Takotsubo Syndrome and Sudden Cardiac Death

Abstract

Takotsubo syndrome (TTS), triggered by intense emotional or physical stress, occurring most commonly in post-menopausal women, presents as an ST-elevation myocardial infarction (MI). Cardiovascular complications occur in almost half the patients with TTS, and the inpatient mortality is comparable to MI (4–5%) owing to cardiogenic shock, myocardial rupture, or life-threatening arrhythmias. Thus, its prognosis is not as benign as previously thought, as it may cause mechanical complications (cardiac rupture) and potentially lethal arrhythmias and sudden cardiac death (SCD). Similar to MI, some patients may perish before reaching the hospital due to out-of-hospital cardiac arrest; this may lead to underestimation of the actual SCD risk. Furthermore, after discharge, some patients may develop late SCD and/or TTS recurrence that may result in SCD. There are risk factors for SCD in TTS patients, such as severe/persistent QT-interval prolongation inciting torsade-de-pointes, other ECG abnormalities (diffuse giant negative T-waves, widened QRS-complex), bradyarrhythmias, comorbidities, concurrent obstructive coronary artery disease or vasospasm, male gender, older age, severe left ventricular dysfunction, and use of sympathomimetic drugs. All these issues are herein reviewed, case reports/series and data from large cohort studies and meta-analyses are analyzed, risk factors are tabulated, and proarrhythmic effects and management strategies are discussed and pictorially illustrated.

Neurohumoral Activation in Heart Failure

“…Yet another prominent manifestation of catecholamine toxicity relates to the development of the Takotsubo syndrome (TTS) or stress cardiomyopathy or apical ballooning [18][19][20]. Takotsubo syndrome is often triggered by intense emotional or physical stress; it occurs most commonly (~90%) in post-menopausal women, manifesting as an acute coronary syndrome (ACS), similar to an ST elevation myocardial infarction (STEMI); it presents as an acute HF syndrome or antero-apical cardiomyopathy with reversible left ventricular (LV) dysfunction involving LV walls in more than one coronary territory, usually in a global pattern, and commonly, albeit not exclusively, without significant underlying coronary artery lesion(s) [19,21].…”

“…A major mechanism for the development of TTS relates to an acute cardiac sympathetic surge with norepinephrine release and spillover; however, circulating catecholamines may not have a direct effect in the pathogenesis of TTS, as the sympathetic activation and surge in norepinephrine release is confined to sympathetic nerve terminals and is considered to play a critical role in the acute phase of TTS producing acute myocardial stunning or paralysis [23,24]. Its prognosis is not as benign as one may think, as it may cause mechanical complications (cardiac rupture) and potentially lethal arrhythmias and sudden cardiac death (SCD) [18,22].…”

New Concepts on the Pathophysiology of Acute Coronary Syndrome

“…The exact pathophysiological mechanisms of TTS are still unclear. Sympathetic stimulation leading to increased circulating and local cardiac tissue catecholamine levels is thought to be the major pathology [ 76 , 77 ]. Elevated catecholamines can induce vascular spasm or cause direct myocardial toxicity, which causes TTS, together with increased cardiac load, resulting in an acute supply-demand mismatch and even post-ischemic shock [ 78 ].…”