Stress-related cardiomyopathies

Neurocardiology has many dimensions, namely divided in three categories: the heart's effects on the brain (i.e., embolic stroke); the brain's effects on the heart (i.e., neurogenic heart disease); and neurocardiac syndromes, such as Friedreich disease [1]. The present review will focus on the nervous system's capacity to injure the heart. The relationship between the brain and the heart, i.e., the brain-heart connection, is central to maintain normal cardiovascular function. This relationship concerns the central and autonomic nervous systems, and their impairment can adversely affect cardiovascular system and induce stress-related cardiomyopathy (SRC) [2]. Even if it is unclear whether myocardial adrenergic stimulation is the only pathophysiological mechanism associated with SRC, enhanced sympathetic tone inducing endogenous catecholamine's stimulation of the myocardium was always reported [3].The first description of suspected SRC was reported by W.B. Cannon in 1942 cited by Engel et al. [4] who published a paper entitled "Voodoo death," which reported anecdotal experiences of death from fright. This author postulated that death can be caused by an intense action of the sympathico-adrenal system. In 1971, Engel et al. collected more than 100 accounts from the lay press of sudden death attributed to stress associated with disruptive life events and provided a window into the world of neurovisceral disease (i.e., psychosomatic illness).It is now widely admitted that this autonomic storm, which results from a life-threatening stressor, can be observed in the four following situations that induce left ventricle (LV) dysfunction [2]:- Takotsubo cardiomyopathy or apical ballooning syndrome [5]- Acute LV dysfunction associated with subarachnoid hemorrhage [6]- Acute LV dysfunction associated with pheochromocytoma and exogenous catecholamine administration [7]- Acute LV dysfunction in the critically ill [8]Emotional and physical stress can induce an excitation of the limb