Canine cobalt cardiomyopathy: A model for the study of heart failure

The purpose in this study was to describe the canine cobalt cardiomyopathy model and the accompanying myocardial histologic features, metabolism, and central and regional hemodynamic properties. Six dogs were treated with cobalt sulfate (given IV) at a dose of 5 mg/kg/day to a cumulative dose of 150 ± 20 mg/kg; another 6 dogs were controls. Evaluation included study of echocardiograms and systolic-time intervals, and uses of cardiac catheterization to record dp/dt max and chamber pressures and of radiolabeled microspheres to determine cardiac output and regional flow distribution. Transmural biopsies of the left ventricle were analyzed for catecholamine concentration, adenine nucleotides, and percentage of fibrosis. Compared with the control group, the cobalt-treated group developed tachycardia, increased ratio of preejection period to left ventricular ejection time, decreased dp/dt max, depressed angiographic ejection fraction, and decreased systemic pressures. There were no significant changes of cardiac index or left ventricular end diastolic pressure. Although total systemic resistance was less in the cobalt-treated dogs, there was redistribution of blood flow from midbrain, cerebral cortex, renal cortex, esophagus, and stomach to the pancreas and myocardium. Epicardial blood flow increased more than did endocardial flow, so that the ratio of endocardial-to-epicardial blood flows (1.40 ± 0.12 in the control group) was 1.14 ± 0.10 (P<0.05) in the cobalt-treated dogs. The ratio of endocardial-to-epicardial adenosine triphosphate concentration was 1.24 ± 0.13 in the control group and depressed to 0.74 ± 0.16 (P<0.05) in the treated dogs. The ratio of fibrosis in the endocardium and that in the epicardium was constant in the 2 groups. In addition, myocardial stores of epinephrine were depleted in the cobalt-treated dogs, whereas urinary catecholamine concentrations were 3 times greater than those in the controls.