Medičnì Perspektivi (Mar 2022)
Remodeling of heart in patients with stable ischemic heart disease combined with chronic obstructive pulmonary disease as a basis for development of heart failure
Abstract
The aim of this study was to determine phenotypes of remodeling of heart and the status of systolic and diastolic function in patients with ischemic heart disease (IHD) combined with chronic obstructive pulmonary disease (COPD) with early symptoms and signs of heart failure (HF). We enrolled 108 males with stable IHD and spirometrically confirmed COPD which preceded the manifestations of IHD – the main group (group 1). As comparison groups 30 males with stable IHD (group 2) and 30 males with COPD (group 3) were examined. Control group included 30 males without IHD and respiratory diseases. All groups were comparable in age, groups 1 and 2 – in the duration of IHD, groups 1 and 3 – in the duration of COPD. The patients of the group 1 were divided into 3 subgroups: subgroup 1 – 45 patients with stable angina, subgroup 2 – 27 patients with postinfarction cardiosclerosis, subgroup 3 –36 patients with combination of stable IHD and arterial hypertension (AH) without history of myocardial infarction. The patients of group 1 had different phenotypes of heart remodeling, which depended on the clinical forms of IHD, the presence of concomitant AH, the severity of bronchial obstruction. The patients of subgroup 1 in 60.0% cases had concentric remodeling and concentric left ventricular hypertrophy (LVH), in 26.7% – normal LV geometry, in all these cases ejection fraction (EF) was preserved. Only in 13.3% of cases eccentric LVH with mildly reduced EF was found. 59.3% of patients in subgroup 2 had eccentric LVH, left atrium dilatation and 55.6% had reduced EF. All patients of subgroup 3 had concentric direction of LV remodeling. The phenotypes of HF with reduced and mildly reduced EF were accompanied by impaired LV diastolic function. In assessing the likelihood of HF with preserved EF the HFA-PEFF score showed better accuracy. Pulmonary hypertension had a mixed cause with predominance of postcapillar component.