Why the study?
Does antimony treatment cause electrocardiographic changes in bilharzia patients?
Does antimony treatment cause electrocardiographic changes in bilharzia patients?
Antimony treatment for bilharzia is associated with significant electrocardiographic changes and bradycardia, indicating potential myocardial toxicity.
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ECG changes may signal antimony cardiotoxicity in bilharzia; hypothesis-generating, no practice change from case data alone.
In twelve bilharzia patients the development of the electrocardiogram was followed up during a course of tartar emetic treatment. In seven cases considerable alterations were found, changes of the S–T interval as well as of the T deflection. The tracings which had in all the cases been absolutely normal assumed a markedly pathological character in three cases. In the other four cases the picture suggested the suspicion of a disturbed heart action. In three persons the electrocardiogram remained unchanged, in two further cases the changes were insignificant. The extent of the electrocardiographic changes was parallel to the degree of chronic bradycardia due to the effect of antimony. In contradiction to the view held hitherto the persistent antimony bradycardia differs in its electrocardiographic characteristics from the slowing of the pulse rate due to vagal stimulus. In two patients in whom the electrocardiogram was considerably changed no bradycardia occurred. The electrocardiographic abnormalities as well as the bradycardia are, therefore, considered as resulting from intoxication of the heart muscle through therapeutic antimony administration, though the process in most cases is not clinically evident. In exceptional cases the condition may result in sudden death, through auricular fibrillation.
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Mainzer et al. (1940) studied this question.
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