There are approximately 60 million cats in the US, of which it is estimated that 11% have heart disease.
There are approximately 60 million cats in the US, of which it is estimated that 11% have heart disease. Of the heart diseases approximately 85% are hypertrophic cardiomyopathy (hCMy); the prevalence of systemic arterial hypertension (SAH) is unknown but probably more prevalent than hCMy. The vast majority of other diseases affecting the heart of cats occur rarely. Hyperthyroidism is the exception and may occur in as many as 1 in 300 cats, with some estimates that 1/5th of them may develop heart failure.
hCMy refers to idiopathic hypertrophy of one or more portions (septum, free-wall, both) of the left ventricle in which myofibers may be more numerous than normal and in disarray, and with arteriole sclerosis leads to patches of myocardial fibrosis. Hypertrophy of the septum may result in obstruction of the flow of blood from the left ventricle—termed dynamic outflow tract obstruction—often accompanied displacement of the anterior leaflet of the mitral valve—termed systolic anterior motion (SAM). The 2 together may limit outflow from the left ventricle and produce a systolic ejection-type murmur, and may produce mitral regurgitation with a typical murmur of that physiology. Typically the left ventricle is excessively stiff, fills less and/or more slowly, and terminates filling more abruptly, giving rise to abnormal gallop sounds. Hypertrophy may be attributed to excessive angiotensin-II or other cytokines that stimulate proliferation of muscle components, and it certainly, in many cases, a genetic disease.
Systemic arterial hypertension refers to elevation of pressure within the systemic arteries. In humans arterial pressure fluctuates from approximately 120 mmHg in systole when the ventricle contracts to 80 mmHg in diastole when the ventricle relaxes. There are no absolute limits of systemic arterial pressure in cats which if exceeded constitute SAH. Upper limits of systolic pressure may be as high as 180 mmHg (in part because cats become agitated when blood pressure is taken, in part depending upon how the pressure is measured), and normal diastolic pressure has been described as anywhere from 50 mmHg to 120 mmHg. Arterial blood pressure is a balance between how much blood the heart ejects (i.e., cardiac output, CO) and the hindrance to flow imposed by the aorta (impedance) or systemic arterioles (systemic vascular resistance). Thus SAH may result from an elevated CO (but rarely so), but more so from stiffening of the arterial walls due to constriction of vascular smooth muscle. In cats, the most common mechanism is probably stiffening of the system arterioles due to primary kidney disease in which the kidney produces renin which activates vasopressor neuroendocrines (e.g., arginine vasopressin, angiotensin-II) and the adrenergic portion of the sympathetic nervous system. This is often called renoprival hypertension. Hyperthyroidism results most often from thyroid adenomas of 12 or both lobes of the gland. These may be palpable in many cats, but of course the detection depends upon experience.
Cats with either hCMy or SAH and with hyperthyroidism may present with similar symptoms/signs. They may be dyspneic due to either pulmonary edema (with louder than usual breath sounds) or more likely pleural effusion (with softer than usual breath sounds), heart rate may be elevated, they may have "extra" heart sounds produced by S3 and/or S4 gallops, and they usually have left ventricular hypertrophy and left atrial enlargement. Those with more severe edema and effusion may be cyanotic and may "mouth" breath. Pressure pulses are unremarkable, and they will (not infrequently) have arrhythmias. Often cats with hCMy will present with thromboembolism affecting (usually but not always) the pelvic limbs causing them excruciating pain and paresis. The greatest number of cats with either hCMy or SAH are asymptomatic; cats with hCMy probably remain asymptomatic for years or for their entire lives. Cats with SAH often develop; retinal hemorrhages, detached retinae, retinal edema, tortuous retinal arteries. Their arterial pulses are usually of normal intensity. Because most often SAH in cats is secondary to other diseases, it is not unusual to observe azotemia from primary renal disease, or denuding and a pendulous abdomen from hyperadrenocorticism, or hyperglycemia from diabetes.
Echocardiography and measurements of blood pressure and T4 will most often allow identification the specific heart disease. Although measuring blood pressure is very difficult in most cats, indirect sphygmomanometry produces pressures in excess of 160/110 in most hypertensives, cats with hCMY seldom have hypertension, and echocardiography reveals the classical hypertrophic pattern, often SAM, and elevated flow velocities through the aortic and/or mitral valves. Furthermore the systolic murmurs of either aortic stenosis or mitral regurgitation are usually significantly louder in cats with hCMy than with SAH. Of course cats with hyperthyroidism often manifest elevated T4 but not T3. Images using radionuclide allow identification of precise regions of the thyroid involved. Whereas cats of any age may develop hCMy, both hyperthyroidism and SAH usually develop in relatively older cats, >6 years of age. Cats with any form of heart disease may manifest arrhythmias, often tachycardias, and (not infrequently) accelerated junction rhythms.
hCMy—Cats with hCMy usually require no therapy, unless they develop either pulmonary edema or pleural effusion. The former is treated with diuretics (e.g., furosemide, 6.25 to 12.5 mg po qd to tid); the latter with pleurocentesis. [It is important to consider lymphoma as a cause for pleural. It is important to consider asthma as a cause for dyspnea.] The differential can be made most often by there being bronchial breath sounds in the former, and diminished vesicular breath sounds in the latter, or (of course) by radiography. Although both B-blockers (e.g., atenolol, 6.25 to 12.5 mg qd to bid, po per cat) and calcium channel blockers (e.g., diltiazem, 7.5 mg tid, po/cat) have been used, there is little evidence of efficacy, although also little evidence of risk. There is significant experimental evidence that ACE inhibitors (e.g., enalapril, 2.5 mg qd po/cat) may delay worsening of disease and that angiotenis-II may of genetic origin be responsible for the disease. In later stages of disease, or if there is massive left atrial enlargement, digitoxin (0.1 mg/cat po, q 7 days) and pimobendan (may be of use by strengthening atrial contraction and improving left ventricular filling, as well as for slowing heart rate and improving appetite. Because thromboembolism occurs in cats with hCMy, if they have very large left atria, have clouds in the atrium on echo exams, or have shed clots before, the cats should be on either 40 mg of aspirin, po q3d or 0.5 mg coumadin po qd. Efficacy of either anticoagulant is unknown, and bleeding may be a complication of Coumadin and gastritis a complication of aspirin.
SAH—Blood pressure may be reduced by decreasing the adrenergic drive to the heart by using atenolol, and/or by relaxing systemic arterial smooth muscle (amlodipine, 0.625 to 1.25 mg/cat po qd or less effectively ACE inhibitors). Many other potential antihypertensives (e.g., prazosin, hydralazine) have been used and may prove more efficacious in certain cats.
Hyperthyroidism—This may be treated with antithyroid drugs (methimazole, 2.5 to 7.5 mg/cat po bid), ablation with radioactive iodine at appropriate centers, or surgical removal of the adenoma.