Asoyan I. Optimization of diagnosis and treatment of chronic heart failure associated with diabetes mellitus type 2, based on the determination of the effect of inflammatory mechanisms in the development heart dyssynchrony.

The dissertation presents a theoretical generalization and a new solution to the current problem of modern therapy, namely, the mechanisms of activation of inflammatory components and their role in the development and progression of cardiac dyssynchrony in patients with combined congestion of chronic heart failure (CHF) of ischemic genesis and diabetes mellitus type 2 (DM 2 type). It has been established that the course of CHF of ischemic genesis in combination with DM 2 type is accompanied by an increase in the frequency of myocardial dyssynchrony, both due to electrical (QRS expansion> 120 ms) and mechanical (Ts, Ts-SD, APEI, PPEI, IVMD) types and increased incidence of the combination types of mechanical dyssynchrony: intraventricular and interventricular (Ts-SD+IVMD), atrioventricular and interventricular (LVFT+IVMD) and associations of all types heart dyssynchrony (Ts-SD+LVFT+IVMD). Joining heart dyssynchrony in such patients is accompanied by negative changes in morpho-functional parameters, which facilitates the transformation of the type of disturbed relaxation into a more severe type of diastolic dysfunction - pseudo-normal. It has been established that the onset and progression of myocardial dyssynchrony is accompanied by a significant increase in the concentrations of inflammatory markers (CRP, TNF-alpha, IL-1.beta, IL-6) in patients with CHF of ischemic genesis comorbid with DM 2 type. It is proved that the increase of the values of inflammatory factors contributes to lowering the ejection fraction, increasing the functional class of CHF and the process of inadequate remodeling of the left ventricle. The relationships between the indicators of dyssynchrony, the markers of inflammation and the structural and functional parameters of the myocardium in patients with CHF of ischemic genesis, type 2 diabetes and heart dyssynchrony were revealed. That is, the activation of systemic inflammation promotes inadequate remodeling of the heart, resulting in disturbances of synchronous reduction of chambers and segments of the myocardium and progression of CHF. It has been proved that additional therapy with coenzyme Q10 in patients with CHF of ischemic genesis with preserved left ventricular ejection fraction and DM 2 type positively affects the structural and functional parameters of the myocardium, synchronization of the reduction of chambers and segments of the myocardium, and also reduces the inflammatory response, thus slowing down the processes of heart remodeling and progression CHF.