Key result
Rattlesnake envenomation mimics acute myocardial infarction biomarkers via skeletal muscle injury without cardiac involvement.
Observational
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The clinical signs and symptoms of Crotalus durissus terrificus envenoming are due to the neurotoxic, myotoxic systemic and thrombin-like coagulating effects of the venom. The rhabdomyolysis observed after envenoming caused by snakes, the venom of which has a systemic myotoxic activity, has been limited thus far to skeletal muscle, with no reports of myocardial damage. In the present paper we report serial measurements of serum creatine kinase (CK), lactic dehydrogenase (LD) and of CK-MB and LD1 isoenzymes in human victims of Crotalus bites. The results were similar to those reported for acute myocardial infarction even though the clinical evolution, electrocardiogram and echocardiogram findings did not show any involvement of cardiac muscle. The enzymatic profile detected, as well as the pattern of focal involvement observed in muscle biopsies obtained from these patients, suggest that there may be a type of skeletal muscle fibre that is preferentially damaged by C. durissus terrificus venom, i.e., type I and/or IIa fibres, the composition of which is richer in CK-MB and LD1, and is similar to that of cardiac fibres.
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Cupo et al. (1990) conducted an observational in Crotalus durissus terrificus envenoming. Crotalus durissus terrificus envenoming was evaluated on Serial serum creatine kinase (CK), lactic dehydrogenase (LD), and CK-MB and LD1 isoenzyme profiles and cardiac muscle involvement. Crotalus durissus terrificus envenoming produced an acute myocardial infarction-like CK-MB and LD1 profile from type I and/or IIa skeletal muscle damage without cardiac involvement on ECG or echo.
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