Cardiomyopathy (CMy) refers to an affectation of the heart not caused by valvular or coronary vascular disease, and is often
of unknown etiology. Infections (e.g., Trympansoma cruzi, viral), toxic agents (e.g., doxorubicin, cobalt), or micronutrient deficiency (e.g., l-carnitine, taurine) may result in
cardiomyopathy. Eleven percent (~6 million dogs) of the dog population (~60 million) in the US have heart disease, but probably
fewer than 10% (~600,000) have cardiomyopathy. Cardiomyopathies are none-the-less important since they often carry high risk
for sudden death (e.g., arrhythmic cardiomyopathy in Boxers, dilated cardiomyopathy in Dobermans), and in Boxers the sudden
death may be unanticipated.
Dilated cardiomyopathy (dCMy) occurs most often in large breed dogs (e.g., Dobermans, Irish Wolfhounds) or in English Cocker
Spaniels; arrhythmic cardiomyopathy (aCMy) occurs most often in Boxers dogs or in dogs that look like Boxers only with different-appearing
heads (e.g., Staffordshire terriers). Because of breed predilections, it may be presumed that cardiomyopathies possess a genetic
basis, but the genetic transference is not established.
Dilated Cardiomyopathy (dCMy)
Dogs with dCMy are usually larger, are thin or skinny because of lack of appetite or increased metabolic activity), have swayed
backs (because of skeletal muscle weakness), often have bloated abdomen due to ascites and/or muscular weakness, and may be
dyspneic with or without cough. [If the cough is due to pulmonary edema, it is usually subtle; if due to cardiomegaly and
compression of the left mainstem bronchus, it is usually hacking.] Often dogs are dehydrated with eyes "sucken-in". Dogs are
usually inactive and may be either cyanotic because of ventilation perfusion mismatch, or have "white" gums produced by poor
circulation and/or anemia.
Dogs with dCMy are often dsypneic, breathing both rapidly (>30/minute) and with increase effort (bulging eyes, head extended,
reluctant to lay down, pulmonary retractions). As mentioned, they may be either cyanotic due to ventilation-perfusion mismatch
or their gums may be white due to poor circulation and/or anemia. Auscultation, palpation, and percussion produce almost always
abnormal findings. With pleural effusion they will have dull notes of percussion and softer than expected vesicular breath
sounds; with pulmonary edema they will have louder than expected vesicular breath sounds (termed bronchial) and crackles that
are usually rather soft and high-pitched. Their femoral pulses are most often rapid and, if dogs are in atrial fibrillation,
they will be irregularly-irregular. If the rhythm is sinus and the arteries are stiff, the pulses may have a sharp, "tapping"
nature. Most dog with dCMy have an audible third heart sound (S3) producing a diastolic gallop (Lub dup uh, instead of merely
a Lub dup). If in atrial fibrillation, heart sounds (in particular the second heart sound, S2) will be highly variable in
intensity, and there can never be a fourth heart sound (S4) because of the absence of atrial contraction.
The ECG will show a rapid heart rate, it will be irregularly-irregular and with no P-waves if in atrial fibrillation, and
the R-waves in lead II will be taller than normal (greater than 3 mV) and longer in duration (greater than 60 ms). Often premature
depolarizations of atrial and/or ventricular origin are observed, and there may be paroxysms (bursts) of tachycardia.
Most often dogs with dCMy will have globular hearts representing left atrial and ventricular dilatation and less right atrial
and ventricular dilatation. Pulmonary veins more than pulmonary arteries will be distended. Commonly dogs will have pulmonary
edema, but not uncommonly also pleural effusion.
The ECHO will confirm dilatation of the left ventricle and enlargement of the left atrium, but of greatest importance, left
ventricular wall motion will be reduced so that shortening fraction is reduced. Doppler interrogation of the mitral orifice
will demonstrate mitral regurgitation, and interrogation of the aortic orifice a brief period of ejection.
Goals of Therapy
1. Reduce pulmonary edema—furosemide and spironolactone often with nitroglycerine and a thiazide diuretic.
2. Slow heart rate—digitalis, diltiazem if atrial fibrillation, B-blocker (carefully)
3. Decrease loading condition on left ventricle—ACE inhibitor, amlodipine
4. Strengthen force of contraction—pimobendan, digitalis
5. Strengthen muscles of respiration—theophylline, digitalis
6. Minimize structural; remodeling—spironolactone, B-blocker (carefully but importantly)
7. Extinguish ventricular arrhythmias—amiodarone, sotalol