Experimental cobalt cardiomyopathy in the dog: A model for cardiomyopathy in dogs and man

Abstract The effect of cobalt cardiomyopathy was studied in 21 mongrel dogs. The dogs were divided into four groups; Group A (5 dogs) contained the normal controls, Group B (5 dogs) was fed a protein- and thiamine-deficient diet, Group C (5 dogs) was fed a normal diet and given cobalt by iv infusion, and Group D (6 dogs) was fed a protein-and thiamine-deficient diet and given cobalt by iv infusion. Cobalt (500 mg) dissolved in saline was given iv through a chronic indwelling venous catheter in the femoral vein for a 10-week period. No changes were seen in the control groups. The primary clinical findings in dogs in Groups C and D were dyspnea, exercise intolerance, and mild systolic murmurs with a prominent gallop rhythm. Abnormal electrocardiograms illustrating sinus tachycardia and lowered QRS complexes in limb leads were characteristic as was microcardia as visualized in thoracic radiographs, elevated left ventricular end diastolic pressure, lowered systolic pressures, angiographic evidence of a small end systolic volume, and slightly enlarged left diastolic volume. The dogs were necropsied in the 10th week, 24 hr after the last infusion and the heart was fixed in formalin, processed, and examined by light microscopy. The principle gross lesions in dogs in both Groups C and D were marked right ventricular dilatation, slight hypertrophy of the left ventricle, uniform paleness of the myocardium and dilatation of both atria. Histologic lesions included vacuolation of myofibers, loss of myofibers with hypertrophy of remaining fibers, and randomly scattered areas of coagulation necrosis. These findings suggest that experimental cobalt-induced cardiomyopathy in the dog is similar to alcoholic cardiomyopathy in man.