Myocardial Ischemia after Severe Scorpion Envenomation: A Narrative Review

Myocardial ischemia after severe scorpion envenomation is rarely reported. The aim of this review was to elaborate on a review of myocardial ischemia after severe scorpion envenomation and to detail the mechanism of this myocardial hypoperfusion. We used the PubMed database and entered the following keywords in MeSH research: scorpion envenomation, myocardial ischemia, myocardial perfusion scintigraphy, echocardiography, and troponins. The literature analysis confirmed that severe scorpion envenomation can be complicated by temporary myocardial ischemia, based on electrocardiographic, histopathologic, echocardiographic, myocardial perfusion scintigraphy, and biological studies. The correlation between clinical manifestations, laboratory and electrocardiographic evidence of myocardial damage, echocardiographic studies, perfusion scintigraphy abnormalities, and histopathologic findings are suggestive of lesions of cardiac fibers secondary to myocardial ischemia. Myocardial hypoperfusion may be due to multiple factors. First, catecholamine storms can induce microvascular constriction. On the other hand, the release of catecholamines through a complex neurohormonal interaction with other neuropeptides and cytokine release can produce/induce major coronary microvascular constriction and/or microvascular injury, leading to microvascular acute coronary syndrome with Takotsubo cardiomyopathy. The management of severe scorpion envenomation with severe myocardial failure and pulmonary edema is based on oxygen with invasive or noninvasive ventilator support. Dobutamine improves cardiac function after scorpion envenomation. Antiplatelet therapy is not recommended. In conclusion, severe scorpion envenomation can be complicated by temporary myocardial ischemia, which can be due to multiple factors.