The Brain-Heart Connection in Takotsubo Syndrome: The Central Nervous System, Sympathetic Nervous System, and Catecholamine Overload

Abstract

Takotsubo syndrome (TTS), also known as stress cardiomyopathy, is a type of acute heart failure syndrome triggered by intense psychological or physiological stress. TTS typically manifests as acute chest pain, dyspnea or syncope that mimics an acute myocardial infarction but does not involve coronary artery obstruction. e current understanding of the pathogenesis of TTS suggests that sympathetic nervous system (SNS) activation plays a central role. Specifically, stress can activate the SNS and lead to the over-release of catecholamine, which have toxic effects on myocardial tissue when present at excessive levels. However, the brain changes associated with TTS and the connection between the brain and the heart in patients with this disease remain unclear. In recent years, several published reports have revealed the role of this brain-heart connection in the pathogenesis of TTS.is review summarizes recent studies regarding SNS activation, catecholamine overload, and the brain-heart connection in patients with TTS from both pathophysiological and mechanistic aspects.

Cardiovascular protective properties of oxytocin against COVID-19

“…In stroke, social pairing in adult mice enhances hypothalamic OXT gene expression and leads to smaller infarct size by reducing neuroinflammation and oxidative stress [ 112 ]. OXT can reduce stress-elicited neuroendocrine, autonomic, and behavioral responses [ 53 ], which can be used to prevent the brain-heart syndrome [ 129 ]. In addition, OXT also has anti-depressive effects [ 130 ] and may be used to relieve social isolation-associated depression in COVID-19 patients [ 48 ].…”

Takotsubo Syndrome: Cardiotoxic Stress in the COVID Era

“…Although HF in TTS has been assumed to be a form of cardiogenic shock, it may be more accurately considered "vasodilatory shock." 41,43 STRESS TRIGGERS OF TTS One-third of patients with TTS report an emotional stressor, another one-third report a preceding physical stressor, and the final third have no apparent trigger. 21 Studies report that chronic anxiety and/or depression are twice as common in patients with TTS compared with patients with ACS (70% vs 36%).…”

“… 41 The central mechanism is aberrant post-receptor β-2 signaling, with consequent activation of nitric oxide synthase and formation of peroxynitrite—a potent oxidant that damages DNA and impairs myocardial metabolism. 41 , 42 , 43 This in turn leads to hypotension, which is often a major issue early in the course of TTS and can be life-threatening. Although HF in TTS has been assumed to be a form of cardiogenic shock, it may be more accurately considered “vasodilatory shock.” 41 , 43 …”

“… 41 , 42 , 43 This in turn leads to hypotension, which is often a major issue early in the course of TTS and can be life-threatening. Although HF in TTS has been assumed to be a form of cardiogenic shock, it may be more accurately considered “vasodilatory shock.” 41 , 43 …”

Stress and Fear

“…In 1942, Cannon’s research into “Voodoo death” — a sudden, unexplained death resulting from a Voodoo curse — formed the basis for much of our modern understanding of the physiological response fight-or-flight systems linking emotions, such as fear, with illness. 75 Sympathetic activation and the subsequent catecholamine release brought on by emotional distress is implicated in the pathophysiology of the “broken heart syndrome.” 76 Thus, a state of fear and panic can potentially worsen clinical outcomes through sympathetic activation, the HPA axis, or other, yet unexplained mechanisms.…”