Cardiac complication following Hemotoxic snake bite: A rare case from Eastern India

Abstract Primary cardiovascular complications following viper envenomation have been sparsely observed and remain poorly characterized in literature, despite South Asia being one of the largest snake bite prevalent zones. Venom induced coagulopathy, endothelial injury and hemodynamic disturbances on the other hand have been well documented events. We report a rare case of an inferior wall ST-segment elevation myocardial infarction (STEMI) following a hemotoxic viper bite in a 55-year-old male. The patient initially presented with localized swelling at the bite site, gross hematuria, and a whole blood clotting time exceeding 20 minutes, necessitating polyvalent antisnake venom administration. Six hours post-envenomation, he developed chest tightness and vomiting. A 12-lead electrocardiogram supported by elevated cardiac enzymes confirmed a diagnosis of inferior wall STEMI, supported by markedly elevated troponin T and I level occurring alongside an active venom-induced coagulopathy. Because of this coexisting bleeding manifestations, standard reperfusion strategies, including thrombolysis, anticoagulation, and antiplatelet therapy were not initiated, and the patient was managed conservatively with polyvalent anti-snake venom, supportive care, and high-intensity statin therapy, achieving resolution of cardiac symptoms within a day and cessation of hematuria by the 22nd hour with improving coagulation parameters over the next 3 days. Coronary angiography performed on follow-up revealed significant proximal right coronary artery stenosis, suggesting that venom-induced mechanisms, such as hypercoagulability or vasospasm, may precipitate acute ischemia in patients with undiagnosed atherosclerotic lesions. This case underscores the rarity of viper envenomation-induced cardiotoxicity, most of which have been documented in patients without identifiable coronary risk factors. It further illustrates the added diagnostic challenges of managing myocardial infarction when conventional reperfusion protocols are precluded by severe hemotoxicity.