visualized.Cardiac CatheterizationWhile cardiac catheterization is not required for most patients with cardiac murmurs, it may be beneficial for diagnosing aortic stenosis when clinical findings do not correlate with echocardiography findings (O’Gara & Loscalzo, 2012). Left heart catheterization is an ACC/AHA class I recommendation for patients with severe aortic stenosis at risk for coronary artery disease, who plan to undergo aortic valve replacement (AVR) (Nishimura et al., 2014). The sensitivity and specificity for cardiac catheterization to identify severe aortic stenosis is 78% and 91%, respectively (Kupfahl et al., 2004). While this patient’s clinical symptoms associate with the echocardiogram findings, cardiac catheterization is performed to rule out CAD, showing heavily calcified aortic valve area with minor irregularities in the major coronary arteries, but no significant blockages. The ascending aorta is not well visualized.Cardiac Magnetic Resonance (CMR)CMR is another noninvasive approach for the diagnosis of severe aortic stenosis. Poor acoustic visibility on echocardiogram or inability to cross the valve by catheterization may call for further testing such as CMR (Kupfahl et al., 2004). In the circumstance of bicuspid aortic valve, the importance of CMR or CT is stressed for the appropriate evaluation and measurement of the aortic root (Svensson et al., 2013). Inability to perform CMR depends on the presence of metallic implants or pacemaker, history of severe claustrophobia, and facility ability. CMR has a sensitivity of 78% and specificity of 89% for the accurate detection and diagnosis of severe aortic stenosis (Kupfahl et al., 2004). Prioritized PlanCurrently, no medical treatment has been established for aortic stenosis. The only effective treatment shown to improve quality of life, relieve symptoms, and increase survival in aortic stenosis is aortic valve replacement (AVR) (Svensson et al., 2013). Cardiothoracic surgery should be consulted in this patient, and surgical risk score and frailty index should be calculated in order to proceed with AVR.AVR is an ACC/AHA class Ia recommendation for any patient with severe aortic stenosis at the onset of symptoms of lightheadedness or syncope, angina, and dyspnea (Svensson et al., 2013). The guidelines also recommend elective aortic root replacement for any patient with bicuspid aortic valve who’s diameter exceeds five cm (class Ia) (Svensson et al., 2013). In patients with severe aortic stenosis presenting with aortic velocity of greater than four m/s or mean pressure gradient of forty mmHg or greater, plus calcified aortic valve with associated symptoms, AVR is recommended (Nishimura et al., 2014). A shared decision making process on the choice of valve intervention between the patient and provider must be carried out to discuss risks regarding each valve type and patient preference and values. Choice of mechanical or bioprosthetic valves should be discussed with the patient, regarding the need for anticoagulation therapy and associated risks, and the durability of each valve with the possible need for future reoperation. For patients who have an exclusion risk for surgical AVR, and post-surgery survival rate of greater than one year, transcatheter aortic valve replacement (TAVR) is recommended (Nishimura et al., 2014). Balloon aortic valvuloplasty (BAV) can be used as a bridge therapy in patients with severe aortic stenosis who are hemodynamically unstable and unable to undergo immediate AVR (Svensson et al., 2013). Bioprosthetic valves are more likely to be considered in patients over the age of 70 due to the increased risk of bleeding complications, but have decreased durability inversely related to the patient’s age (Nishimura et al., 2014). Since patients do not require anticoagulation therapy with bioprosthetic valves, some patients may prefer to avoid the “hassle” of long term therapy such as dietary and medication interactions, frequent laboratory monitoring, and athletic activity restrictions (Nishimura et al., 20140. In patients already treated with anticoagulation therapy for a pre-existing medical condition, mechanical valve is suitable. Patients less than 60 years of age without contraindication for life-long anticoagulation therapy, may benefit from a mechanical valve, and is an ACC/AHA class II recommendation (Nishimura et al., 2214). Studies have shown a decrease in reoperation rate and lower mortality rate associated with mechanical valves in patients younger than 60 (Nishimura et al., 2014). For patients between the age of 60 and 70, either valve choice is reasonable with similar long term outcomes, and is based on patient preference (Nishimura et al., 2014). This patient decides to undergo bioprosthetic valve to avoid the complications and lifestyle alteration associated with life-long therapy. Prophylactic antibiotic with gram-positive and gram-negative coverage is recommended for any patient undergoing AVR (Svensson et al., 2013). If mechanical valve was chosen, warfarin therapy to achieve a goal INR of 2.5-3.5 is recommended for the prevention of thromboembolism due to abnormal flow conditions which cause platelet activation, with frequent laboratory monitoring to ensure therapeutic dose range (Nishimura et al., 2014). Even with bioprosthetic AVR, anticoagulation therapy should be started and continued for the first three months post-operatively, until the valve is endothelialized, due to the increased risk of peripheral embolism and ischemic stroke associated with bioprosthetic valves (IIb) (Nishimura et al., 2014). Regardless of valve type, 81 mg daily aspirin dosing is a class IIa recommendation for the further prevention of thromboembolism (Nishimura et al., 2014).Follow-upPatients who have endured valve replacement are still considered to have a serious heart disease, and routine follow-up is essential. Seven to ten days following discharge from the hospital, the patient will follow-up with the cardiothoracic surgeon for history and physical exam, and assessment of vital signs, wound healing, and activity tolerance post-operatively. CXR and ECG may be performed at that time. To evaluate the outcomes of surgery and assess valve hemodynamics, echocardiogram should be performed during this time (Nishimura et al., 2014). Baseline post-AVR images and measurements are obtained from the echocardiogram at this time for comparison regarding valve compliance should problems develop in the future. Routine follow up with a cardiologist is essential, with varying interval in visits depending on valve type, clinical factors, and other comorbid conditions. In patients with bioprosthetic valves, annual 2D echos should be performed for the first ten years post AVR, and is an ACC/AHA class II recommendation (Nishimura et al., 2014). Due to the increased risk of endocarditis, prophylactic antibiotic therapy is required for any patient with a history of AVR who undergoes surgical, endoscopic, or dental procedures (Svensson et al., 2013). Health Promotion ActivitiesImmediate post-operative health promotion activities are aimed toward infection prevention with adequate hand washing and increased pulmonary exercises to prevent atelectasis contributing to pneumonia. Cardiac rehabilitation is generally recommended to assist with normal activities of daily living and reduce the risk of future problems. The patient should be instructed on eating heart healthy items and participating in normal cardiovascular exercise to inhibit atherosclerosis. Encouraging the patient to stay up to date on annual influenza vaccination and every five year pneumococcal vaccination is also important for health promotion. ReferencesAminoff, M. & Kerchner, G. (2013). Nervous system disorders. In M. Papadakis & S. McPhee (Eds.), Current Medical Diagnosis and Treatment, 52nd edition (pp. 962-1037). New York: McGraw Hill.Bashore, T., Granger, C., Hranitzky, P., & Patel, M. (2013). Heart disease. In M. Papadakis & S. McPhee (Eds.), Current Medical Diagnosis and Treatment, 52nd edition (pp. 324-432). New York: McGraw Hill. Child, J. & Aboulhosn, J. (2012). Congenital heart disease in the adult. In D. Longo, A. Fauci, D. Kapser, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s Principles of Internal Medicine, 18th edition (pp. 1925-1928). New York: McGraw Hill.Etchells, E., Glenns, V., Shadowitz, S., Bell, C., & Siu, S. (1998). A bedside clinical prediction rule for detecting moderate or severe aortic stenosis. Journal of General Internal Medicine, 13, 699-704. Kupfahl, C., Honold, M., Meinhardt, G., Vogelsberg, H., Wagner, A., Marholdth, H., Sechtem, U. (2004). Evaluation of aortic stenosis by cardiovascular magnetic resonance imaging: comparison with established routine clinical techniques. Heart, 90, 893-901. doi: 10.1136/hrt.2003.022376Li, X., Lijun, T., Lei, Z., Yuqing, D., Sheng, Y., Rong, Y., …& Xiangquing, K. (2009). Aortic valve stenosis and regurgitation: assessment with dual source computed tomography. International Journal of Cardiovascular Imaging, 25, 591-600. Doi: 10.1007/s10554-009-9456-zNishimura, R., Otto, C., Bonow, R., Carabello, B., Erwin, J., Guyton, R., ., …& Thomas, J. (2014). ACC/AHA Practice guidelines for the management of patients with valvular heart disease: executive summary. Circulation, 129, 2440-2492. doi: 10.1161/CIR.0000000000000029O’Gara, P. & Loscalzo, J. (2012). Valvular heart disease. In D. Longo, A. Fauci, D. Kapser, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s Principles of Internal Medicine, 18th edition (pp. 1929-1950). New York: McGraw Hill.Seeley, W. & Miller, B. (2012). Dementia. In D. Longo, A. Fauci, D. Kapser, S. Hauser, J. Jameson, & J. Loscalzo (Eds.), Harrison’s Principles of Internal Medicine, 18th edition (pp. 3300-3316). New York: McGraw Hill.Svensson, L., Adams, D., Bonow, R., Kouchoukos, N., Miller, C., O’Gara, P., …& Williams, M. (2013). Aortic valve and ascending aorta guidelines for management and quality measure. The Annals of Thoracic Surgery, 95, 1-66. doi: 10.1016/j.athoracsur.2013.01.083 ................
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