Physiological Influences of Active and Passive Acute Mental Stress on Cardiac Repolarization: A Preliminary Investigation into Pathophysiological Mechanisms of Adult Cardiac Arrhythmias

Background: Adult cardiac arrhythmias cause adverse health effects including death. While the underlying mechanisms of arrhythmiogenesis have yet to be elucidated, the cardiac autonomic nervous system (ANS) is suggested to play a notable role. As part of the stress response the cardiac ANS is activated under conditions of acute mental stress, yet, little is known about the cardiac ANS stress response and adult arrhythmiogenesis in acute mental stress conditions. This systematic review offers insight into the influences of acute mental active and passive stress and their potential roles in generating proarrhythmic environments, and provides a primary foundation for future clinical research investigating prospective arrhythmiogenic pathophysiological pathways for the prediction, prevention and treatment of adult arrhythmias. Methods: An extensive literature search was performed by two independent reviewers using Pubmed, PsycINFO, and Scopus electronic databases (up to December 2018). All English language articles which assessed adult cardiac electrophysiological, autonomic, and hemodynamic responses, to acute mental stress conditions were included. Results: Eleven studies were identified; 5 studies included active stress tasks, 3 studies included passive stress tasks, and 3 studies included both active and passive stress tasks. Both active and passive stress were associated with pro-arrhythmic electrocardiographic changes, along with increased hemodynamic and autonomic responses. Conclusions: Active and passive stress create a pro-arrhythmic environment through repolarization alterations, increased sympathetic nervous system activity, and concurrent diminished parasympathetic activity. Further studies should include distinctions between active and passive stress cardiac electrophysiology profiles to better understand how mental stress contributes to cardiac arrhythmia etiology