The feline heart is a hollow, muscular organ located in the center of the chest. Both the right and left sides of the heart have an upper chamber (atrium), which collects circulating blood, and a lower chamber (ventricle), which serves as the primary pump to move blood away from the heart into the circulation.

Cardiomyopathy, which literally means “disease of the heart muscle,” refers to primary diseases of this heart muscle (myocardium) itself, as opposed to diseases of the heart valves, blood vessels, and the tissue that conducts electrical activity through the heart. Feline cardiomyopathies can cause the (usually ventricular) heart muscle to become too thick, too thin, and/or inflamed. These changes in heart structure are commonly accompanied by a decreased ability of the heart to efficiently pump blood that can lead to congestive heart failure (CHF), paralysis-causing blood clots, and, in some cases, sudden death.

The cause of the majority of feline cardiomyopathies is currently unknown, and many have been shown to be or are presumed to be genetically mediated. Some, however, occur secondary to other diseases such as hyperthyroidism, high blood pressure, inflammation within the myocardium, or (much less commonly) growth hormone excess.

Far and away the most common type of feline cardiomyopathy is hypertrophic cardiomyopathy (HCM, affecting up to 15% of the feline population), which is characterized by thickening of the left ventricular myocardium. This thickening results in poor filling of the ventricle between contractions and, sometimes, obstruction of blood flow from the ventricle to the body. These problems can cause the left atrium to become dilated (enlarged), and ultimately to an increase in fluid pressure in the blood vessels in the lungs that can progress to the leakage of fluid from vessels into the lung tissue, called pulmonary edema. This process is referred to as congestive heart failure (CHF). Cats suffering from CHF usually show signs of an increased respiratory effort and an accelerated respiratory rate (above 35 breaths/minute when resting). Blood clots (thrombi) may also develop in the dilated left atrium of affected cats, and if one of these breaks up, small pieces of it may be ejected from the heart and travel to other parts of the body where they can lodge in arteries and block blood flow to muscles and/or other organs (celled thromboembolism). The most common place for these thrombi to lodge is in the arteries that supply blood to the hind limbs (called a saddle thrombus). Cats that suffer from a saddle thrombus usually experience a sudden onset of hind limb lameness or paralysis, usually accompanied by severe pain.

Breeds predisposed to HCM include the Maine Coon, Ragdoll, Sphynx, British Shorthair, Chartreux, and Persian breeds.

The second most common type of feline cardiomyopathy is restrictive cardiomyopathy (RCM). This condition is characterized by the excessive buildup of scar tissue on the inner lining and muscle of the ventricle that prevents it from relaxing completely, filling adequately, and emptying appropriately with each heartbeat. Cats with RCM are also at risk of developing CHF and thromboembolism.

A third type of cardiomyopathy called dilated cardiomyopathy (DCM). This condition is characterized by a dilated, thin walled left ventricle that cannot generate sufficient pressure to eject blood when it contracts. Cats with DCM are similarly at risk for the development of CHF and thromboembolism. The condition is usually due to dietary deficiency of an important amino acid called taurine, and since the vast majority of cat food manufacturers now routinely supplement their products with sufficient taurine, the incidence of feline DCM has become very low.

More recently, a phenomenon referred to as transient myocardial thickening (TMT) has been recognized in cats. As its name implies, the thickening seen in affected cats is transient and resolves on its own. TMT is usually seen in younger cats than the other cardiomyopathies and is often preceded by a stressful event such as anesthetic administration, bite wounds, car accidents, tooth extraction, vaccination, and pneumonia. The cause of TMT is current unknown, but transient inflammation of the myocardium has been proposed as being contributory to this condition. Importantly, the prognosis for cats with TMT is generally much better than for the other feline cardiomyopathies.

Many cats with cardiomyopathies don’t show any signs of disease early in their progression. The most common clinical signs (symptoms) of cats with cardiomyopathies once they develop include rapid/labored breathing due to CHF, lethargy, and decreased appetite. Cats that suffer from thromboembolism may experience a sudden onset of paralysis of (most commonly, but not exclusively) the hind limbs. Rapid/labored breathing and/or sudden paralysis are considered medical emergencies that must be addressed immediately. Unfortunately, cats with cardiomyopathies are at risk of sudden death.

The gold standard for the diagnosis of feline cardiomyopathies is echocardiography (ultrasound of the heart). Radiographs (X-rays) of the chest will often be taken to determine whether CHF is present, and sometimes an electrocardiogram will be recommended. A type of blood test called NT pro-brain-derived natriuretic peptide (NT-pro BNP) may be used as a screening tool in some cases in which echocardiography is not immediately available. This protein is released into the bloodstream by the heart when it is dilated, and elevated NT-pro-BNP may be an indicator of left atrial dilation in affected cats. Importantly, NT-pro-BNP cannot be used to make a definitive diagnosis of feline cardiomyopathy, but can assist in identifying cases that may benefit from further diagnostic testing.

The treatment of cats with cardiomyopathies is dictated primarily by whether they have dilated left atria, in which cases anti-clotting drugs may be prescribed to decrease the likelihood of thrombus formation, and whether they are experiencing CHF, in which case oxygen therapy, diuretics, and other cardiac drugs may be required. Many cats do not require treatment early in their disease progression, and some may go years without requiring therapy.

With appropriate care, a cat diagnosed with cardiomyopathy may survive for years, depending upon whether CHF and/or thromboembolism occurs. Cats diagnosed with TMT generally have the most favorable prognosis among all feline cardiomyopathy patients, as they carry a good prognosis even if they develop CHF. Many cats diagnosed with HCM live normal or near-normal lifespans. The prognosis of cats diagnosed with RCM is less favorable than that of cats with HCM, with a median survival time of 1-2 years if they are not initially diagnosed with CHF. Cats diagnosed with either HCM, RCM, or DCM generally carry guarded prognoses once they develop CHF, with expected medial survival times ranging between 2 and 12 months. Cats that experience thromboembolism, regardless of type of the type of cardiomyopathy that causes it, generally carry a guarded to poor prognosis.

Updated March 2024