Paul Pion United States
Objectives of the Presentation
Review the clinical skills and diagnostic tests used to screen feline patients for cardiac disease.
Summarize current knowledge, opinion, and controversies about myocardial diseases in cats.
Encourage therapeutic decisions based upon clinical findings, not the disease you assign to a patient.
Encourage a conservative approach to therapy that involves owner participation.
Encourage healthy dose of skepticism—don’t believe everything you hear or read.
Key Clinical Diagnostic Points
Murmurs are common in cats.
Not all murmurs represent cardiomyopathy, or even significant pathology, in cats.
Gallop sounds commonly signify significant cardiac pathology.
Echocardiography is the primary tool for diagnosing feline cardiomyopathies.
Radiography is an important tool for determining the need for therapy and monitoring efficacy of therapy.
In the absence of dysrhythmia, electrocardiography adds little to the diagnosis of feline cardiac disease.
Key Etiologic and Pathophysiologic Points
Taurine deficiency causes a nutritional secondary dilated cardiomyopathy in cats.
Hypertrophic cardiomyopathy (HCM) is, in many cases, a familial disease
Likely a sarcomeric protein defect inherited as an autosomal dominant trait in the Maine Coon cat.
Believed familial in the Maine Coon, Rag Doll, British and American Shorthair, and Rex breeds.
The cause of other forms of feline cardiomyopathy remains unknown.
Morbidity and mortality in cats with cardiomyopathy most commonly manifest as congestive heart failure, aortic thromboembolism, arrhythmia, or sudden death.
Other than in dilated cardiomyopathy, diastolic dysfunction predominates in most cases.
Dynamic outflow obstruction due to systolic anterior motion (SAM) of the mitral valve is common in HCM.
The pathologic and prognostic significance of this finding is unknown.
Key Therapeutic Points
A diagnosis of cardiomyopathy does not necessarily mean treatment is currently, or ever, required.
Educate owners about possible outcomes:
No clinical significance; congestive heart failure; aortic thromboembolism; sudden death.
Teach owners to monitor and log respiratory rate at home; call if increasing or > 30/min.
Always consider secondary cardiomyopathies that may be reversible:
Taurine supplementation for cats with myocardial failure secondary to taurine deficiency.
Treatment of underlying endocrinopathies (e.g., hyperthyroidism, acromegaly?)
The most common (and perhaps only) absolute indications for therapeutic intervention are:
Congestive heart failure.
Pleural effusion -> thoracocentesis followed by diuretic and ACE inhibitor
Pulmonary edema -> diuretics and ACE inhibitor
Caution: The stress of handling and manipulation can kill a dyspneic cat. The author recommends doing the minimum needed to determine and implement emergency therapy: pleurocentesis or drugs (diuretics for CHF, steroids for asthma, etc) prior to proceeding to a definitive diagnostic workup.
Aortic thromboembolism -> controlling pain and hyperkalemia are most critical
Myocardial failure -> taurine supplementation should be attempted in all arrhythmias that appear hemodynamically significant or life threatening.
Beyond this short list, the indication for and efficacy of therapy is highly controversial.
Current preventive measures for aortic thromboembolism are not highly efficacious in practice.
Key Drugs, Doses, and Indications
Key Prognostic Points
Early diagnosis permits more careful monitoring but early intervention may not alter the ultimate outcome.
Left atrial size is a key prognostic factor in predicting onset of CHF in cats with LV diastolic dysfunction.
Response to initial aggressive therapy for congestive heart failure:
Some patients will stabilize; slow downward dose titration or withdrawal can be attempted.
Other patients require continued aggressive monitoring and remain fragile. Short-term prognosis is worse for this group.
Aortic thromboembolism (ATE) is most commonly seen with severe left atrial enlargement (LA:Ao > 2.0).
Approximately 50% of cats with ATE die during the first hospitalization.
Most who survive the first episode will rethrombose within a year despite preventive measures.
Development of atrial fibrillation in cats with left atrial enlargement is a poor prognostic indicator.
Rapid and frequent ventricular arrhythmias likely predict a higher probability of sudden death.
Cats with myocardial failure secondary to taurine deficiency who survive two weeks will likely recover.
Knowing breed and familial patterns in cats with HCM may be helpful for predicting prognosis.
Background and Detail
Derivation and Definitions: cardio- = heart; myo- = muscle; pathos- = disease
A primary (idiopathic) cardiomyopathy is a disease of heart muscle with no known underlying etiology.
A secondary cardiomyopathy is a heart muscle disease resulting from other disease processes.
Primary Cardiomyopathies are diagnosed by the morphologic and functional appearance of the patient’s heart and ruling out other causes for these “patterns”.
Hypertrophic cardiomyopathy (HCM): concentric (symmetric or asymmetric) hypertrophy.
Idiopathic Dilated cardiomyopathy (DCM): eccentric hypertrophy with myocardial failure.
Restrictive cardiomyopathy (RCM).
Unclassified cardio(myo)pathy (UCM).
Note: The author and others use the term unclassified cardio(myo)pathy in place of intermediate form or restrictive cardiomyopathy as a reminder that we are unsure if these cases represent a true cardiomyopathy. Classification of these cases as a primary cardiomyopathy is tenuous, at best.
Proven or strongly suspected causes of Secondary Cardiomyopathy in Cats:
Nutritional (taurine deficiency).
Metabolic (hyperthyroidism, acromegaly).
Infiltrative (neoplasia, amyloidosis).
Inflammatory (toxins, immune reactions, infectious agents).
Genetic (strong evidence in HCM in some breeds; may play a role in the susceptibility to taurine deficiency induced myocardial failure).
Toxic (doxorubicin, heavy metals).
Within each class, wide ranges of morphologic and clinical presentations are seen.
The lines between forms and classifications begin to blur as we unravel the facts. I suppose that as we define the etiology of myocardial diseases we concurrently redefine each as a secondary cardiomyopathy. Perhaps genetic/heritable causes should remain classified as primary causes?
Diagnosis of Feline Cardiomyopathies—Echocardiography
Hypertrophic Cardiomyopathy (HCM)—concentric hypertrophy
Any or all of the following is/are observed:
Left ventricular wall or interventricular septum thickness (diastolic) > 5.5 mm.
Enlarged papillary muscle(s) in the left ventricle.
Left ventricular (LV) dynamic outflow obstruction secondary to systolic anterior motion (SAM) of the anterior mitral valve leaflet and/or marked thickening of the septum during systole.
Obliteration of the left ventricular cavity during systole.
Note: Upon identification of the genetic marker for HCM a more specific blood test may be possible.
In the absence of:
A LV pressure overload: fixed LV outflow obstruction or systemic hypertension.
Abnormal thyroid function (hyper), abnormal growth hormone status (hyper).
Dilated Cardiomyopathy (DCM)—myocardial failure/systolic dysfunction.
LV end-systolic dimension > 12 mm in cats with a shortening Fraction < 35%.
In the absence of:
Valvular, ischemic, or other disease that might underlie myocardial failure.
Taurine deficiency myocardial failure: same as DCM in a taurine deficient (and responsive) patient.
Restrictive (RCM) and Unclassified (UCM) Cardio(myo)pathies: diastolic dysfunction.
Enlarged left (and sometimes also right) atrium in cases that don’t fit criteria or other diagnoses.
Diagnosis of RCM requires demonstration of histopathologic changes to the myocardium such as endomyocardial fibrosis, inflammatory cell infiltration, deposition of amyloid, etc. Antemortem differentiation is not usually possible.
Rules I live by: and most agree with:
Dyspneic cats should not be stressed.
Pleural effusion should be drained.
Furosemide and angiotensin converting enzyme inhibitors are indicated for CHF.
Cats with myocardial failure should receive taurine in hope that it is taurine responsive.
Rules I live by but not all agree with:
There is no proven benefit to “treating” in the absence of congestive heart failure.
Beta blockers are effective antiarrhythmics; whether they alter the risk of sudden death is unknown.
Beta blockers are effective in the reduction of dynamic outflow obstruction (DOO) in cats, though we are unsure if DOO contributes significantly to morbidity or mortality and needs to be treated.
Diltiazem appears to reduce the amount of diuretic needed to control CHF in some cats with HCM.
Regression of LV wall thickness as a result of prescribing calcium entry blockers, ACEIs, or beta blockers is not a realistic therapeutic expectation.
Left atrial size is the best predictor of the risk of left heart failure and aortic thromboembolism. As LA size approaches 20 mm I worry more.
Current strategies for treating and preventing ATE are not very effective.
Involving owners in the process by teaching them to count and record heart rate and respiratory rate at home helps them feel involved and satisfied they have “gotten something” and minimize the natural tendency to want to treat when it may not yet be indicated.
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