Virginia Luis Fuentes,     Hatfield, Hertfordshire, United Kingdom

Karsten Eckhard Schober,     Columbus, Ohio

Definition of Myocardial Disease

Myocardial disease in cats is a heterogeneous group of conditions, paralleling the spectrum of diseases that make up human cardiomyopathy. Feline cardiomyopathies originally were categorized according to morphology and function, in line with the contemporary human classification. The main categories were hypertrophic, dilated, restrictive, and unclassified cardiomyopathy, with the later addition of arrhythmogenic right ventricular cardiomyopathy (ARVC). Human cardiomyopathies now are divided into primary cardiomyopathies in which the myocardial changes are the major abnormality (e.g., hypertrophic cardiomyopathy, or HCM) and secondary cardiomyopathies in which a multiorgan systemic disease (e.g., hyperthyroidism) affects the myocardium (Maron et al, 2006). Primary cardiomyopathies are divided into those with a genetic basis, those with an acquired cause, and those involving a combination of genetic and acquired factors (mixed). Hypertrophic cardiomyopathy and ARVC are considered genetic in humans, whereas dilated cardiomyopathy (DCM) and restrictive cardiomyopathy (RCM) are classed as mixed. There is evidence that HCM can be genetic in cats: two separate mutations in the cardiac myosin-binding protein C gene have been identified in Maine coon and Ragdoll cats with HCM. A deficiency in dietary taurine can result in a feline DCM phenotype. Secondary cardiomyopathies found in cats include myocardial disease related to hyperthyroidism, systemic hypertension, and chronic anemia, which commonly affect cardiac chamber size and function.

Despite this classification, there is considerable overlap among groups. Cats may progress from one phenotype to another. Myocardial infarction can complicate HCM, resulting in regional wall thinning and hypokinesis that resembles a DCM phenotype. An end-stage form of HCM also has been described in human and feline patients, characterized by left ventricular hypertrophy with dilation and reduced systolic function. Left ventricular remodeling in HCM with interstitial fibrosis and loss of cardiac myocytes can result in a morphology that is closer to RCM than to classic HCM, and chronic myocarditis may mimic RCM or DCM. Even on a genetic level, some sarcomeric mutations are associated with both DCM and HCM phenotypes. In addition, abnormal mitral valve morphology can be associated with dynamic outflow tract obstruction and left ventricular hypertrophy, which blurs the boundaries between congenital heart disease and primary cardiomyopathy.

Diagnostic Approach

In addition to the difficulties in trying to assign a particular label to the cardiomyopathy in individual cats, feline cardiac disease presents a number of other diagnostic challenges.

Healthy cats may have innocent heart murmurs that are not associated with any structural cardiac abnormality. The prevalence of murmurs in the healthy cat population is high, but as many as half of all feline murmurs may be functional and not actually caused by structural heart disease (Wagner et al, 2010). These low- to moderate-intensity systolic murmurs often are associated with conditions characterized by increased sympathetic tone and high cardiac output, such as stress, anemia, hyperthyroidism, and fever, with the murmur arising from the left or the right ventricular outflow tract. Dynamic right ventricular outflow tract obstruction can be normal in cats. The best way to differentiate cats with functional murmurs from those with heart disease is with echocardiography. Unfortunately, interpretation of echocardiograms in cats requires a high level of expertise, particularly in distinguishing between normal cats and cats with mild structural cardiac changes. Thoracic radiography may be used to identify cardiomegaly in asymptomatic cats, but the sensitivity of this method is low, especially in cats with mild structural changes. Plasma biomarker assays such as those for N-terminal prohormone B-type natriuretic peptide (NT-proBNP) and high-sensitive cardiac troponin I are showing promise as screening tests for cardiomyopathy in this setting but always should be used in conjunction with other tests (Fox et al, 2011). It is relatively easy to screen for secondary cardiomyopathies by measuring blood pressure, thyroxine concentration, and hematologic parameters.

Noncardiac disease can cause respiratory distress that must be distinguished from congestive heart failure (CHF). Auscultation of a gallop sound in a cat with tachypnea is highly suggestive of CHF. Radiography can be helpful if cardiomegaly or venous engorgement is detected. If the cardiac silhouette is obscured or interpreted as normal, radiography is less useful as a discriminatory test because the distribution of pulmonary infiltrates with cardiogenic pulmonary edema is very variable in cats, and the presence of a pleural effusion is nonspecific. The careful positioning necessary for diagnostic radiography also can jeopardize patient safety when the cat is tachypneic. Although plasma NT-proBNP concentration may discriminate well between cardiac and noncardiac causes of respiratory distress in cats, it is not yet available as a cage-side test, and the delay in receiving results limits its usefulness.

Cats with myocardial disease may have no detectable abnormalities on physical examination. The extent of this problem is unclear, although a recent study evaluating 103 apparently normal cats found heart murmurs in only 5 of the 16 cats with echocardiographic evidence of cardiomyopathy (Paige et al, 2009). Additionally, it is common for cats brought for treatment of aortic thromboembolism (ATE) and advanced cardiomyopathy to have shown no signs of cardiac disease at previous examinations. Without preemptive screening, these at-risk cats likely will continue to be denied the opportunity for cardiac therapy.

Therapeutic Approach

Clearly it is never appropriate to treat a cat for heart disease based solely on the presence of an auscultatory abnormality such as a murmur or even a gallop sound or click. Most cats with heart disease have cardiomyopathy, but those with secondary cardiomyopathies must be identified because their treatment should be directed at the underlying disease. It is more important to determine symptomatic status than to try to categorize the cardiomyopathy phenotype because cats with clinical signs are managed differently from those without. Treatment decisions ideally should be evidence based, but relevant data mostly are lacking in feline heart disease. In the absence of valid evidence, management should focus on targeting cats at risk of recognized complications of cardiomyopathy. The most common sequelae of cardiomyopathy are CHF and ATE, although the incidence of sudden death is probably underestimated. When specific hemodynamic disturbances (e.g., systolic dysfunction) are identified, therapy should be tailored to the specific functional problem. Nevertheless, it is important to recognize that many cats with myocardial disease remain asymptomatic for long periods without any intervention (Payne et al, 2010), and any incremental benefit from therapy in these cats may not justify the additional expense, time, and stress. Management strategies are presented in the following sections according to risk stratification for stages of heart disease (Table 180-1).