Page 301 - Clinical Small Animal Internal Medicine

27 Feline Myocardial Disease 269

regurgitation. Outflow tract obstruction can be severe HCM with myocyte loss or ES‐HCM, and they may in
VetBooks.ir enough to result in a pressure gradient across the LV out- fact be part of the same wide spectrum of HCM.
flow tract of over 100 mmHg for much of systole. In
human HCM patients, the additional myocardial oxygen
consumption associated with outflow tract obstruction DCM
can cause myocardial ischemia, which is further exacer- This form of cardiomyopathy is now very uncommon in
bated by the concurrent narrowing of small coronary cats, despite being the most common phenotype in dogs.
arteries that is a feature of HCM in both humans and A DCM phenotype is characterized by systolic dysfunc-
cats. Clinical signs of outflow tract obstruction in human tion with normal or reduced LV wall thickness and is
HCM patients include exertional dyspnea and chest pain. associated with an increase in diastolic and systolic ven-
The exact clinical effect in cats is difficult to determine, tricular dimensions. An association was identified in the
as chest pain could easily pass unnoticed by owners, and late 1980s between DCM in cats and dietary taurine bio-
the majority of affected cats appear to be subclinical. availability, and since that time, a change in pet food
Some owners report open‐mouth breathing during play, manufacturing processes has resolved this problem.
despite an absence of documentable pulmonary edema. Accordingly, most cats with a DCM phenotype are found
With progression of HCM, diastolic filling of the LV to have normal plasma taurine concentrations.
may be further impaired as interstitial fibrosis worsens, Congestive heart failure, arterial thromboembolism, and
and the LV myocardium becomes stiffer. Ischemic epi- low‐output signs are all common presentations for DCM.
sodes can result in focal areas of myocardial damage,
resulting in replacement fibrosis. Neurohormonal acti- Arterial Thromboembolism
vation adds to the problem by causing plasma volume All of the above forms of cardiomyopathy may lead to
expansion through sodium and water retention, and intracardiac thrombus formation if disease is sufficiently
signs of chronic congestive heart failure become more advanced (i.e., with left atrial enlargement and dysfunc-
likely. Signs include pulmonary edema, pleural effusion tion). Arterial embolization of thrombus (ATE) into the
or both. Cats at this stage are also at risk of arterial systemic circulation causes vascular occlusion and acute
thromboembolism, as LA contractile function deterio- ischemia of downstream tissues, resulting in severe pain,
rates with chronic LA enlargement. A minority of cats electrolyte disturbances, acute renal injury, and for those
will develop generalized LV systolic dysfunction, or large surviving the initial embolic episode, a high long‐term
areas of ventricular “scarring” with regional wall thin- risk of ATE recurrence or CHF. Nevertheless, a minority
ning and replacement fibrosis. Cats with increased wall of cats can survive for periods in excess of a year if they
thickness but systolic dysfunction are sometimes recover from the acute crisis.
described as “end‐stage HCM” (ES‐HCM). Although
these cats may start with a nondilated hypertrophied LV,
over time the LV wall thickness may decrease and LV ARVC
diameter increases, so that ultimately they may bear little Arrhythmogenic right ventricular cardiomyopathy also
resemblance to the classic HCM phenotype. occurs in humans and dogs, and is characterized by
Occasionally, cats with HCM will present with acute fibrofatty replacement of myocytes. The extent and dis-
signs of cardiogenic shock, including hypotension, hypo- tribution of myocyte replacement are variable, and may
thermia, and, often, bradycardia. These low‐output signs result in tachyarrhythmias and/or right atrial and right
may or may not be accompanied by congestive signs. ventricular dilation. Affected cats may be presented with
signs of syncope associated with tachyarrhythmias, but
RCM can also develop right‐sided congestive signs with ascites.
Two forms of RCM have been reported: an endomyocar-
dial form characterized by LV bridging scar (eRCM); and Epidemiology
a myocardial form where the LV appears structurally
normal but is poorly compliant (mRCM). Varying The prevalence of HCM in cats is high; approximately
degrees and distribution of myocardial fibrosis are com- 15% of apparently healthy cats are affected, with a preva-
mon to both forms. Biatrial enlargement and increased lence increasing to nearly 30% of cats over 9 years of age.
atrial pressures are also common to both. Cats diagnosed The prevalence of RCM, DCM, and ARVC is harder to
with RCM usually demonstrate clinical signs, which can gauge, but is likely considerably lower. HCM is the most
include congestive heart failure, arrhythmias, arterial common type of feline cardiomyopathy, regardless of age,
thromboembolism, or low‐output signs. It is difficult to breed or presenting signs. In the absence of longitudinal
differentiate RCM from the more advanced forms of epidemiologic studies, it is impossible to determine