Page 196 - Small Animal Internal Medicine, 6th Edition

168 PART I Cardiovascular System Disorders

15% of hyperthyroid cats; most have normal to high FS, but difficult to differentiate “true” RCM from end-stage remod-
a few have poor contractile function. Cardiac therapy, in eled HCM.
VetBooks.ir addition to treatment of the hyperthyroidism, is indicated RCM, including marked perivascular and interstitial fibrosis,
There are a variety of histopathologic findings in cats with
for cats with severe hyperthyroid heart disease. Treatment
for CHF is the same as that described for HCM. Treat-
trophy, as well as areas of degeneration and necrosis. Some
ment for preclinical disease with marked LA enlargement intramural coronary artery narrowing, and myocyte hyper-
also is similar to that for HCM, including thromboprophy- cats have extensive LV endomyocardial fibrosis with chamber
laxis with clopidogrel and potentially, vasodilation with an deformity or fibrous tissue bridging between the septum and
ACEI. Concurrent systemic hypertension should be treated LV wall. In such cases, the mitral apparatus and papillary
with amlodipine. A β-blocker can temporarily control many muscles may be fused to surrounding tissue or distorted. LA
of the adverse cardiac effects of excess thyroid hormone, or biatrial enlargement is prominent in cats with RCM as a
especially tachyarrhythmias; for this reason, atenolol is a consequence of chronically high ventricular filling pressure
common adjunct treatment for hyperthyroid heart disease. from increased wall stiffness. The LV may be normal to
Cardiac therapy, including a β-blocker, is not a substi- reduced in size or mildly dilated. Intracardiac thrombi and
tute for antithyroid treatment. Regression of myocardial systemic thromboembolism are common.
hypertrophy (“reverse remodeling”) can sometimes occur LV fibrosis impairs diastolic filling. Most affected cats
in cats after treatment for hyperthyroidism, particularly have normal to only mildly reduced contractility, but this can
definitive treatment with I-131. Treatment with methima- progress with time as more functional myocardium is lost.
zole might or might not resolve or prevent hyperthyroid Some cases develop regional LV dysfunction, possibly from
heart disease, presumably because periodic spikes in cir- myocardial ischemia or infarction. If mitral regurgitation is
culating thyroid hormone can still occur despite apparent present, it is usually mild. Chronically elevated left heart
disease control. filling pressures, combined with compensatory neurohor-
LV concentric hypertrophy is the expected response to monal activation, lead to left-sided or biventricular CHF. The
increased ventricular systolic pressure (afterload). Systemic duration of subclinical disease progression in RCM is
arterial hypertension (see Chapter 11) increases afterload unknown.
because of high arterial pressure and resistance. Increased
resistance to ventricular outflow also occurs with a fixed Clinical Features
(e.g., congenital) subaortic stenosis. In addition, cardiac Middle-aged and older cats are most often diagnosed with
hypertrophy develops in cats with hypersomatotropism RCM, though young cats are sometimes affected. Clinical
(acromegaly) as a result of the trophic effects of growth features are similar to those seen with HCM. Preclinical
hormone on the heart. Increased myocardial thickness occa- disease might be discovered by detection of abnormal heart
sionally results from infiltrative myocardial disease, most sounds or arrhythmias on routine examination or radio-
notably from lymphoma. Cats with hypertensive heart graphic evidence of cardiomegaly. Clinical signs of CHF
disease, acromegalic heart disease, or myocardial lymphoma most commonly involve respiratory signs from pulmonary
might require cardiac medications in addition to treatment edema or pleural effusion; inactivity, poor appetite, vomit-
for the underlying disease. In general, treatment for second- ing, and weight loss also are common in the history. Clinical
ary myocardial hypertrophy is the same as that described for signs can be precipitated or acutely worsened by stress or
HCM. concurrent disease that causes increased cardiovascular
demand. Signs associated with thromboembolic events
depend on the location and extent of vascular obstruction
RESTRICTIVE CARDIOMYOPATHY but can be severe (see Chapter 12, p. 224).
Physical examination might reveal a systolic murmur of
Etiology and Pathophysiology mitral or tricuspid regurgitation, an S 4 gallop sound, and/or
RCM is a myocardial disease phenotype associated with an arrhythmia. Pulmonary sounds can be abnormal in some
extensive endocardial, subendocardial, or myocardial fibro- cats with pulmonary edema, or muffled with pleural effu-
sis of unclear, but probably multifactorial, etiology. Char- sion. Femoral arterial pulses could be normal, slightly weak,
acteristic features include diastolic dysfunction (restrictive or absent (if caudal aortic thromboembolism has occurred).
filling physiology) and severe LA enlargement in the absence Jugular vein distention and pulsation are common in cats
of myocardial hypertrophy. This condition could be a conse- with right-sided CHF. Acute signs of distal aortic (or other)
quence of endomyocarditis or infiltrative neoplastic disease thromboembolism may be the reason for presentation.
(e.g., lymphoma), or may be idiopathic; no specific familial
associations or genetic mutations have been identified. It is Diagnosis
important to remember that advanced HCM also is charac- Diagnostic test results are similar to those in cats with HCM.
terized by restrictive LV filling, and that chronic ischemia Routine clinicopathologic findings are nonspecific, although
and fibrosis can result in an end-stage or “remodeled” HCM NT-proBNP can be useful in some clinical scenarios, as in
phenotype with minimal hypertrophy and focal areas of wall HCM (see p. 162). Radiographs indicate LA or biatrial
thinning. Thus without serial echocardiography it can be enlargement (sometimes massive) and LV or generalized