Electrocardiographic abnormalities in patients bitten by taipans (Oxyuranus scutellatus canni) and other elapid snakes in Papua New Guinea

Abstract

Envenoming by a number of species of snake may affect the myocardium or cause electrocardiographic changes; several different mechanisms have been proposed. In a prospective study of snake bite in Papua New Guinea, electrocardiographic changes were observed in 36 of 69 patients (52%) envenomed by the taipan (Oxyuranus scutellatus), 2 of 6 (33%) envenomed by death adders (Acanthophis sp.) and one envenomed by the brown snake (Pseudonaja textilis). Septal T wave inversion and bradycardias, including atrioventricular block, were the commonest abnormalities. There was no haemodynamic deterioration. The cause of these changes is uncertain; only 2 of 24 patients (8.3%) with electrocardiographic changes had markedly elevated plasma concentrations of cardiac troponin T, a sensitive and specific marker of myocardial damage. This suggests that myocardial damage is uncommon following bites by these species. Electrocardiographic abnormalities are most likely to have been caused by a direct toxic effect of a venom component upon cardiac myocyte function; in taipan bites, taicatoxin, a calcium channel blocker, might be responsible.

Molecular basis of cardiotoxicity upon cobra envenomation

“…The results of this investigation clearly indicate that NS venom is cardiotoxic, and this is likely true of cobra venoms in general, given their similarities in composition [7]. This is interesting because cobra venoms, as used here, are not mainly known for their cardiotoxic activity, though studies have been carried out over the years to suggest this [9,53,54]. It has been argued that most cases of cardiac instability by cobra envenomation are actually caused by hypoxia or acidosis secondary to respiratory paralysis.…”

Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure

“…MI as a result of snake envenomation has been reported (116 ), with rare occurrences of non-AMI increases in cTn related to snake envenomation (117 ). In a prospective study of 45 patients who complained of snake bite, none were found to have increased cTn (118 ).…”

Antivenomic Characterization of Two Antivenoms Against the Venom of the Taipan, Oxyuranus scutellatus, from Papua New Guinea and Australia

“…3 Envenomings by this large elapid snake are characterized by minor local effects and severe systemic manifestations, including irreversible flaccid paralysis, coagulopathy associated with systemic spontaneous bleeding, myotoxicity, acute kidney injury, and cardiac damage. [2][3][4][5][6] The therapy for envenomings by O. scutellatus in PNG is based on the intravenous administration of either CSL Polyvalent Antivenom or CSL Taipan Antivenom (both manufactured by bioCSL Limited in Melbourne, Victoria, Australia; CSL). They are F(ab') 2 antivenoms generated by pepsin digestion and ammonium sulphate precipitation of plasma of hyperimmunized horses.…”