BACKGROUND: After recovery from COVID-19 patients may develop new risk factors that lead to changes in cardiopulmonary interactions, i.e. an increase in the afterload on the right ventricle due to increased pressure in the pulmonary artery and change in pulmonary vascular resistance. It can be assumed that the presence of such a spectrum of problems can influence the severity of dyspnea and the development of pathogenetic events (pulmonary hypertension, right ventricular failure, subendocardial ischemia), which in turn can determine the outcome.
AIM: To identify the characteristics of acute coronary syndrome after a COVID-19, taking into account angiographic data on coronary artery lesions and hemodynamic manifestations.
MATERIALS AND METHODS: A comparative analysis of the clinical and hemodynamic consequences of the COVID-19 and the development of acute coronary syndrome in 157 patients was carried out. The group 1 included 69 patients who had had COVID-19 (vaccinated — 24.6%) during the 6 months preceding acute coronary syndrome; group 2 — 88 patients without a history of COVID-19 (vaccinated — 42%). The 12-lead electrocardiogram has been used in the diagnosis of subendocardial ischemia in acute coronary syndrome. The ST segment displacement in lead aVR was analyzed.
RESULTS: After COVID-19, dispnoe occurred in 52% of the patients and in 14.8% without previous infection. Echocardiographic signs of right ventricular overload were present in 42% of the patients in group 1 and 10.2% in group 2. The mean pressure in the pulmonary artery was increased after COVID-19 in 58% of the patients in group 1 and in 10.2% of group 2 in the range from 20 to 24 mm Hg and in the range from 25 to 36 mm Hg in 29% of the patients in group 1 and 2.3% of the patients in group 2. The average value of left ventricular ejection fraction in the patients who had had COVID-19 was 55.9 ± 14%, which was less than in the patients in the control group (63.2 ± 5.5%; p 0.001). ST segment elevation in lead aVr indicated high incidence of subendocardial ischemia. 40.6% in group 1, and 11.4% in group 2 (χ2 = 17.9; p 0.001); in group 1 vaccinated — 17.6%, and not vaccinated — 48.1% (χ2 = 4.9; p = 0.027), in group 2 vaccinated — 8.1%, and not vaccinated — 13.7% (χ2 = 0.7; p = 0.41). All the patients had drug-eluting stents implanted in the infarct-related artery. After stenting, no recurrence of pain or further increase in chest pain was observed.
CONCLUSIONS: After coronavirus infection COVID-19, 58% of patients have increased mean pressure in the pulmonary artery in the range from 20 to 24 mm Hg and in the range from 25 to 36 mm Hg in 29%. Atherothrombosis is the main mechanism of acute coronary syndrome after COVID-19 coronavirus infection. The main feature of acute coronary syndrome after a coronavirus infection COVID-19 is increased pressure in the pulmonary artery after a lung injury, which must be taken into account when planning surgical treatment tactics and management tactics in the postoperative period.
