Takotsubo syndrome: Unraveling the mystery behind its triggers (Review).

Abstract

Takotsubo syndrome (TTS) is a clinical condition characterized by left ventricular dysfunction, clinically mimicking acute coronary syndrome. Despite significant advancements in understanding TTS, more questions about its underlying pathological mechanisms remain unresolved. The present review offered current data on the underlying pathological mechanisms of TTS, including central nervous system structural and functional alterations, sympathetic nervous system overstimulation, excessive catecholamine secretion, shifts in adrenergic receptors (ARs) distribution and balance, hormone influences, epicardial vasospasm, endothelial dysfunction and genetic predispositions. For example, stressors from physical or emotional triggers induce central neurohumoral activation by influencing the hippocampus and amygdala, which results in excessive local or systemic secretion. This catecholamine surge affects the myocardium by altering cellular metabolism, disrupting signaling pathways and impairing endothelial function. The regional myocardial effects are influenced by the modified ARs distribution and the density of autonomic innervation, which are pivotal in the onset of TTS. These insights suggest potential therapeutic strategies, including cognitive behavioral therapy, endothelin A antagonists and β‑blockers. However, the complex interplay of these factors in TTS onset remains poorly understood. Further research is essential to elucidate the intricate mechanisms and interactions underlying this syndrome, paving the way for improved prevention and treatment approaches.