Page 198 - Small Animal Internal Medicine, 6th Edition

170 PART I Cardiovascular System Disorders

simple deficiency of this essential amino acid are likely to Echocardiography is an important tool to differentiate
be involved in the pathogenesis, including genetic factors DCM from other myocardial pathophysiology. Findings are
VetBooks.ir and a possible link with potassium depletion. Not all cats analogous to those in dogs with DCM (see p. 144). Poor FS
(<26%), increased LV end-systolic (e.g., >1.1 cm) and end-
fed a taurine-deficient diet develop DCM, and taurine
deficiency can occur even in cats fed a balanced commer-
septal separation (>0.4 cm) have been described as diagnostic
cial diet. Relatively few cases of DCM are identified now, diastolic (e.g., >1.8 cm) diameters, and wide mitral E point–
and most of these cats are not taurine deficient. DCM in criteria for DCM in cats. Cats with only focal hypokinesis
these cats could be idiopathic or represent the end stage (for example, of only the LV wall or septum) may actually
of another myocardial metabolic abnormality, toxicity, have UCM or end-stage remodeled HCM, particularly if
or infection. focal areas of hypertrophy are present. In DCM, ventricular
Doxorubicin can cause characteristic myocardial histo- wall thickness is normal or decreased. An intracardiac
pathologic lesions in cats as it does in dogs, and in rare thrombus is identified in some cats, usually within the LA.
instances echocardiographic changes consistent with DCM As with other feline heart diseases, routine clinicopatho-
can occur after cumulative doses of 170 to 240 mg/m . logic testing is generally nonspecific. Prerenal azotemia,
2
However, clinically relevant doxorubicin-induced cardiomy- mildly increased liver enzyme activity, and a stress leuko-
opathy is not an issue in the cat; anecdotally, total cumulative gram are common. Elevated NT-proBNP and cardiac tropo-
doses of up to about 600 mg/m (23 mg/kg) have been nin concentrations are expected, particularly in cats with
2
administered without evidence of cardiotoxicity. CHF.
Plasma or whole blood taurine concentration measure-
Pathophysiology ment is recommended to detect possible deficiency, even in
DCM in cats has a similar pathophysiology to that in dogs cats fed commercial diets. Specific instructions for sample
(see p. 141). Poor myocardial contractility is the character- collection and mailing should be obtained from the labora-
istic feature. Usually, all cardiac chambers become dilated. tory used. Plasma taurine concentrations are influenced by
AV valve insufficiency occurs secondary to chamber enlarge- the amount of taurine in the diet, the type of diet, and the
ment and papillary muscle atrophy. As cardiac output time of sampling in relation to eating; an 8-hour fast is rec-
decreases, compensatory neurohormonal mechanisms are ommended. A plasma taurine concentration of less than
activated, leading eventually to signs of CHF and low cardiac 40 nmol/mL in a cat with DCM is diagnostic for taurine
output. Pulmonary edema, pleural effusion, and arrhythmias deficiency. Nonanorexic cats with a plasma taurine concen-
are common in cats with DCM. tration of less than 60 nmol/mL probably should receive
taurine supplementation or a different diet. Whole blood
Clinical Features samples produce more consistent results than plasma
DCM can occur at any age, although most affected cats are samples. Normal whole blood taurine concentrations exceed
late-middle aged to geriatric. There is no breed or sex predi- 200 nmol/mL; < 150 nmol/L is diagnostic for taurine
lection. Clinical signs of CHF often include anorexia, leth- deficiency.
argy, and increased respiratory effort or dyspnea. Evidence
of poor cardiac output is usually found in conjunction with Treatment and Prognosis
congestive signs (right-sided, left-sided, or biventricular The goals of acute and chronic CHF treatment are similar to
CHF). Hypothermia, jugular venous distention, an attenu- those for cats with other cardiomyopathies (see p. 164) and
ated precordial impulse, weak femoral pulses, a gallop sound analogous to those for dogs with DCM. Emphasis is placed
(usually S 3 ), and a left or right apical systolic murmur (of on inotropic support; pimobendan is indicated in all cases
mitral or tricuspid regurgitation) are common. Bradycardia and should be instituted as soon as oral medication can safely
and arrhythmias can be present, although many affected cats be given. Dobutamine (or dopamine) is administered by CRI
have normal sinus rhythm. Increased lung sounds and pul- for critical cases (see p. 62 and Box 3.1). Frequent ventricular
monary crackles may be auscultated, but pleural effusion tachyarrhythmias might respond to lidocaine, mexiletine,
often muffles the lung sounds. Some cats have signs of arte- conservative doses of sotalol, or combination antiarrhyth-
rial thromboembolism (see p. 224). mic therapy (see Table 4.2). However, β-blockers (including
sotalol) must be used cautiously (if at all) in cats with DCM
Diagnosis and CHF because of their negative inotropic effect. Hemo-
Generalized cardiomegaly with rounding of the cardiac apex dynamically significant supraventricular tachyarrhythmias
is often seen on radiographs. Pleural effusion is quite are treated with diltiazem, again with caution because of
common and may obscure the heart shadow and coexisting the drug’s negative inotropic effect. Management of throm-
evidence of pulmonary edema or venous congestion. Hepa- boembolism is described in Chapter 12, p. 227. Hypother-
tomegaly and ascites also might be detected. Normal sinus mia is common in cats with decompensated DCM; external
rhythm predominates; variable ECG findings can include warming is provided as needed.
ventricular or supraventricular tachyarrhythmias (although Supplemental taurine is recommended for taurine-
AF is rare), AV conduction disturbance, and an LV enlarge- deficient patients. Taurine (250-500 mg orally q12h) is insti-
ment pattern. tuted as soon as practical in cases where plasma taurine