Feline heart disease can take on many forms, and can be congenital or acquired. The complex anatomy of the heart requires all components to be functioning in perfect balance for long term health. Increases as well as decreases in the efficiency of blood flow through the four chambers of the heart, to and from the lungs, and out to the body can become progressive and lead to heart failure by a variety of pathways and compensatory feedback mechanisms. Any abnormalities upon auscultation such as heart murmurs, arrhythmias, gallop rhythms, tachycardia, or bradycardia should be carefully evaluated even in a patient that is otherwise asymptomatic regardless of age. Cats are notorious for hiding clinical signs until the condition advances to a dangerous level, and the most common cardiac diseases in cats are best managed early.
Heart disease may result from disruptions in function of any of the valves of the heart, function of the papillary muscles or cords that attach to the valves, the size or tone of the major vessels flowing into or out of the heart, the size of the chambers, or the thickness of the chamber walls. In the geriatric feline, the most common cause of heart disease is myocardial, or related to heart muscle. The chamber walls are composed of cardiac muscle tissue, and are susceptible to excess or insufficient development from multiple causes. This discussion will focus primarily on cardiomyopathies commonly seen in the geriatric feline.
First, a brief summary of the flow of blood through the heart may be useful. After circulating through the body and delivering oxygen to tissues, blood returns to the heart via the vena cava. It empties into the right atrium, passes through the right atrioventricular valve (tricuspid valve) into the right ventricle, then passes through the pulmonary valve into the pulmonary artery where it is carried to the lungs to become oxygenated. Fresh, oxygenated blood returns to the heart via the pulmonary vein and empties into the left atrium. From the left atrium, it passes through the left atrioventricular valve (mitral valve) into the left ventricle, which pumps fresh blood through the aortic valve and into the aorta. The aorta is the primary artery which leads oxygenated blood away from the heart to feed the body.
Hypertrophic cardiomyopathy (HCM) is a primary condition of enlargment or thickening of the wall of the left ventricle and interventricular septum, as well as possible thickening of the papillary muscles which control the mitral valve. There is a wide variation in the extent of hypertrophy between patients, not only in terms of size but also in terms of uniformity and symmetry, or lack thereof. As the disease progresses, secondary atrial dilation often occurs as blood flow from the lungs is restricted. The cause of HCM is often idiopathic, but in many cases there is evidence of a strong hereditary component of an autosomal dominant gene which alters the protein formation and development of the sarcomere of the muscle. Because of this genetic component, HCM is not exclusively a disease of the geriatric feline and can occur in cats of all ages. When considering all cases of idiopathic and inherited, the documented average age of diagnosis is approximately 7 years.
Function of the heart in an HCM patient is impaired in several ways. Thickening of the papillary muscles which control the mitral valve create a malpositioning of the valve which can partially obstruct the outflow of blood from the left ventricle to the aorta. In addition, a malfunctioning mitral valve, which is normally designed for one way flow, may allow backflow of blood from the ventricle back into the atrium, causing a heart murmur. Compounding the complication with the mitral valve, the thickening of the ventricle walls causes stiffening, which inhibits the ability of the ventricle to relax sufficiently to fill with blood at the proper pressure. The increased pressure in the left ventricle increases the pressure in the left atrium, which compensates by dilating. If the problem persists, the lungs also become affected. Blood that normally drains from the lungs, into the atrium, and into the ventricle becomes backed up in the capillary beds of the lungs and chest cavity. Increased pressure in the capillaries forces fluid from these capillaries and results in excessive perfusion of lung tissue, pulmonary edema, and eventually pleural effusion (congestive heart failure). A final complication results from the slowed blood flow through the atrium. Somewhat stagnant flow increases the chance of blood clots to form within the left atrium, which can move through the heart, into the aorta, and become lodged at some point in the body where the arteries decrease in diameter. A common location for this is where the aorta splits into two smaller branches to feed the hind legs. A clot lodged at this location is referred to as a saddle thromboembolus, and results in rear leg paralysis.
As mentioned previously, feline patients tend to hide their signs and show few symptoms in the early stages of HCM (or any other heart disease). Heart murmurs (mitral or aortic) and other signs detectable on auscultation are not always present in the early stages, but are often the first detectable sign on basic physical examination. As the disease advances, some signs that may become apparent are varying degrees of dyspnea, anorexia, cyanosis, lethargy, and of course rear leg paralysis. Unfortunately, HCM can result in congestive heart failure and death quite suddenly, with little to no history of detectable symptoms.
Hypertrophic cardiomyopathy must be differentiated from secondary myocardial hypertrophy caused by a host of other diseases. HCM is, by definition, a primary disease of the heart. Myocardial hypertrophy is also characterized by excessive thickening of the left ventricle (and sometimes the right) and can result in the same chain of events leading to congestive heart failure, but the thickening is caused by a known and usually treatable disease separate from the heart. Examples of diseases that can cause thickening of the left ventricle are systemic hypertension, hyperthyroidism, aortic stenosis, kidney disease, and excessive growth hormone (acromegaly).
Hyperthyroidism is particularly important in aged feline patients. In some cases, myocardial hypertrophy is detected first, and thyroid screening tends to be standard practice to help determine if the patient has primary HCM or secondary hypertrophy. Hyperthyroid patients, if left untreated, have a high rate of occurrence of secondary myocardial hypertrophy and congestive heart failure.
Excess thyroid hormone, which increases metabolic rate throughout the body, directly stimulates heart rate by stimulating the action of the sympathetic nervous system. The sympathetic nervous system increases heart rate by direct impulses to beta adrenergic receptors within cardiac muscle, increasing contractility. In addition, alpha receptors in peripheral tissues are stimulated, which causes peripheral vasodilation to accommodate increased cardiac output. Finally, thyroid hormone directly upregulates gene expression for the synthesis of contractile proteins within cardiac muscle cells. These direct effects are compounded by the increased oxygen demand in all areas of the body and a call for more blood flow to feed the increased metabolic rate. In a nutshell, hyperthyroidism increases demand on the heart, and the heart hypertrophies to meet those demands. If the hemodynamic stress of hyperthyroidism is not relieved, the damage can become permanent and progressive, either in the form of wearing out the heart like an old machine that just quits, or in a nearly identical series of events as described for HCM.
Restrictive Cardiomyopathy (RCM) describes non-hypertrophied ventricles with normal systolic function. RCM includes a variety of phenotypes resulting in a physiological restriction in ventriclar filling, except those that fall under the category of HCM. In fact, areas of the chamber wall may have regional scarring or thinning possibly due to atrophy or infarction. If thickening is present, it is usually due to excess scarring and fibrous tissue rather than hypertrophy or hyperplasia of cardiac muscle cells. Fibrous bands can bridge areas of myocardial thinning, or completely fill in the left ventricular apex by bridging from the septum to the papillary muscles of the chamber wall. Like HCM, ventricular relaxation and chamber compliance are restricted, which progressively increases left atrial pressure and can lead to pleural effusion or congestive heart failure. There are likely several causes of RCM, most of which are not fully understood. It tends to be a disease of middle aged to geriatric cats. Suggested causes include primary HCM with secondary myocardial infarcts, myocarditis, endomyocarditis, eosinophilic myocardial infiltration, diffuse small vessel disease, or any inflammatory cell infiltration that damages cardiac muscle.
DILATED Dilated Cardiomyopathy (DCM) in cats was once a common condition primarily caused by dietary taurine deficiency. The prevalence has decreased as more pet cats are being fed commercial foods supplemented with taurine, but can still occur with or without a regular healthy diet. There appears to be a genetic inheritance to a predisposition to the development of DCM in other species, but has not been proven in cats. DCM is characterized by a global wall thinning and dilation of all four cardiac chambers, with overall cardiomegaly, which often results in elevation of the trachea by secondary compression. Enlargement is usually most pronounced in the left ventricle and systolic function is markedly reduced. Inflammation tends to be absent in DCM patients, or when present it is unrelated. Chronic passive congestion of the lungs and abdominal viscera is the most common progression in cats, which leads to pleural and abdominal effusion. DCM is also appropriately referred to as congestive cardiomyopathy.
Each of the cardiomyopathies described have two things in common.
They are difficult to recognize early without a full evaluation, and they each have the potential to rapidly progress to full congestive heart failure. When discovered early, they may be managed and kept under control, and sometimes cured depending on the etiology of onset. As damage progresses, prognosis also progresses from good to guarded or grave. In late stage cardiomyopathy, there are drug therapies to manage symptoms and temporarily alleviate discomfort, which are a topic for a later discussion, but there is usually no cure for advanced congestive heart failure. Early detection is the key to recovering from cardiomyopathy of any kind.