Abstract:

Sinus tachycardia in young individuals represents an increasingly recognized multidimensional phenomenon arising from the dynamic convergence of psychosocial stress, autonomic disequilibrium, and intrinsic myocardial excitability. Rather than a benign epiphenomenon, persistent sinus tachycardia in structurally normal hearts is now understood as a potential surrogate marker of subclinical autonomic dysfunction, characterized by sustained sympathoexcitation and vagal withdrawal. Chronic exposure to psychosocial stressors, sleep deprivation, and lifestyle factors such as high caffeine intake and physical inactivity fosters a state of functional hyperadrenergia, promoting maladaptive remodeling of sinoatrial nodal electrophysiology. At the cellular level, augmented β-adrenergic receptor sensitization, dysregulated calcium cycling, and impaired baroreflex integration collectively enhance pacemaker automaticity and reduce heart rate variability. These processes may further engage downstream molecular cascades implicated in oxidative stress and altered ion channel expression, thereby predisposing susceptible individuals to arrhythmogenic potential despite the absence of overt structural pathology. Recognizing sinus tachycardia as a harbinger of early autonomic and electrophysiologic perturbation underscores the need for comprehensive assessment and targeted modulation of autonomic tone. This review delineates the mechanistic continuum linking stress, neurocardiac regulation, and cardiac excitability in the young population, with emphasis on emerging diagnostic paradigms and evolving therapeutic interventions.