SINCE the advent of penicillin in the treatment of subacute bacterial endocarditis, it has become increasingly obvious that certain patients are being cured of the infection only to suffer cardiac failure later. Many reports of treatment with penicillin mention cases in which there were unsatisfactory results, not because the drug failed to eliminate the bacteria but because of subsequent deterioration of cardiac function.1 Inasmuch as the infection occurs in persons who have more or less damaged hearts to begin with and who might therefore be expected at some time to show symptoms of myocardial weakness, it seems illogical to blame penicillin unless its use can be shown to have hastened cardiac insufficiency. Obviously the drug cannot be expected to repair damage already done either by the original cardiac disease or by the bacterial endocarditis; the question is whether penicillin is likely to promote destructive processes. The purpose of this
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