: 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, lack of coronary artery obstruction, 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%. In many patients with TS, but not in all, physical or emotional stress precedes the disease. Many patients with TS, but not all, have neurological or mental illnesses. The level of catecholamines is increased in patients with TS, therefore, the occurrence of TS is associated with the 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 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.

No abstract

The purpose was to study the utility of technetium 99m - pyrophosphate in the diagnoses of inflammatory changes of the heart in patients with persistent atrial fibrillation. The study included 30 patients (20 men and 10 women, mean age is 46 ± 9.92 years) with idiopathic persistent atrial fibrillation. To identify the foci of inflammatory changes in the myocardium the scintigraphy with 99mTc-Pyrphotech and myocardial perfusion scintigraphy with 99mTc-methoxy-isobutyl-isonitrile (99mTc-MIBI) was performed before the operation. Later, both scintigrams were combined. During the surgical intervention, in all patients an endomyocardial sampling for histological and immunohistochemical study was performed. Pathological accumulation of 99mTc-Pyrphotech in the myocardium was detected in 8 (26%) of examined patients. In 20% of cases the cause of "idiopathic" form of AF is latent lymphocytic or polymorphocellular myocarditis of viral etiology. Scintigraphy with 99mTc-Pyrphotech can serve as one of the primary methods for non-invasive diagnosis of myocardial inflammation at the given form of arrhythmia.

No abstract

The purpose of this study is to research the use of the radiopharmaceutical99mTc-HMPAO in the evaluation of drug prevention of cerebral complications in patients with coronary heart disease after coronary artery bypass grafting (CABG) performed with cardiopulmonary bypass (CPB). The study included 30 patients, in whom surgical revascularization was performed with CPB. 11 patients in this group were prescribed instenon. All the patients underwent brain tomoscintigraphy with99mTc-HMPAO and neuropsychological testing before CABG and 10-15 days after it. The results showed that99mTc-HMPAO is useful radiopharmaceutical for evaluation of cerebral complications in patients after CABG. Thus, coronary artery bypass grafting using CPB can be complicated by the deterioration of cerebral perfusion and cognitive dysfunction, while preventive medication with instenon can prevent or significantly reduce the violations of cerebral hemodynamics and neuropsychological status of the patients.