Cardiomyopathy refers to an affectation of the heart not caused by valvular or coronary vascular disease, and is often of unknown etiology.
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.
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
A cardiomyopathy characterized by periods of rapid heart action originating most often from irritable foci in the right ventricle. There may be no structural contribution, or the right ventricle may be infiltrated with fatty materials.
Most commonly dogs are asymptomatic, but they may faint during longer and more rapid periods of tachycardia (rapid heart action). Frequently the initial presentation is sudden, unexpected death, or sudden death in a Boxer known to have ventricular premature depolarizations occurring either rarely or frequently.
Most dogs are without symptoms or signs of arrhythmia, but Boxers will often have soft, ejection murmurs of subaortic stenosis heard best midway between the left apex and base. The subaortic stenosis rarely affects either duration or quality of life.
Often within limits of normal, but often with rare ventricular premature depolarizations in which the QRS complexes are positive in leads in which the beats of sinus origin are normally positive. The best method for identifying this disease is Holtor monitoring in which an apparatus is placed on the thorax that records the ECG for 24 hours, and the recording is then scanned by computer to determine the nature of the ectopic activity, i.e., beats originating from other than within the SA node.
Most often within normal limits.
Goals of Therapy
1. No therapy unless dog is fainting or manifests unexplained periods of weakness
2. Suppress ventricular ectopy with sotalol, amiodarone, or mexiletine and procainamine.
Many dogs live full lives or some may die the next day, seemingly independent of therapy or frequency of premature depolarizations. All drugs that might suppress the arrhythmia are known to provoke the very same arrhythmia, therefore therapy is contentious.