The purpose of the review is the analysis of clinical and experimental data on the etiology
and pathogenesis of takotsubo syndrome (TS). TS is characterized by contractile dysfunction,
which usually affects the apical region of the heart without obstruction of coronary artery, moderate
increase in myocardial necrosis markers, prolonged QTc interval (in 50% of patients), sometimes
elevation of ST segment (in 19% of patients), increase N-Terminal Pro-B-Type Natriuretic Peptide
level, microvascular dysfunction, sometimes spasm of the epicardial coronary arteries (in 10% of
patients), myocardial edema, and life-threatening ventricular arrhythmias (in 11% of patients).
Stress cardiomyopathy is a rare disease, it is observed in 0.6 - 2.5% of patients with acute coronary
syndrome. The occurrence of takotsubo syndrome is 9 times higher in women, who are aged 60-70
years old, than in men. The hospital mortality among patients with TS corresponds to 3.5% - 12%.
Physical or emotional stress do not precede disease in all patients with TS. Most of patients with TS
have neurological or mental illnesses. The level of catecholamines is increased in patients with TS,
therefore, the occurrence of TS is associated with excessive activation of the adrenergic system.
The negative inotropic effect of catecholamines is associated with the activation of β2 adrenergic
receptors. An important role of the adrenergic system in the pathogenesis of TS is confirmed by
studies which were performed using 125I-metaiodobenzylguanidine (125I -MIBG). TS causes edema
and inflammation of the myocardium. The inflammatory response in TS is systemic. TS causes impaired
coronary microcirculation and reduces coronary reserve. There is a reason to believe that an
increase in blood viscosity may play an important role in the pathogenesis of microcirculatory dysfunction
in patients with TS. Epicardial coronary artery spasm is not obligatory for the occurrence
of TS. Cortisol, endothelin-1 and microRNAs are challengers for the role of TS triggers. A decrease
in estrogen levels is a factor contributing to the onset of TS. The central nervous system appears to
play an important role in the pathogenesis of TS.