ACUTE AND CHRONIC HEART FAILURE AFTER MYOCARDIAL INFARCTION: CLINICAL AND FUNCTIONAL MARKERS

Abstract

Вackground. The last decade has seen an increase in the number of people who have had myocardial infarction (MI). This phenomenon contributes to an increase in the long-term incidence of chronic cardiovascular diseases, including chronic heart failure.\nPurpose of the study. To identify the most significant clinical and functional indicators characterizing acute and chronic heart failure after myocardial infarction.\nPatient Characterization and Research Methods. This analysis included 186 patients who had myocardial infarction from January 2019 to January 2020: 86 people, the main subgroup, with signs of CHF above FC 2 (NYHA) (mean age 64.3 g) and 100 people, the comparison subgroup, without signs of CHF or had CHF 1 FC (NYHA) (mean age 62.6 l). After 1 year, clinical outcomes were assessed: cardiovascular death, repeated hospitalizations due to decompensation of CHF, death from other causes, stroke, repeated myocardial infarction, unplanned coronary revascularization.\nResults. In the acute period of myocardial infarction in the main subgroup (MI + CHF more than 2cl NYHA), all patients had symptoms of acute heart failure (AHF) in the form of Killip II and Killip III. Predictors of the development of chronic heart failure were the presence of a history of ischemic heart disease, confirmed in accordance with the recommendations, before myocardial infarction; decreased fraction of the left ventricle, detected before discharge and on the 30th day of myocardial infarction; the presence of atrial fibrillation (AF). One-year unfavorable outcomes in the main group were significantly more frequent. Subanalysis of long-term drug therapy showed that cardiovascular death was significantly less common in the subgroup of patients taking ARNI than in the subgroup of enalapril.\nConclusion. In the present study, we studied postinfarction myocardial remodeling, which is realized in the form of the formation of a syndrome of acute and chronic heart failure. It has been shown that immediate reperfusion and restriction of the necrosis zone, as well as long-term use of drugs that inhibit SAS and RAAS, stimulating NPP, can inhibit the development of AHF and death. The CHF problem requires further fundamental research in order to develop new approaches that can affect more subtle mechanisms, such as the expression of specific genes involved in the disease, in order to reduce the persisting excess mortality for this pathology.