Cardiac toxicity following cobra envenomation

To the Editor:

Ismail et al.¹ have brought out an unusual form of cardio toxic effect of cobra envenomation and discussed the role of cardiotoxin (CTX) and phospholipases A₂ (PLA2) for different manifestations. In addition, neural and molecular mechanisms also contribute to cardiac toxicity. The possible involvement of the autonomic nervous system following cobra envenomation has to be considered, as the patient had tachycardia, hypertension and hypotension. The electrocardiogram (ECG) displayed reveals prolonged QTc. The cobra venom stimulates the autonomic nervous system first and manifests in the form of tachycardia, and augments blood pressure. Both of which increase the myocardial oxygen demand which results in cardiac ischemia with coronary vasospasm, depolarized block, hypotension, loss of cardiovascular reflex, as well as inhibition of cardiac conduction with prolongation of QTc intervals and ventricular ectopics.² From the experimental models, it is known that venom induces alteration of genes expressed in the heart,³ which is responsible for the mediators of immune response, apoptosis, ion transport, signal transduction, hypotension, energy metabolism and electron transport. However, the role of gene alteration as a possibility for the cardiac involvement in human beings needs further clinical research.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.