Journal of Cardiology and Heart Failure

INTRODUCTION

Syncope is defined as a self-limited, transient loss of consciousness [1]. Vasovagal syncope (VVS), also known previously as neurocardiogenic syncope, is the most common type, with 60-70% of all syncopes [2]. Though accurate pathophysiology remains poorly understood, the most documented mechanism is the autonomic dysfunction, sympathetic activity withdrawal, and increased parasympathetic tone, which leads to vasodilation, bradycardia, and decreased peripheral resistance, which eventually leads to cerebral hypo perfusion [3,4]. The trigger behind this initiation of autonomic dysfunction is still debated; it is said to be a defense mechanism against the brain stem shutting down by the higher centers or ventricular mechanoreceptors' paradoxical firing [5,6]. However, other sources debate it as a psychological issue, like anxiety that activates sympathetic stimulation [7]. Also, Family history and sex of the subject are important predictors of vasovagal syncope in offspring [8]. The prevalence of syncope for a lifetime of 70 years is 42%, with an annual rate of 6%. Moreover, the incidence ranges from 18.1 to 39.7 per 1,000 patients [9].