Page 199 - Small Animal Internal Medicine, 6th Edition

CHAPTER 8 Myocardial Diseases of the Cat 171

concentration is low or cannot be measured. Clinical valve apparatus appears structurally normal. Other possible
improvement, if it occurs, generally is not apparent until findings include abnormal muscular trabeculation, aneurys-
VetBooks.ir after a few weeks of taurine supplementation. Improved sys- mal dilation, areas of dyskinesis, and paradoxical septal
motion. Tricuspid regurgitation appears to be a consistent
tolic function is seen echocardiographically within 6 weeks
of starting taurine supplementation in most taurine-deficient
enlargement, if the LV myocardium is affected.
cats. In some taurine-responsive cats, cardiac medications finding on Doppler examination. Some cats also have LA
might be tapered and discontinued after 6 to 12 weeks (with The prognosis is guarded once signs of heart failure
close monitoring for recurrence of CHF). For cats previously appear. Recommended therapy is similar to that for other
eating a taurine-deficient diet, it may even be possible to causes of CHF in cats, and includes diuretics as needed, an
transition from taurine supplementation to a diet known to ACEI, pimobendan, and prophylaxis against thromboembo-
support adequate plasma taurine concentrations (e.g., most lism. Additional antiarrhythmic therapy may be necessary
name-brand commercial foods). Dry diets with 1200 mg of (see Chapter 4). In people and Boxer dogs with ARVC, ven-
taurine per kilogram of dry weight and canned diets with tricular tachyarrhythmias are a prominent feature and
2500 mg of taurine per kilogram of dry weight are thought sudden death is common. Right heart dysfunction and right-
to maintain normal plasma taurine concentrations in adult sided CHF are a more consistent feature of ARVC in cats
cats. Requirements could be higher for diets incorporating compared with Boxer dogs.
rice or rice bran. Reevaluation of the plasma taurine concen-
tration 2 to 4 weeks after discontinuing the supplement is UNCLASSIFIED CARDIOMYOPATHY
advised. UCM is a term used in people to describe cases of myocar-
Taurine-deficient cats that survive a month after initial dial disease that do not fit within other defined categories
diagnosis appear to have approximately a 50% chance for (HCM, RCM, DCM, or ARVC). In cats, this label is most
1-year survival. It might be possible to wean the cat off some often applied to cases with severe LA or biatrial dilation
or all cardiac medications long-term. The prognosis for cats despite normal LV size, wall thickness, and systolic function,
with DCM that are not taurine deficient is guarded to poor, and without obvious evidence of endomyocardial fibrosis
with median survival time of 49 days even with pimobendan (which would otherwise denote RCM). It is unclear whether
treatment. UCM represents a distinct disease entity in cats; more likely,
UCM includes end-stage or “remodeled” phenotypes of
other cardiomyopathies, particularly HCM. Prevalence of
OTHER MYOCARDIAL DISEASES UCM varies significantly among reports, likely owing to dif-
ferences in diagnostic criteria. Most commonly it is esti-
ARRHYTHMOGENIC RIGHT mated that UCM comprises approximately 10% of feline
VENTRICULAR CARDIOMYOPATHY cardiomyopathy cases.
Arrhythmogenic RV cardiomyopathy (ARVC) is a rare idio- Clinical features of UCM are similar to those for other
pathic cardiomyopathy similar to ARVC in people. Charac- feline cardiomyopathies. The median age at diagnosis in one
teristic features include moderate to severe RV chamber small study (8.8 years) is higher than for HCM or RCM,
dilation, with either focal or diffuse RV wall thinning. RV again supporting the notion that UCM may represent a
wall aneurysm also can occur, as can dilation of the RA and, common end-stage disease phenotype. Heart murmurs and
less commonly, the LA. Myocardial atrophy with fatty and/ arrhythmias are common on physical examination. The ECG
or fibrous replacement tissue, focal myocarditis, and evi- may show ventricular or supraventricular tachyarrhythmias,
dence of apoptosis are typical histologic findings. These are and/or evidence of LA or LV enlargement. Radiographs indi-
most prominent in the RV wall. Fibrous tissue or fatty infil- cate cardiomegaly with LA or biatrial enlargement; pleural
tration is sometimes found in the LV and atrial walls. effusion is more common than pulmonary edema. Echocar-
Signs of right-sided CHF are common, including jugular diography confirms atrial enlargement, with characteristics
venous distention, ascites or hepatosplenomegaly, and of ventricular structure and function inconsistent with other
labored respirations caused by pleural effusion. Syncope cardiomyopathy categories.
occurs occasionally. Lethargy and inappetence without overt Treatment of UCM is identical to treatment for RCM.
heart failure are the presenting signs in some cases. Patients in CHF receive furosemide, pimobendan, and ACEI,
Thoracic radiographs indicate right heart and sometimes and thromboprophylaxis with clopidogrel, as well as dietary
LA enlargement. Pleural effusion is common. Ascites, caudal and lifestyle management. Prognosis is variable and probably
vena caval distention, and evidence of pericardial effusion similar to that for other cardiomyopathies.
could also be evident. The ECG can document various
arrhythmias in affected cats, including VPCs, ventricular CORTICOSTEROID-ASSOCIATED
tachycardia, AF, and supraventricular tachyarrhythmias. A HEART FAILURE
right bundle branch block pattern appears to be common; CHF has been reported in cats approximately 3 to 7 days
some cats have first-degree AV block. Echocardiography after receiving injectable long-acting corticosteroids (such as
shows severe RA and RV enlargement similar to that seen Depo-Medrol). The proposed mechanism is the diabetogenic
with congenital tricuspid valve dysplasia, except that the effect of glucocorticoids causing a transient hyperglycemia