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Hypertrophic Cardiomyopathy 505
• Renal function before and during treatment is Technician Tips SUGGESTED READING
important. Cats with an initial combination • Serum submitted for T 4 should be free of Carney HC, et al: AAFP guidelines for the manage-
VetBooks.ir developing post-treatment azotemia should • Serum submitted for FT 4ED should be free AUTHOR: Sylvie Daminet, DVM, PhD, DACVIM, Diseases and Disorders
hemolysis.
of azotemia and hyperthyroidism and cats
ment of feline hyperthyroidism. J Feline Med Surg
18:400-416, 2016.
of hemolysis and lipemia; a fasted sample is
be approached differently.
Prevention recommended. DECVIM
Avoid foods containing soy isoflavones or cans EDITOR: Ellen N. Behrend, VMD, PhD, DACVIM
with plastic linings or easy open lids (pop-tops).
Hypertrophic Cardiomyopathy Client Education
Sheet
BASIC INFORMATION Scottish fold, Bengal, Persian, Himalayan, hypertrophy. Myocardial replacement fibrosis
Birman, and rex; DSH remains the most (dead myocardial cells and interstitial fibrosis)
Definition commonly diagnosed breed. is likely mediated by angiotensin II and
A common, primary myocardial disease charac- aldosterone levels +/− coronary artery
terized by increased left ventricular wall thick- RISK FACTORS abnormalities.
ness (concentric left ventricular hypertrophy • Precipitating events that can lead to conges- • Diastolic dysfunction from altered calcium
[LVH]) in the absence of secondary causes of tive heart failure (CHF) in cats with previ- handling, LVH, myofiber disarray, and
hypertrophy such as systemic hypertension and ously compensated (asymptomatic) HCM myocardial fibrosis
hyperthyroidism include intravenous fluid administration, • Elevated left ventricular filling pressure leads
recent glucocorticoid administration (e.g., to elevated left atrial and pulmonary venous
Synonyms methylprednisolone acetate), and recent pressure and development of left-sided CHF
• Idiopathic hypertrophic cardiomyopathy anesthesia/surgery. (pulmonary edema +/− pleural effusion).
(HCM) • In Maine coon cats with the A31P myosin- • Left atrial thrombus may form secondary to
• Hypertrophic obstructive cardiomyopathy binding protein C3 mutation, the risk blood stasis in the dilated left atrium and
(HOCM) if systolic anterior motion (SAM) ratio for developing LVH is 9.9 or 35.5 if can lead to ATE.
of the mitral valve is present, which obstructs heterozygous or homozygous, respectively.
the left ventricular outflow tract DIAGNOSIS
ASSOCIATED DISORDERS
Epidemiology CHF (pp. 408 and 409), aortic thromboem- Diagnostic Overview
SPECIES, AGE, SEX bolism (p. 74), sudden cardiac death Diagnosis is made by echocardiographic
• A common disease in cats, HCM is rarely Clinical Presentation demonstration of LVH with no identifiable
recognized in dogs. cause. Thoracic radiographs are necessary to
• Juvenile (6 months) to adult age routinely HISTORY, CHIEF COMPLAINT evaluate CHF, but radiographs alone cannot
recognized; average age ≈6 years. Purebred • Often, cats show no clinical signs, and HCM confirm or refute HCM and are often normal
cats often younger (average age at diagnosis: is discovered incidentally (e.g., murmur on for cats with mild or moderate HCM without
Ragdoll = 15 months, Maine coon = 2.5 physical exam). left atrial enlargement and/or CHF. Plasma
years, Sphynx = 3.5 years, British shorthair = • Respiratory abnormalities (CHF): tachypnea, N-terminal pro-brain-type natriuretic peptide
2.3 years). The age is often older for Persian, dyspnea, orthopnea, uncommonly cough (NT-pro-BNP) levels are elevated in a majority
domestic shorthair (DSH), and chartreux (8, • Nonspecific: lethargy, anorexia, vomiting of symptomatic cats with clinically significant
8, and 11 years, respectively). • Lameness, inability to move limb, signs of HCM.
• Males tend to be more severely affected, but intense pain (aortic thromboembolism)
there is no sex-linked heritability. • Sudden death Differential Diagnosis
Echocardiographically, HCM is a diagnosis of
GENETICS, BREED PREDISPOSITION PHYSICAL EXAM FINDINGS exclusion after other causes of LVH have been
• Autosomal dominant heritability with incom- • Systolic murmur (30%-80% of cases) ruled out:
plete penetrance in Maine coon and Ragdoll • Gallop (S 3 or S 4 ) heart sound: varies (≈30%), • Hyperthyroidism
cats. Two different missense mutations of the more likely with CHF • Systemic hypertension
sarcomeric protein myosin-binding protein • Arrhythmia: premature beats, irregular • Subaortic stenosis
C cause HCM in these two breeds; there rhythm (20%-70% of cases) • Acromegaly
likely are additional causative mutations to • Respiratory abnormalities common if CHF:
be discovered in these and other breeds. tachypnea, dyspnea, increased breath sounds, Initial Database
• Worldwide prevalence of genotypically paradoxic breathing, ventrally dampened • Echocardiogram: interventricular septum
affected Maine coon cats is 34% (91% of lung sounds if pleural effusion and/or left ventricular free wall end diastolic
them are heterozygous). • Signs of arterial thromboembolism (ATE) thickness ≥ 6 mm. Papillary hypertrophy is
• Autosomal dominant (one family of American (p. 74) often present (subjective or quantitative).
shorthair cats); probable autosomal dominant SAM of the mitral valve with mitral regur-
heritability with incomplete penetrance Etiology and Pathophysiology gitation and left ventricular outflow tract
(Sphynx) • Initial defect is myocyte dysfunction due obstruction may be variably present. Left
• Other predisposed breeds: Siberian, British to primary sarcomeric defect; remaining atrial enlargement is variably present; a left
shorthair, Norwegian forest cat, Turkish van, sarcomeres develop compensatory concentric atrial to aortic ratio greater than 1.5 or left
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