Characteristics of clinical current and structural-functional state of left ventricular in decompensation of chronic heart failure in patients with ischemic chronic heart failure with systolic dysfunction and inflammation of the myocardium

The aim was to study the clinical course of CHF decompensation and the structural and functional state of the left ventricle in patients with ischemic CHF with systolic dysfunction and myocardial inflammation. Material and Methods. This study is open, non-randomized, prospective, registered on the ClinicalTrials.gov website, identification number: NCT02649517. The analysis included 25 patients (84% men, LVEF 29.17±9.4%) with ADHF of ischemic etiology. The average age of the patients was 60.12±9.3 years. All the patients underwent an echocardiography including 2D-speckle tracking technique to assess LV deformation. All patients underwent invasive coronary angiography to exclude the progression of coronary atherosclerosis, as a cause of CHC decompensation. An endomyocardial biopsy was performed to diagnose the presence of myocardial inflammation. We performed a comparative analysis of clinical, laboratory, instrumental indicators depending on the fact of diagnosis of inflammation in the myocardium. Results. There were no specific features of the clinical course of decompensation of ischemic CHF with systolic LV dysfunction depending on the inflammation in the myocardial tissue. However, in patients with inflammation, aortocoronary bypass surgery was more often performed (p=0.00650). In addition, in patients with inflammation, there was a decrease in apical rotation (p=0.0313), its systolic velocity (p=0.0157 with decompensation of CHF. A year later, improvement in LV biomechanics, but a continuing decrease in the absolute modulus of global longitudinal LV deformation (p=0.0431) after the anti-inflammatory treatment. Also a year later, in both groups there was an increase in the LV end-diastolic volume index (p=0.0180 and p=0.0280, respectively), a decrease in the interventricular septum of the LV (p=0.0491) in the group with inflammation, and an increase in the myocardial mass index of the LV (p=0.04995) in patients with inflammation. Conclusion. Decreased apical LV rotation and its systolic velocity in patients with ischemic CHF and LV systolic dysfunction, in view of the lack of clinical improvement after optimal myocardial revascularization, may be an additional criterion of concomitant inflammation in the myocardium. Among patients with ischemic CHF and LV systolic dysfunction, more pronounced cardiac remodeling, manifested by LV dilatation and thinning of LV wall, was observed in the group with inflammation.