Role of the Sympathetic Nervous System in Stress-Mediated Cardiovascular Disease

Abstract

A high incidence of acute cardiovascular events and sudden cardiac death following unexpected acute emotional stress or a natural catastrophic disaster has been well-documented over the past decades. Chronic psychosocial factors have been shown to be directly linked to the development of hypertension, cardiovascular disease and stroke. Activation of various neurogenic pathways is an important mediator of acute and chronic stress-induced hypertension and heart disease. Heightened sympathetic activation has been shown to be a critical contributor linking psychogenic effects on cardiovascular regulation to serious and often fatal CV outcomes. Accordingly, several therapeutic approaches that attenuate autonomic imbalance via modulation of increased sympathetic outflow by either non-pharmacological or interventional means have been shown to alleviate clinical symptoms. Likewise stress reduction per se achieved with transcendental medicine has been linked to improved patient outcomes. Therapies that oppose adrenergic activity and/or have the potential to attenuate negative emotions are likely to reduce cardiovascular risk and its adverse consequences attributable to chronic mental stress.