THE EFFECTS OF SODIUM ANTIMONY TARTRATE ON THE MYOCARDIUM

Abstract

A West African girl, aged 23, developed severe chest pain, circulatory collapse, and Stokes-Adams attacks at the end of a course of treatment with sodium antimony tartrate (SAT). A cardiogram showed S-T and T wave changes suggestive of myocardial infarction and also a ventricular tachycardia with bizarre mutlifocal QRS complexes. Complete clinical and ecg recovery followed. Cardiograms of 59 patients receiving SAT treatment were recorded before and after treatment. They showed reduction in amplitude of T, characteristic upward sloping S-T segment with terminal dipping and later frank T wave inversion, most frequently in the precordial leads V2 to V4, and prolongation of the Q-T duration. These changes are divided into 4 grades of severity; one patient alone showed no change; one showed grade I change; 22, grade II; 18, grade III; and 17, grade IV changes. Severity of change is not closely related to age, sex, or total dose, but Africans and Asians are particularly prone to show more severe changes. Serial records show progressive increase in severity of change,and, after treatment, gradual return to normal after 6 weeks or more. The changes are attributed to cumulation of antimony in the myocardium producing metabolic and functional changes and possibly actual necrosis. They are regarded as being a sign of impeding clinical myocardial damage with potentially serious or lethal consequences. A second West African girl, aged 21, who died during treatment is described. No serial cardiograms were recorded, but autopsy revealed a septal infarct and a high concentration of antimony in the myocardium. It is suggested that until SAT is supplanted by a safer but equally effective drug, a wise precaution is to record a cardiogram after the administration of 15-20 grains (0.9-1.2 g) and modify the course of treatment if severe changes are seen.