Restenosis of Coronary Arteries in Patients with Coronavirus Infection: Case Series.

Abstract

Introduction: Coronavirus infection is a risk factor for vascular thrombosis. This is of particular importance for patients undergoing myocardial revascularization since this infection can be a trigger for the formation of restenosis in the area of a previously implanted coronary stent. Understanding the risk factors for stent thrombosis and restenosis is of particular importance in individuals at risk for adverse outcomes. The rarity of such situations makes the present study unique.

Objective: Studying the peculiarities of restenosis and thrombosis of the coronary arteries in patients after coronavirus infection.

Methods: The study was performed in the Department of Cardiovascular Surgery of Emergency Hospital, Semey City, in 2021. We have examined the medical records of 10 consecutive patients with restenosis of coronary arteries after coronavirus infection and 10 matched-by-age patients with similar restenosis of coronary arteries who did not have coronavirus infection as a comparison group. To determine statistically significant differences between independent samples, we calculated the Mann-Whitney U test.

Results: The average age of patients was 65.7 years. Only one case was classified as early restenosis (within 8 days of previous revascularization), two cases represented late restenosis, and seven cases were very late restenoses. In 70% of cases, restenosis was localized in the left anterior descending artery, in 30% of cases, it was in the right coronary artery, and in 40% of cases, it was in the left circumflex artery. In comparison with patients who did not have a coronavirus infection, there were statistically significant differences regarding IgG (P < 0.001) and fibrinogen (P=0.019).

Conclusion: Patients with myocardial revascularization in the past have a higher risk of stent restenosis against the background of coronavirus infection due to excessive neointimal hyperplasia, hypercoagulability, increased inflammatory response, and endothelial dysfunction.