АннотацияВ данной работе обсуждаются современные клинико-фундаментальные аспекты диагностики и лечения пациентов с ишемической кардиомиопатией (ИКМП). Рассматриваются патофизиологические, морфологические и иммуногистохимические аспекты ремоделирования левого желудочка (ЛЖ) при ИКМП. Приводится подробная характеристика и показана роль методов оценки функциональных резервов миокарда при ИКМП. Акцентировано внимание на методиках хирургического лечения при ИКМП. Статья рассчитана на кардиологов, терапевтов, кардиохирургов. Ключевые слова:хроническая сердечная недостаточность, ишемическая кардиомиопатия, магнитно-резонансная томография, стресс-эхокардиография. Конфликт интересов:авторы заявляют об отсутствии конфликта интересов. Прозрачность финансовой деятельности:никто из авторов не имеет финансовой заинтересованности в представленных материалах или методах.

It was established that in patients with chronic heart failure (CHF), including CHF with reduced ejection fraction, as well as acute decompensated CHF, the level of serum inflammatory markers was increased. Moreover, experimental studies have shown repeatedly that activation of mechanisms of immune response in the myocardium provokes left ventricular remodeling and progression of left ventricular dysfunction. Nonetheless, clinical studies of anti-inflammatory drugs, including those aimed at blockage of cytokines have been neutral or negative with respect to the primary end points of the trials, and in some patients, resulted in worsening CHF or death. This review discusses variants of the types of inflammation in the myocardium, their immune mediators involved in the pathogenesis of CHF and its progression. Mechanisms of the pathogenesis of inflammatory cardiomyopathy leading to HF are discussed. A more precise conclusion about inflammatory phenotype in myocardial tissue, which will identify therapeutic targets in the treatment of CHF is necessary. Additionally, the review presents modern data about tactics for managing patients with acute decompensation of CHF with systolic dysfunction, which includes optimal medication, invasive and device therapy.

Background. The high prevalence of cardiac damage in resistant hypertensive patients signifcantly increases the risk of cardiovascular complications. Despite the antihypertensive effcacy of renal denervation (RDN), the cardioprotective effect has not been suffciently studied.Objective. To study the changes in left ventricular mass (LVM) and volume of myocardial damage after the RDN and to detect a possible connection of the studied parameters with blood pressure (BP) reduction after RDN.Design and methods. RDN was applied to 84 patients with resistant hypertension. Initially, at 6 and 12 months after treatment, patients underwent the measurements of the “offce” BP, 24-h BP, echocardiography and cardiac contrast-enhanced magnet-resistance tomography.Results. At baseline, “offce” BP averaged 175,3 ± 22,1 / 100,4 ± 16,1 mmHg and the prevalence of left ventricular hypertrophy (LVH) was 84,5 %. “Offce” BP reduced signifcantly at 6 month by –27,5 (–74,0; 12,0) / –14,2 (–39,4; 10,3) mmHg (p < 0,001), at 12 month by –31,6 (–78,7; 8,3) / –15,5 (–43,3; 10,2) mmHg (p < 0,001). 24-h BP reduced signifcantly at 6 month by –13,0 (–45,2; 17,6) / –6 (–27,8; 8,9) mmHg (p < 0,001), at 12 month by –14,3 (–52; 25) / –7,3 (–26; 15,0) mmHg (p < 0,001). At 12 month after RDN LVM decreased by 6,9% (p = 0,015), LV mass index by 5,5 % (p = 0,020). According to MR study, subendocardial damage was detected in 100% of patients in the absence of coronary atherosclerosis. A volume of subendocardial damage signifcantly reduced by 29 % at 6 month (p = 0,031) and by 41,4% at 12 months after RDN (p = 0.008). LVM reduced signifcantly by 18,3 % (р = 0,008). LVM also reduced signifcantly in non-responder’s group at 6 month after RDN (р = 0,046). The regression of subendocardial damage correlated with the change in systolic BP at 12 months after RDN (р = 0,034). There was no signifcant correlation between LVH regression and baseline BP and its change after RDN.Conclusions. One year after RDN, LVH decreased independently from the BP change. Subendocardial damage was detected in 100% patients, regressed at 6 months after RDN and correlated with the regression of systolic BP at 12 month after the RDN.