DESCRIPTION

• Transient stress cardiomyopathy (TSC) is a unique cause of reversible left ventricle (LV) dysfunction with a presentation indistinguishable from the acute coronary syndromes (ACS), particularly ST-segment elevation myocardial infarction (STEMI).
• Typically, the patient is a postmenopausal woman who presents with acute chest pain, dyspnea, or syncope and an identifiable “trigger” (i.e., an acute emotional or physiologic stressor).
• First reported by authors from Japan as “takotsubo” (the Japanese word for octopus trap, due to the characteristic shape of the LV at the end of systole) cardiomyopathy (1)
• Presenting clinical features include:
  • Chest pain/pressure, dyspnea and/or syncope
  • ECG changes, including ST-segment elevations or diffuse T-wave inversions
  • Mild elevation in cardiac biomarkers (creatine kinase [CK], troponin)
  • Transient wall motion abnormalities that may involve the base, midportion, and/or lateral walls of the LV
  • The apex of the right ventricle (RV) may be affected in up to 25% of cases.
• Clinical features may vary on a case-by-case basis, and formal diagnostic criteria have not been established.
• Authors from the Mayo Clinic have proposed that three of the four following criteria establish the diagnosis (1):
  • Transient akinesis or dyskinesis of the LV apical and midventricular segments with regional wall motion abnormalities extending beyond a single epicardial vascular distribution
  • Absence of obstructive coronary artery disease (CAD) or angiographic evidence of acute plaque rupture
  • New ECG abnormalities, either ST-segment elevation or T-wave inversion
  • Absence of recent significant head trauma, intracranial bleeding, pheochromocytoma, obstructive epicardial CAD, myocarditis, hypertrophic cardiomyopathy
• Synonym(s): takotsubo cardiomyopathy; apical ballooning syndrome; stress cardiomyopathy; broken heart syndrome; ampulla cardiomyopathy

EPIDEMIOLOGY

ETIOLOGY AND PATHOPHYSIOLOGY

• The precise pathophysiologic mechanisms of TSC are not well understood (3).
• There is considerable evidence that sympathetic stimulation is central to its pathogenesis. A clear emotional or physiologic triggering event precipitates the syndrome in most cases, and TSC has been associated with conditions of catecholamine excess (e.g., pheochromocytoma, central nervous system disorders) and activated specific cerebral regions.
• Occurs primarily in subjects with increased susceptibility of the coronary microcirculation and of cardiac myocytes to stress hormones leading to temporary left ventricular dysfunction with secondary myocardial inflammation
• A perturbation in the brain–heart axis, originating in the insular cortex, may be the inciting event.
• Subsequent overwhelming activation of the sympathetic nervous system initiates a cascade of events, including the following: catecholamine-induced LV dysfunction: “biased agonism” of for β₂-adrenergic receptors, located predominantly at the cardiac apex; endothelial dysfunction and vasospasm; cellular metabolic injury: myocardial norepinephrine release, calcium overload, contraction band necrosis

RISK FACTORS

Female sex, postmenopausal state; emotional stress (i.e., argument, death of family member); physiologic stress (i.e., acute medical illness); chronic neurologic or psychiatric disease