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Congestive Heart Failure - Diagnosis and Therapy May 2019, WITS branchDr. Dave Miller.Johannesburg Specialist Veterinary centreDave.miller@jsvc.co.zaIntroduction:Knowing how to treat congestive heart failure / left heart failure is of little help if you do not diagnose the CHF first. Much of the data you need to diagnose heart failure can be obtained with a good history and physical exam. There are extra tests one can do to help with the diagnosis like:Very high NT-proBNP tends to support CHF, but there's a lot of overlap between subclinical & clinical disease.Radiographs are notoriously unreliable for diagnosing CHF.Echocardiography is expensive and often suggestive but not always diagnostic.The huge majority of dogs presented in CHF will be small breed dogs with MMVD and the primary variables for diagnosing CHF in small breed dogs are mainly obtained with a good history and physical exam and the findings of a loud murmur, no arrhythmias, presence of dyspnoea or panting, and a large LA on radiographs.ACVIM/ECVIM CHF Classification Scheme:Stage A: Patient at high risk of developing cardiac disease but with no evidence of structural disease (e.g. Cavalier King Charles spaniel with no heart murmur) Stage B: Patient with evidence of structural cardiac disease (i.e. heart murmur) but no clinical signs of CHF 1) Stage B1: Asymptomatic patient with no evidence of cardiomegaly/heart enlargement on radiography or echocardiography2) Stage B2: Asymptomatic patient with cardiomegaly/heart enlargement on radiography and/or echocardiography Stage C: Patient with clinical signs (past or current) of CHF secondary to structural cardiac diseaseStage D: Ongoing, refractory CHF unresponsive to standard therapy with furosemide 2 mg/kg PO q 8-12 hrs, pimobendan 0.25 mg/kg PO q 12 hrs, and enalapril 0.5 mg/kg PO q 12 hrs or an equivalent drug, and requiring advanced or specialized treatments Aetiology of CHF:Left-sided CHF results from cardiac diseases that cause volume and/or pressure overload of the left heart. Most diseases fall into one of three categories:1) Myocardial failure/systolic dysfunction, e.g. dilated cardiomyopathy2) Volume overload secondary to valvular regurgitation, e.g. mitral regurgitation, aortic insufficiency3) Increased myocardial stiffness/diastolic dysfunction, e.g. HCM, aortic stenosisOverlap between categories is also possible, such as the patient with severe mitral regurgitation and systolic dysfunction, or the patient with subaortic stenosis and myocardial failureNoteworthy examples of potentially reversible causes of CHF in the dog include some congenital heart defects (e.g., patent ductus arteriosus), taurine-responsive dilated cardiomyopathy, pericardial disease, and some sustained tachy- or brady-arrhythmias.Presenting Signs of CHF:Small breed dogs are predisposed to myxomatous mitral valve degeneration (MMVD), and large breed dogs are prone to dilated cardiomyopathy (DCM). Dogs with MMVD are generally older when CHF is diagnosed. Dogs with DCM are generally middle-aged. CHF precipitated by congenital cardiac abnormalities (e.g. patent ductus arteriosus, aortic stenosis, mitral valve stenosis, tetralogy of Fallot) usually occurs in young dogs.Some owners may witness “exercise intolerance” but this is often a subtle finding and is likely to go unnoticed. Eventually clinical signs manifest at rest and are typically secondary to elevated venous pressures leading to pulmonary congestion (oedema) and/or body cavity effusions. These signs commonly include tacchypnoea, dyspnoea, and maybe/rarely a cough secondary to a large heart vibrating on the mainstem bronchi or less commonly pulmonary oedema or pleural effusion. Abdominal distension and vague gastrointestinal signs (e.g., decreased appetite, vomiting, and diarrhoea) might also occur secondary to ascites and passive congestion affecting abdominal organs. Exertional syncope also occasionally occur secondary to severe cardiac disease and CHF.The Struggle to diagnose CHF – Why we get it wrong.Some cases have obvious CHF and the diagnosis is instant due to presenting signs of severe respiratory distress with cyanosis but many cases presented for a 2nd opinion already on CHF meds [often for years] are not in heart failure. Part of the problem is what we've all been taught: that if you hear a murmur, and you've got a dog that's coughing, and you've got what you interpret to be a big heart on films or peri-hilar oedema - therefore we've diagnosed congestive heart failure. I think we've been actually taught incorrectly on this. Add in the fact that most of us struggle to interpret chest films because they are affected by breathing, position movement and differing heart shapes in different breeds. So here is a question algorithm for one to go through to improve one’s diagnostic ability in CHF cases: Question 1 - Do we need a murmur in dogs to diagnose congestive heart failure? It does depend on the type of dog. Small breed dog, the answer is absolutely yes. There are virtually no diseases of little older dogs that cause heart failure without a murmur, because almost all of them have mitral valve disease as the cause. [except Cocker Spaniels with cardiomyopathy]. So older small breed dogs that don't have a murmur, DO NOT HAVE congestive heart failure.? Puppies - The answer is also yes, because most congenital diseases that cause heart failure also have murmurs [shunts, defects, valvular defects or stenosis, mitral dysplasia or PDA or VSD]A puppy with congestive heart failure that doesn't have a murmur is really rare.? Larger, giant breed dogs, the answer is no. A number of those can develop heart failure without having an auscultable murmur, or when they do have a murmur, it's going to be quite mild or soft. You may not hear it, especially if there are other arrhythmias. Doberman cardiomyopathy & Boxer cardiomyopathy don't have to have a murmur.So - in a small breed dog or a puppy - if you don't hear a murmur, you've essentially moved on to something else as your differential.Question 2 - Loudness of the murmur Small breed dog and a murmur. Does it matter how loud it is in order for it to be considered consistent with congestive heart failure?Studies show that there are basically no dogs with soft murmurs (or low-grade murmurs) in heart failure groups. Almost all soft murmurs were in the really mildly affected group, and occasionally a little more severely affected, but none with actual pulmonary oedema. Groups with high-grade murmurs, is when you started to see heart failure. The level of intensity of the murmur was predictive, but not always diagnostic.When one classifies murmurs as soft, moderate, loud, or thrilling, and compares them to the size of the left atrium. Soft murmurs are found virtually only in a normal heart size range. It is shown that the heart size does get bigger as you get louder and louder murmurs, so the heart size is associated with murmur intensity, but there are still dogs that have mild or even moderate enlargement that can have very loud or even palpable murmurs.? So, soft murmurs are either normal or mild disease, but once you start to get louder you start to develop a proportion of dogs that might have congestive heart failure. Question 3: What about heart rate and the heart rhythm? Sinus arrhythmia - It speeds up. It slows down. It speeds up. It slows down....with every breath. Sinus arrhythmia rules out heart failure. Heart failure is when you lose vagal dominance and you become sympathetically driven, because now you're panicking about the next breath because you're struggling to breathe, your heart rate is racing, and you're stressed. So, if you've got a sinus arrhythmia or a sinus bradycardia, both of which can indicate high vagal tone, you've essentially ruled out heart failure BUT, having a loss of vagal tone doesn't mean you have heart failure. Question 4 - Coughing. "This little dog has got a murmur and a coughCoughing is usually a function of a big heart, and in heart esp. LA vibrating on the mainstem bronchus, and in heart failure this tends to happen but we can have a big heart without heart failure. Trials show that coughing really isn't a function of heart failure per se, but just having a big heart, which a lot of these little dogs do. Remember - little old dogs cough, so we need to try forget about the coughing when trying to work out if we have CHF, even though that's why the client brought the pet in, So coughing might be a sign of CHF but only when all the other signs we have and will discuss are present and never diagnostic on its own. If the client tells you the cough has been going on for a long time, it's not heart failure related because dogs don't live for a long time with heart failure, not without treatment. BUT if we have both coughing and tacchypnoea, then are we getting closer to call this CHF.Question 5 - Pulmonary oedema on auscultation? People say, oh, the lungs sounded wet, or they sounded crackly. Do we hear crackles? Do we hear other things with heart failure?Most of these types of sounds come from large airways. If you know someone with asthma, you know exactly what it's like to wheeze. It's a constriction of the smaller airways and even some of the larger airways. Crackles occur because of snapping open of small bronchioles. It's either a slapping together or a popping open. In dogs CHF causes thickening of the actual interstitium. It's not in the alveoli. They're not full of fluid. Essentially the fluid is being deposited in the tissues around the alveoli. Well, if the fluid is in the tissues around the alveoli, there's no fluid to be snapping the bronchioles open and closed. The crackles in CHF comes from the human literature, as they get alveolar oedema therefore crackles. So we might hear some “more harsh” lung sounds just because they’re breathing harder. In very severe progressive CHF crackles might occur.Question 6 - Respiratory rate at rest? Can dogs with left-sided CHF have a normal respiratory rate at rest? Most of our dogs with subclinical valve disease—even if they had bad subclinical valve disease with severely enlarged hearts, still have normal breathing rates. These are mainly at-home resting rates. Try allowing the dog to relax and hopefully lie down while you chat to owners and watch it out of the corner of your eye. A low respiratory rate tends to tell us that we don't have heart failure. A high respiratory rate r panting can make us suspicious, but fear, pyothorax, pneumonia,pneumothorax and heat, all could cause high respiratory rates.So, there are other conditions that can cause an elevated respiratory rate, but if it's normal, we probably don't have heart failure, look for something else.Question 7 - What about biomarkers? NT-proBNP – IN MMVD and small breed dogs.In studies of MMVD with heart failure, biomarkers were actually all over the place. If you look at the overlaps between well less than 1000 to somewhere up about 4500, which was where most of our CHF dogs are going to lie, there's just no way that one can tell whether you're in heart failure or not. Subclinical dogs versus CHF dogs - you see a fair bit of overlap. CHF cases - A lot of dogs still have normal NT-proBNP, or they're not that much different from dogs that have subclinical valve disease.If you have a really high BNP it tends to support heart failure, but we have a lot of overlap here too. So their value in helping us figure out what's going on with these little dogs is probably of little help.In Large bred dogs with potential DCM [NT-proBNP & cTn1]:NT-proBNP Assay a circulating peptide created and released by cardiomyocytes as a reaction to stretching. NT-proBNP combined with 24-Holter monitoring to detect early evidence of DCM, particularly in Doberman pinschers [In this breed NT-proBNP is elevated in all stages of DCM] withCardiac Troponin 1 [cTn1] is a marker of cardiac myocyte damage. Elevation of cTn1 was found in Dobermans with both occult and clinical DCM. A cut-off value >0.22 ng/mL had a sensitivity of 79.5% and a specificity of 84.4% for detecting DCM.So, in large breed dogs both biomarkers can be helpful in diagnosis and pro BNP in monitoringQuestion 8 - How big should the heart be?Generally, it takes "overwhelming heart disease" in these little dogs to cause heart failure Dr. Peter Lord followed MMVD dogs for years and found:Go back five years and their hearts are pretty normal. As they get closer to heart failure [remember it's a slow progressive disease]Once you're approx. a year out, size starts to climb, Once in CHF - virtually all the dogs had a very large heart.?The answer to this question is yes, most of the time we need to have a big heart—but not always because if we rupture a chord all of a sudden; So - If we see mild or moderate enlargement, it tends to rule out heart failure and an absolutely yes, we do need big hearts in these little dogs.. Question 9 – SRR If the dog has a loud murmur and is tacchypnoeic in the exam room, then we can move on, but if it's not obviously tacchypnoeic or if it has fear type panting all the time in clinic we can look at breathing at home. Average sleeping respiratory rate in a dog is somewhere around about 15 breaths a minute. None of them were above 25. These are absolutely normal dogs, and some as low as 8 or 9.When not in heart failure even though they have severe valve disease, they're down in the same range as what the healthy dogs are, maybe a little higher but normal.SRR < 45 with no other lung disease present is 100% diagnosticEven dogs with CHF, when treated appropriately, will, within a day or two, be subclinical again with SRR well below 30 for the most part, so we use SRR to diagnose and monitor CHFSo, a dog with a normal sleeping respiratory rate less than 30 breaths a minute tends to rule out heart failure.? Question 10: How reliable are radiographs at identifying left-sided CHF?If one looks at a full expiratory vs a full inspiratory film, what we might think is interstitial pulmonary oedema, disappears. Also breeds have different heart shapes so often 1 view looks like large heart esp Dachsies, Yorkies, JRT. All this makes chest films notoriously difficult to read. So, chest films with a very large left atrium is definitely linked with a higher chance of CHF but presence or absence of oedema is to subjective and unreliable to be an essential tool in diagnosis.Question 11 - Lasix trial or a diuretic trial for a cough..? "Oh, I gave the dog some Lasix because I thought it might be in heart failure and the owner said the cough is way better," BUT Lasix bronchodilates and it interferes with coughing mechanisms. We can't use elimination of a cough to diagnose congestive heart failure when we give Lasix. What we can do is watch the respiratory rate.So just because the cough went away doesn't mean you had CHF.Question 12 - Lasix trial for raised SRRIf we reduce the respiratory rate to less than 30 [fairly rapidly] after administering 1-2 mg/kg of Lasix, if the respiratory rate comes down dramatically and normalizes, then ones made the likely diagnosis of heart failure.Summary of diagnosis of CHF diagnosis:We have covered presence of crackles and wheezes and murmurs. We covered the loudness of the murmur and presence of bradycardia’s and sinus arrhythmias as well as tacchypnoea and about the size of the left atrium on x-rays. What we came away with is a lot of the cases that you see, if you just pay attention to four things in the exam room, you can probably figure out whether or not the dog in front of you is a likely candidate for a Lasix trial or not. That is, all you need to have is a loud murmur, a lack of a sinus arrhythmia, dyspnoea or constant panting in the exam, and hopefully a really big left atrium on radiographs.OTHER TALKS IN CARDIOLOGY:Heart Murmurs in Asymptomatic DogsA heart murmur is a relatively common physical exam abnormality in dogs. The characteristics of the murmur, including the point of maximal intensity, timing, and grade, can also help narrow the list of possible causes.Review of Auscultation Technique in DogsQuite room with a calm patient:1.??Palpate both sides of the thorax to identify the apex beat and to identify any thrill 2.??Auscult the left side of the thorax at the apex beat. This is generally where the heart sounds are loudest and is near the mitral valve.3.??Auscult the left heart base region by inching the stethoscope cranio-dorsally. Murmurs emanating from the great vessels, aortic and pulmonic valves are best heard at this location.4.??Auscult the right side at the level of the apex.5.??Palpate the femoral pulses while ausculting and assess the heart rhythm.Murmurs in Puppies, Physiologic murmurs - systolic, grade 3 or quieter, with a point of maximal intensity at the left heart base, generally gone by about 6 months of age. A murmur that is continuous, loud, or has a PMI on the right side is not a physiologic juvenile ejection murmur and should be further evaluated. Murmurs in Adult Dogs:Some healthy dogs have ejection murmurs. These are systolic, grade 3 or quieter, with a point of maximal intensity at the left heart base, and are most common in large to giant breed dogs and Boxers. Echocardiography is indicated to rule out structural heart disease.In predisposed breeds such as Dobermans, Boxers, Great Danes, and Irish Wolfhounds, a murmur may indicate occult cardiomyopathy. Echocardiography and possibly Holter monitoring are indicated.Murmurs in cats:thoracic auscultation, allowing for identification of heart murmurs, gallop rhythms, and arrhythmias. 40% of cats have heart murmurs and 1 in 3 of those asymptomatic cats with heart murmurs had heart disease the majority of cats with heart murmurs (2 out of 3) having benign or physiological flow murmurs so the presence of a heart murmur in a cat is not an accurate indicator of the presence of heart disease. Cats with loud heart murmurs (grade >3/6) should be considered at high-risk for having heart disease. Thoracic Radiology in the Dog and CatAlways minimum two views; the left lateral view and either the dorsoventral (DV) or ventrodorsal (VD) view. A more complete exam will include three views of the thorax, L and R lateral and either the DV or VD view. DV - preferred for cardiovascular examinations because the heart is more consistent in position, the caudal lobar vessels are seen and its the less stress view with the critical patient. VD - if a pleural effusion is present; All chest rads done at the height of inspiration. Symmetrical patient positioning is essential. With patient rotation in the lateral view, the trachea will appear elevated creating the false impression of cardiomegaly. Subjective cardiac size guidelines are: a width of 2.5 to 3.5 intercostal spaces and height of less than 2/3 of the thoracic height on the lateral view. In the DV view, the heart should be less than 2/3 the thoracic width. Narrow chest breed dogs will tend to have a narrower, taller heart shape and barrel-chest breeds will have a wider, rounder heart. Subjective feline cardiac measurements - no more than two intercostal spaces in width and less than 70% of the thoracic height on the lateral view.Objective cardiac measurements rely on the vertebral heart sum (VHS) method. Pulmonary veins are central and veins are ventralCanine DCM.Dilated cardiomyopathy (DCM) is one of the most common acquired heart diseases of medium to giant breed dogs. It occurs rarely in small breed dogs and cats. DCM causes decreased contractility, with secondary, compensatory, ventricular dilation.Patients may have a soft, left apical systolic heart murmur from functional mitral regurgitation. Femoral pulses may be normal or decreased in strength. An arrhythmia may be detected [usually AF]. Early in the course of disease, affected animals may be asymptomatic [just mild lethargy or exercise intolerance or drop off in appetite]. Later, signs of left-sided CHF such as tacchycardia, tacchypnoea, dyspnoea, cough, cyanosis, and syncope develop. Nonspecific signs include anorexia, lethargy, weakness, weight loss, and poor weight gain in young animals. Although less common, signs of right-sided CHF may occur, such as abdominal distension from ascites.Monitoring of asymptomatic dogs involves Echocardiography, ECG, and/or Holter monitoring and Biomarkers. Sleeping respiratory rate can be monitored at home by owners. Therapy:Preclinical DCM: The PROTECT study demonstrated that the administration of pimobendan (0.25-0.3 mg/kg PO q 12 hrs) to Dobermans with subclinical DCM (i.e. systolic dysfunction on echocardiography) increased time to onset of CHF and extended survival. A retrospective study also suggested that benazepril may delay the progression of occult DCM.Clinical DCM: Goals of therapy are to reduce clinical signs of CHF, diminish life-threatening arrhythmias, and prolong survival. In addition to inotropic support (e.g. pimobendan, dobutamine), therapy often involves use of diuretics (e.g. furosemide, spironolactone, thiazides, Torsemide), and angiotensin-converting enzyme inhibitors (e.g. enalapril, benazepril). Digoxin may be useful in certain cases. SUPPORTIVE THERAPYCarnitine - 50 mg/kg PO 8 hrs in certain breeds (boxer, American cocker spaniel) efficacy unknown. Taurine - 500-1000 mg PO 12 hrs for dogs with suspected/confirmed taurine deficiency. Some grain-free diets with clinical evidence of heart disease often return to normal with dietary change alone. Torsemide and Right heart failure (RHF) [DCM/AF/PH/Tricuspid disease/Restrictive disease]Torsemide is more effective than furosemide in RHF. Furosemide needs rapid absorption to reach effective levels because it has such a short half life (2 hrs tops). In right heart failure the GI capillary congestion limits absorption (and oral furosemide is only 60% bioavailable under the best of circumstances). Torsemide has 80-100% bioavailability (much better absorption) and a 9 hour half life so delayed absorption is less a factor. Torsemide also appears to also have aldosterone blocking properties while furosemide stimulates aldosterone (causing sodium & H20 retention). Several human studies (and meta analyses) show improved results for torsemide vs furosemide in heart failure, and now there is a large canine study (MMVD dogs) that showed a clear benefit. Orally it is shown to be the drug of choice BUT that being said, what works best and fastest is showing owners how to give bid SQ furosemide injections (100% absorption and good peak levels). Most marked ascites cases clear without centesis within a week. We start with 2-3 mg/kg furosemide SQ bid until ascites is resolved, then either oid SQ furosemide or go to Torsemide if they prefer pills.?If CHF is responding to therapy, respiratory rate, serum NT-proBNP, and diastolic function on echocardiography should all improve.48PROGNOSISPrognosis varies depending on the severity of disease at the time of diagnosis and type of DCM. Dogs with occult DCM may remain asymptomatic for years, and their longevity may be improved with use of pimobendan. Typically, the younger the age at time of diagnosis, the faster the disease progresses and the worse the prognosis. Poor prognostic indicators include prolonged QRS duration (>60 msec) on ECG and decreased ejection fraction on echocardiography, the class of heart failure present, and the presence of ascites. So far, the only predictor of sudden death in Dobermans is echocardiographic documentation of severe volume overload of the left ventricle.Survival of dogs with CHF is generally short (i.e. 3-12 months). About 75% of Doberman pinschers with CHF die within 3 months of developing clinical signs.1 However, trials with pimobendan have suggested that survival may be increased to 9-12 months in these dogs. MMVD – Myxomatous Mitral valve DiseaseBy far the number 1 cause left heart CHF in companion animal medicine.The primary goals of the management of CHF are threefold: 1) Determine and, if possible, correct the underlying cause, 2) Alleviate clinical signs and improve quality of life by improving haemodynamic derangements, and 3) Prolong life by maintaining improved haemodynamic’s and blocking adverse neuro-hormones that, in the long-term, perpetuate the vicious cycle of heart failure. Despite this, unfortunately, most causes of CHF in the dog are irreversible and will progress over time. Therefore, it is important to emphasize to dog owners that treatment is almost always life-long and focused on improving quality of life while attempting to prolong life by slowing the progression of the underlying cardiac disease. Stabilization of acute left-sided CHF (i.e., cardiogenic pulmonary oedema causing breathing difficulty and respiratory distress) is focused on alleviating clinical signs and correcting increased preload and increased venous pressures (i.e., “congestion”). Therefore, cardiac medications used for acute CHF are intended to reduce venous pressures, alleviate congestion, and ease the anxiety associated with difficulty breathing (sedation). Mnemonic, “Someone Please Obtain Furosemide”S = sedation, typically butorphanol 0.1–0.4 mg/kg IM/IV as needed; P = pimobendan 0.25–0.3 mg/kg PO q 8 h–12 (I prefers q 8 h dosing while hospitalized); O = oxygen, provide supplemental oxygen; and F = furosemide, 2–4 mg/kg IV initially. Some clinicians may also utilize transdermal nitroglycerin ointment (?–1 inch, depending on the size of the dog, applied to the inside of the ear pinna/unhaired skin) as a venodilator to help reduce preload/congestion. One should consider administering furosemide intravenously if possible due to addition benefits with this route (quicker onset of action and adjunct vasodilatory properties). Following this initial therapy, dogs should be permitted to rest in an oxygen-enriched environment, which allows time for meds to take effect. Respiratory rate and effort should be monitored closely (e.g., every 30–60 min) and throughout the duration of hospitalization, and furosemide (typically 2 mg/kg IV) can be re-administered every hour until breathing improves. Once breathing rate and effort begins to improve, the frequency of furosemide administration should be reduced to, for example, every 4–8 hours with a “rescue” 2 mg/kg IV bolus given as needed.Some clinicians prefer to use a furosemide constant rate infusion (CRI) for acute CHF, particularly when radiographic pulmonary edema is severe (diffuse interstitial and alveolar pulmonary pattern). Furosemide CRIs or modified CRIs regimens vary and are largely clinician dependent. For severe CHF cases, start with a rate of 0.5–1 mg/kg/h (for a maximum of 4–6 hours) with reduction in the rate once breathing rate and effort improve. The risk for severe dehydration increases with azotemia if rates of 1 mg/kg/h are administered longer than 4–6 hours. Management of chronic (outpatient) CHF in dogs can be remembered with the Mnemonic, “Dogs Are For Special People” D = diet (low sodium, cardiac friendly diet; avoid salty treats/snacks); A = angiotensin converting enzyme (ACE) inhibitors 0.5 mg/kg PO q12 h; F = furosemide, typically ～2 mg/kg PO q 12 h; S = spironolactone 1 mg/kg PO q 12 h; P = pimobendan 0.2–0.3 mg/kg PO q 12 h.Pimobendan (0.25-0.3 mg/kg PO q 12 hrs) is a calcium-sensitizing agent with vasodilator and positive inotropic actions. It improves myocardial contractility, with little effect on myocardial oxygen demand. It is the treatment of choice for dogs with CHF secondary to MMVD. Prolonged survival was noted in a study of Doberman pinschers treated during the occult phase of dilated cardiomyopathy, and delayed onset of CHF was documented in dogs with MMVD. Improved appetite and attitude, and decreased sleeping respiratory rates have been reported in many dogs treated with pimobendan.Atrial Fibrillation (Canine)Atrial fibrillation (AF) is a type of supraventricular arrhythmia characterized by an irregularly, irregular rhythm [the “tennis shoes in the clothes drier” rhythm]. Usually associated with severe cardiac disease [DCM, myxomatous degeneration] however, in large and giant breed dogs it can occur in the absence of structural disease (sometimes called idiopathic, spontaneous, primary or lone atrial fibrillation). A small subset of dogs develop AF without evidence of significant cardiac disease. In one study, the Irish wolfhound, Newfoundland, and German shepherd dog were overrepresented. An irregularly, irregular rhythm is always present associated with variable pulse quality and pulse deficits. Frequently, a soft heart murmur is present (primary AF is an exception). Signs of congestive heart failure may also be present. ECG features include 1) irregularly, irregular rhythm, 2) absent P waves that are replaced by an undulating baseline or f waves, 3) supraventricular (narrow) complexes in leads II, III, and 4) a fast, usually irregular ventricular rate [features 2-4 may not always be reliably present]Why will you see this case? Lethargy, generalized weakness, exercise intolerance, tachycardia, variable pulse quality, pulse deficits, weakness, syncope, partial anorexia and signs of congestive heart failure (e.g. increased respiratory rate, coughing, rales) could be present. In some asymptomatic dogs, AF is only discovered upon routine physical examination. AF Therapy: Rate ControlIn patients with severe underlying cardiac disease, rate control (i.e. slowing down the ventricular response rate) is typically the treatment of choice. Therefore, medical management primarily aims to slow conduction through the AV node. Calcium channel blockers (e.g. diltiazem), and digoxin. *Combination therapy with digoxin (0.005 mg/kg PO q 12 hrs) and extended-release diltiazem (diltiazem XR 3-5 mg/kg PO q 12 hrs) provides better control of ventricular response rate than monotherapy. We start with diltiazem monotherapy, diltiazem XR 3-5mg/kg PO q 12 hrs) in most cases. Heart rate assessment and ECG is performed approximately one week following initiation of therapy. An ECG is recommended because some dogs can also have an underlying ventricular arrhythmia that is initially masked by fast AF. If no improvement in heart rate is appreciated, digoxin 0.003-0.005 mg/kg PO q 12 hrs is started. Target heart rate in a clinical setting is <140-160 bpm. Extreme caution must be used when considering beta-blockers in patients with systolic dysfunction, especially those with congestive heart failure and dilated cardiomyopathy. Beta-blocker therapy is typically avoided in these patients. Atrial fibrillation is a poor prognostic indicator for dogs with structural heart disease, such as mitral valve degeneration and heart failure.Challenges in Feline Cardiology:Heart disease is common in cats and cardiomyopathies, affect approximately 1 in 8 healthy cats. While a notable proportion of cats with cardiac disease have a normal life expectancy cats with severe or advanced disease have a high morbidity and mortality from heart failure, sudden death or cardiologists regarding the "best" way to identify and treat these cases. This reflects the difficulties faced with diagnosing and classifying cardiac disease in cats, the high prevalence of functional murmurs in cats, and the paucity of evidence to support the benefit of therapy for both preclinical cardiomyopathies and cats with heart failure.Diagnosing Feline Cardiac DiseaseHypertrophic cardiomyopathy with or without dynamic outflow tract obstruction (HCM or HOCM) is by far the most common heart disease, followed by restrictive or unclassified cardiomyopathies (RCM or UCM) and dilated cardiomyopathy (DCM). thoracic auscultation, allowing for identification of heart murmurs, gallop rhythms, and arrhythmias. 40% of cats have heart murmurs and 1 in 3 of those asymptomatic cats with heart murmurs had heart disease the majority of cats with heart murmurs (2 out of 3) having benign or physiological flow murmurs so the presence of a heart murmur in a cat is not an accurate indicator of the presence of heart disease. Cats with loud heart murmurs (grade >3/6) should be considered at high-risk for having heart disease. A common cause for a benign murmur is the phenomenon of dynamic right ventricular outflow tract obstruction, which can give a grade 1–3 parasternal murmur, typically (but not always) with a right parasternal point of maximal intensity.The absence of a heart murmur does not necessarily mean absence of cardiac disease. In cats presenting with respiratory signs, the presence of a gallop or an arrhythmia were far more accurate predictors of heart failure than the presence of a murmur or Cough - when present in a cat, it is far more likely to indicate respiratory than cardiac disease.When a cat presents with clinical signs and physical examination findings that suggest cardiac disease, further investigations are necessary. Echocardiography is the gold standard diagnostic test for detecting and classifying feline cardiomyopathies. Thoracic radiography is a very useful screening test for detecting congestive heart failure, by identification of cardiomegaly, pulmonary venous congestion, pulmonary parenchymal abnormalities consistent with cardiogenic oedema, and pleural effusions. It lacks accuracy for distinguishing normal heart size from hearts with mild cardiomegaly. It is also limited by the fact that cats with the preclinical stage of HCM, the most common cardiac disease, will typically have no abnormalities on thoracic radiography. Managing Arterial ThromboembolismArterial thromboembolism (ATE) can be a devastating consequence of cardiomyopathy in cats, resulting in pain, paresis, paralysis, or end-organ damage. Oral antiplatelet drugs (aspirin, clopidogrel) used to prevent platelet or coagulation function. In a prospective, multi-center clinical trial comparing the efficacy of aspirin (81 mg PO q72h) and clopidogrel (18.75 mg PO q24h) for prevention of ATE recurrence in cats with cardiac disease and prior ATE reported a significant survival benefit for clopidogrel. Its use is recommended in severe left atrial dilatation, poor systolic function, spontaneous echocardiographic contrast and intracardiac thrombus. This highlights the need for echocardiography to evaluate ATE risk in any cat with suspected cardiac disease. A newer oral antiplatelet drug, the factor Xa inhibitor, rivaroxaban (Xarelto), is currently the subject of clinical trial in cats, comparing its ATE prevention efficacy with that of clopidogrel.SummaryAny cat with a heart murmur, gallops, or arrhythmia would benefit from further testing to screen for cardiac disease. The presence of a heart murmur is not an accurate indicator that heart disease is present.NT-proBNP is a widely available and clinically useful screening tool for determining whether cardiac disease is likely to be present in a cat. Cats with elevated NT-proBNP should undergo echocardiographic examination.Echocardiography is the "gold standard" test for determining whether cardiac disease is present, determining the type of cardiac disease present, and assessing disease severity.Thoracic radiography is a poor screening tool for preclinical heart disease, but it very useful for determining whether congestive heart failure is present.We lack a strong evidence base to advocate any medical therapy in cats with preclinical cardiomyopathies. Atenolol is the preferred drug for most cardiologists to treat cats with severe DLVOTO.Furosemide is the first-line therapy for cats with congestive heart failure.There is no convincing evidence for the benefit of any medical therapy in addition to furosemide in cats with heart failure due to HCM, RCM, or UCM.There is some evidence to advocate the use of pimobendan in addition to furosemide in cats with DCM and heart failure, and convincing evidence that taurine supplementation can treat DCM caused by taurine deficiency.Clopidogrel is recommended over aspirin as antiplatelet therapy for cats with pre-existing cardiogenic ATE or for those at high-risk for ATE.References:Heart Murmurs in Asymptomatic Dogs, Southwest Veterinary Symposium 2017, Caryn Reynolds, DVMDove Lewis Veterinary Emergency and Specialty Hospital, Portland, OR, USAManagement of Congestive Heart Failure in the Dog, Source: Conference Proceedings : International Vet Emerg Crit Care : IVECCS 2018. Lance C. VisserManagement of Congestive Heart Failure in the Dog, International Veterinary Emergency and Critical Care Symposium 2018 Lance C. Visser, DVM, MS, DACVIM (Cardiology) VIN Associate, Atrial Fibrillation?, Last updated on 3/17/2017, Contributors: Geri Lake-Bakaar DVM, DACVIM (Cardiology)VIN Associate, Cardiomyopathy, Dilated?, Last updated on 10/17/2018. Revised by Geri Lake-Bakaar DVM, DACVIM (Cardiology)Original author was Mark Rishniw BVSc, DACVIM (Small Animal Internal Medicine & Cardiology), 12/13/2004VIN Associate, Heart Failure, Left-Sided (Canine), Last updated on 3/9/2018 Revised by Jacqueline Brister DVM and Geri Lake-Bakaar DVM, DACVIM (Cardiology)Original author was Mark Rishniw BVSc MS, DACVIM (Cardiology & Internal Medicine), 10/20/2004Vin Associate, Myxomatous Tricuspid Valve Degeneration (Canine), Last updated on 8/15/2018 Revised by Geri Lake-Bakaar DVM, DACVIM (Cardiology)Original author was Mark Rishniw BVSc, DACVIM (Small Animal Internal Medicine & Cardiology), 10/13/2004CHF Diagnosis Made Easy: A Simple Algorithm to Reduce Inaccurate DiagnosesJuly 1, 2018 (published), Mark Rishniw, DVM, DACVIM, Carla Burris:Challenges in Feline Cardiology, Atlantic Coast Veterinary Conference 2017, Simon Dennis, BVetMed, MVM, DECVIM (CardiologyThoracic Radiology in the Dog and Cat, Atlantic Coast Vet Conference : ACVC 2014. Dennis E. BurkettHope Veterinary Specialists, Malvern, PA, USA ................
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