Asymptomatic Cardiomyopathy (Low Risk)

Cats with occult cardiomyopathy exhibit a spectrum of risks, from those cats that will survive to old age and never experience any clinical signs associated with their heart disease to those at imminent risk of CHF or ATE. Cats at the low-risk end of this spectrum are likely to have a normal-sized left atrium (Payne et al, 2010) and may be difficult to differentiate from healthy cats if ventricular changes are subtle. Echocardiography is the most effective test for evaluating left atrial size in cats, although radiography can provide an approximate assessment in cats with moderate or severe atrial enlargement. Alternatively, plasma NT-proBNP concentrations may be used to provide an initial risk assessment to guide further testing (Fox et al, 2011).

It is difficult to justify therapy in cats with a normal-sized left atrium as a means of improving survival because most cats in this category do well without treatment, including cats with dynamic left ventricular outflow tract obstruction (DLVOTO), which typically is associated with systolic anterior motion of the mitral valve apparatus and mitral-septal contact. It is not known whether cats with DLVOTO experience the chest pain that some human HCM patients experience. Moreover, whether the well-known effect of moderate and severe DLVOTO on activity and exercise level in people also occurs in cats is largely undetermined. These are some potential reasons for treating feline DLVOTO in the absence of any demonstrated effect on survival (see the later section on DLVOTO).

Note that although cats with mild occult disease are unlikely to require treatment and often remain in stable condition for long periods, the risk remains that CHF will develop in response to interventions such as intravenous fluid therapy, anesthesia, or depot corticosteroid administration, or to periods of prolonged tachycardia associated with stress. Worryingly, cats in this category also may be at risk of sudden death (Payne et al, 2011).

Asymptomatic Cardiomyopathy (at Risk)

Cats at the high-risk end of the occult cardiomyopathy spectrum are likely to have left atrial enlargement. Such cats have an increased likelihood of developing CHF or ATE compared with those with no left atrial enlargement. Although results of a few short-term trials of therapy in asymptomatic cats have been published, no therapy has been reported to be unequivocally beneficial. However, enrollees frequently have included cats with normal-sized left atria, which minimizes the likely benefit of intervention over a short period.

Without experimental evidence to provide guidance, therapeutic decisions are based on extrapolation from human treatment protocols or knowledge of pathophysiology. This is the patient group about which there is the most controversy in terms of treatment decisions for feline cardiomyopathy. The theoretical goals of therapy in cats at high risk of decompensation might include improvement of hemodynamic function, reduction of left ventricular filling pressures, counteraction of neurohormonal activation, and modulation of platelet function. Treatments suggested include β-adrenergic antagonists (atenolol), calcium channel blockers (diltiazem), angiotensin-converting enzyme (ACE) inhibitors, and antiplatelet drugs (aspirin and clopidogrel).

β-Blockers reduce myocardial oxygen consumption, an effect that should reduce demand ischemia. This benefit, along with slowing of the heart rate and prolongation of diastolic filling, may have some overall benefit on diastolic function in HCM. Atenolol also reduces or eliminates dynamic outflow obstruction (see following paragraph). Anecdotal evidence suggests that relief of moderate and severe outflow tract obstruction may be associated with increased activity and exercise level in some cats that were previously classified as asymptomatic. Moreover, poor tolerance of tachycardia frequently has been documented in people with HCM and has been proposed as a mechanism for the development of CHF in patients with occult HCM. Prevention of unwanted tachycardia therefore may be beneficial in some cats. The total daily dosage of atenolol is generally 1 to 4 mg/kg q12h PO. Liquid atenolol can be easier to dose than tablets in some cats, but in others the relatively small pill fractions can be hidden in food, treats, pill pockets, or gelatin capsules. Many clinicians dose atenolol to a heart rate effect (e.g., to achieve a rate of 120 to 160 beats/min during physical examination in a hospital setting). Doppler echocardiography can be used to confirm that the dose of atenolol is sufficient to control DLVOTO, and the associated murmur should decrease in intensity or disappear completely. Adverse effects of atenolol in asymptomatic cats can include excessive bradycardia and cardiac dilation.

The calcium channel blocker diltiazem has been said to improve left ventricular relaxation, although definitive evidence of this effect in cats is lacking. Diltiazem also slows heart rate, although less consistently than atenolol. Standard-release diltiazem is dosed at 7.5 mg per cat q8h PO, which is impractical for most cat owners. Extended-release preparations of diltiazem such as Dilacor XR permit once- or twice-daily dosing at 15 to 30 mg per cat q12-24h PO. These long-acting diltiazem compounds can achieve therapeutic plasma levels, but precise dosing guidelines for cats have not been reported. Adverse effects of diltiazem include salivation, anorexia, and weight loss.

Although ACE inhibitors have theoretic benefits in cardiomyopathy, there are no data supporting their use in asymptomatic cats. Well-controlled studies in asymptomatic Maine coon cats failed to show a benefit of 12 months of treatment with ramipril at 0.5 mg/kg q24h PO (MacDonald et al, 2006). Another randomized, controlled study (Taillefer and Di Fruscia, 2006) comparing the effects of benazepril (0.5 mg/kg q24h PO) and diltiazem CD (10 mg/kg q24h PO) in 21 cats with preclinical HCM did not identify any relevant difference between groups after 6 months, although a control group was not studied. However, some cardiologists do consider an ACE inhibitor for treatment of asymptomatic cats demonstrating moderate and severe left atrial enlargement.

Although severe left ventricular hypertrophy has been identified as an independent risk factor in people with HCM, and thus therapeutic targeting of left ventricular hypertrophy has been suggested, similar information is not available in feline HCM. Moreover, the mechanisms of hypertrophy may be so diverse in different forms of HCM that one common therapeutic strategy may not be capable of achieving the desired result. ACE inhibitors or angiotensin II receptor antagonists, spironolactone, diltiazem, and statins all have been used successfully in experimental HCM models. However, neither the ACE inhibitor regimen in the study cited previously nor 4 months of treatment with the aldosterone antagonist spironolactone (2 mg/kg q12h PO) showed any effect on estimates of left ventricular diastolic function or chamber dimensions in cats with preclinical HCM (MacDonald et al, 2006, 2008). In the spironolactone study, several cats developed skin lesions with chronic administration.

The specific risk of ATE in asymptomatic cats with HCM has not been reported. Most clinicians view left atrial enlargement as a likely risk factor for this complication, and many consider antithrombotic therapy appropriate in cats with HCM with this echocardiographic finding. This treatment is discussed in the following paragraphs and in Chapter 181. Evaluation of size, content, and flow velocity in the left auricle may contribute to the decision on whether to use antithrombotic treatment (Schober and Maerz, 2006).