Abstract
Background. The coronavirus pandemic has caused a rapid increase in the number of cases and high deaths worldwide. A new coronavirus infection in the presence of an initial cardiac pathology can provoke decompensation of chronic heart failure.
Aim. To study the clinical features of postinfarction chronic heart failure occurring against the background of a new coronavirus infection.
Material and methods. The study included 80 patients with decompensated chronic heart failure. Three groups have been formed. In patients of the first group (n=40), who underwent inpatient treatment for a new coronavirus infection, the cause of chronic heart failure was a previous Q-myocardial infarction. In patients of the second group (n=20), who did not tolerate COVID-19 earlier and at the time of the current hospitalization, the cause of chronic heart failure was a previous Q-myocardial infarction. The third group (n=20) consisted of patients with chronic heart failure of ischemic etiology without postinfarction cardiosclerosis, not previously and at the time of examination infected with the SARS-Cov-2 virus. Statistical analysis was carried out using the IBM SPSS Statistics V26 program. The KolmogorovSmirnov, KruskalWallis, and Pearson 2 tests were used.
Results. Symptoms of left and right ventricular heart failure were equally common in all groups. Patients of the studied groups had a history of paroxysmal and permanent forms of atrial fibrillation, while the latter variant was more common in patients of the first group with chronic heart failure with postinfarction cardiosclerosis and coronavirus infection. According to echocardiography, the most pronounced structural and functional changes in the myocardium were also found in patients of the first group with postinfarction heart failure and a new coronavirus infection. Thus, statistically significant differences related to the size of the left atrium, end diastolic volume and end systolic volume of the left ventricle, systolic pressure in the pulmonary artery. An increase in the end systolic volume of the left ventricle by 94.6% was registered in the first group compared with the third group of patients (p=0.001). Systolic pressure in the pulmonary artery in the first group was 14.2% higher than the normal values (p 0.001), while in patients of the second and third groups this indicator was within the normal range.
Conclusion. In patients with postinfarction cardiosclerosis suffering from a new coronavirus infection, symptoms of chronic heart failure are more pronounced, characterized by a significant decrease in exercise tolerance; cardiac arrhythmias are more often recorded, and structural and functional changes in the myocardium are of a maladaptive nature.