Cobalt Cardiomyopathy: A Critical Reappraisal in Light of a Recent Resurgence

Cobalt can cause a distinctive, rapidly progressive and reversible depression of cardiac systolic function, which is readily distinguished from other causes of cardiomyopathy. Patients present with the subacute onset of severe heart failure, which is accompanied by hypotension and cyanosis, pericardial effusion, low voltage on the electrocardiogram, marked elevation of serum enzymes, and lactic acidosis. They typically have a history of lethargy, anorexia, and weight loss in the months preceding the illness and exhibit other evidence of cobalt's effects on the body (eg, polycythemia and goiter). The course of cobalt-related cardiomyopathy may be progressive and fatal, but those who survive and cease exposure generally demonstrate complete resolution of symptoms and recovery of cardiac function. Patients presenting with rapid onset of cardiomyopathy, who also exhibit polycythemia, pericardial effusion, or goiter should be evaluated for cobalt exposure. Exposure can be confirmed by the measurement of cobalt in the serum, but serum levels of the ion are not reliably predictive of clinical cardiotoxicity. The clinical emergence of cobalt cardiomyopathy seems to require the coexistence of one or more cofactors, particularly a low-protein diet, thiamine deficiency, alcoholism, and hypothyroidism. As the medicinal use of cobalt has waned and measures to reduce industrial exposure have been implemented, subacute cobalt-related cardiomyopathy had become rare. However, reports describing classical features of the disease have recently surged among patients with a malfunctioning cobalt-alloy hip prosthesis.