Page 187 - Small Animal Internal Medicine, 6th Edition

CHAPTER 8 Myocardial Diseases of the Cat 159

hypertrophy in cats with HCM are variable. Many cats have often causes an ejection murmur of variable intensity in
symmetric hypertrophy, but some have asymmetric septal these cats. Cats with HOCM are thus more likely to have
VetBooks.ir thickening, and a few have hypertrophy limited to the free heart murmurs than cats with nonobstructive HCM. A dia-
stolic gallop sound (usually S 4 ) might be heard, associated
wall or papillary muscles. The LV lumen usually appears
small. Focal or diffuse areas of fibrosis occur within the
Several factors probably contribute to the development of
endocardium, conduction system, or myocardium. Narrow- with high LV filling pressure.
ing of small intramural coronary arteries is commonly noted myocardial ischemia in cats with HCM. These include nar-
and probably contributes to ischemia-related fibrosis. Areas rowing of intramural coronary arteries, increased LV filling
of myocardial infarction and myocardial fiber disarray can pressure, decreased coronary artery perfusion pressure, and
be present. Cats with pronounced systolic anterior motion insufficient myocardial capillary density for the degree of
(SAM) of the anterior mitral leaflet could have a fibrous hypertrophy. Tachycardia contributes to ischemia by increas-
endocardial patch on the interventricular septum (IVS) ing myocardial O 2 requirements while reducing diastolic
where repeated valve contact has occurred. coronary perfusion time. Ischemia impairs early active ven-
Myocardial hypertrophy and the accompanying changes tricular relaxation, which further increases ventricular filling
increase ventricular wall stiffness. Additionally, early active pressure, and over time leads to myocardial fibrosis. Ische-
myocardial relaxation may be slow and incomplete, espe- mia can provoke arrhythmias and, potentially, sudden death.
cially in the presence of myocardial ischemia or abnormal If present, atrial fibrillation (AF) and other tachyarrhyth-
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Ca kinetics. This further reduces ventricular distensibility mias further impair diastolic filling and exacerbate venous
and promotes diastolic dysfunction. The increased ventricu- congestion; the loss of the atrial “kick” and the rapid heart
lar stiffness impairs LV filling and increases diastolic pres- rate associated with AF are especially detrimental. Ventricu-
sure. LV volume remains normal or decreased. Reduced lar tachycardia or other arrhythmias can lead to syncope or
ventricular volume results in a lower stroke volume, which sudden death.
may contribute to neurohormonal activation. Higher heart Eventually, pulmonary venous congestion and edema
rates further interfere with LV filling, promote myocardial result from increasing LA pressure. Cavitary effusions also
ischemia, and contribute to pulmonary venous congestion occur commonly in cats with HCM and CHF; in addition
and edema by shortening the diastolic filling period. Con- to pulmonary edema, approximately half of cats develop
tractility, or systolic function, usually is normal in cats with pleural effusion, and nearly 25% of cats have mild peri-
HCM. However, some cats experience progression to ven- cardial effusion. These effusions usually are modified tran-
tricular systolic failure and dilation. sudates, although they can be (or become) chylous. These
Higher LV filling pressures lead to increased left atrial cavitary effusions, usually associated with right-sided CHF,
(LA) and pulmonary venous pressures. Progressive LA dila- often occur despite echocardiographic appearance of pre-
tion, as well as pulmonary congestion and edema, can result. dominately left heart involvement. This pattern of fluid
LA enlargement can become massive over time. Intracardiac distribution could relate to feline-specific patterns of lym-
thrombi can form, usually within the left auricle but occa- phatic drainage of body cavities, could suggest postcapillary
sionally in the body of the left atrium (LA) or left ventricle pulmonary hypertension with reactive vasoconstriction, or
(LV), or attached to a ventricular wall. Arterial thromboem- might represent underdiagnosis of right heart dysfunction
bolism is a major complication of HCM and other forms of in HCM. Recent evidence suggests that up to 30% to 50% of
cardiomyopathy in cats (see Chapter 12). Mitral regurgita- cats with HCM may have right heart involvement, character-
tion develops in some affected cats and usually is associated ized by segmental or diffuse right ventricular hypertrophy
with changes in LV geometry, abnormal papillary muscle and right atrial (RA) dilation. Cats that manifest CHF with
structure, and/or mitral SAM that prevent complete valve pleural effusion have decreased LA function and larger RA
closure. Valve insufficiency exacerbates increases in LA size volumes compared with cats that develop pulmonary edema
and pressure. exclusively.
Dynamic LV outflow obstruction occurs during systole in
some cats with HCM. This variant is known as hypertrophic Clinical Features
obstructive cardiomyopathy (HOCM). LV papillary muscle HCM is most commonly identified in middle-aged cats,
hypertrophy and abnormal LV or mitral valve geometry are with an average age at diagnosis of approximately 6 years;
thought to produce abnormal hemodynamic forces that pull however, diagnosis at any age is possible. The disease has a
the anterior mitral leaflet toward the IVS during ejection male sex predilection. Overall prevalence of HCM in cats is
(SAM; see echocardiography images later). Excessive asym- estimated to be at least 15% and increases with age. Affected
metric hypertrophy of the basilar IVS can contribute to the cats have a relatively long occult period before development
dynamic obstruction. Both mitral valve SAM and basilar IVS of clinical disease. Many cats are not diagnosed until compli-
hypertrophy can interfere with normal LV outflow. Systolic cations arise. The natural history of HCM is highly variable
outflow obstruction increases LV pressure, wall stress, and among cats. Some cats have relatively mild hypertrophy that
myocardial oxygen demand and promotes myocardial ische- does not worsen or cause clinical disease during the cat’s
mia as well as LV hypertrophy. SAM also causes or exacer- lifetime. Other cats have more rapidly progressive disease.
bates mitral regurgitation. Increased LV outflow turbulence The overall median survival time for cats diagnosed with