Relationship of Atherosclerotic Plaque Structure with the History of COVID-19 in Patients Undergoing Coronary Computed Tomographic Angiography.

Although there is no sign of reinfection, individuals who have a history of coronavirus disease 2019 (COVID-19) may experience prolonged chest discomfort and shortness of breath on exertion. This study aimed to examine the relationship between atherosclerotic coronary plaque structure and COVID-19. This retrospective cohort comprised 1269 consecutive patients who had coronary computed tomographic angiography (CCTA) for suspected coronary artery disease (CAD) between July 2020 and April 2021. The type of atherosclerotic plaque was the primary outcome. Secondary outcomes included the severity of coronary stenosis as determined via the Coronary Artery Disease-Reporting and Data System (CAD-RADS) classification and the coronary artery calcium (CAC) score. To reveal the relationship between the history of COVID-19 and the extent and severity of CAD, propensity score analysis and further multivariate logistic regression analysis were performed. The median age of the study population was 52 years, with 53.5% being male. COVID-19 was present in 337 individuals. The median duration from COVID-19 diagnosis to CCTA extraction was 245 days. The presence of atherosclerotic soft plaque (OR: 2.05, 95% confidence interval [CI]: 1.32-3.11, P = 0.001), mixed plaque (OR: 2.48, 95% CI: 1.39-4.43, P = 0.001), and high-risk plaque (OR: 2.75, 95% CI: 1.98-3.84, P < 0.001) was shown to be linked with the history of COVID-19 on the conditional multivariate regression analysis of the propensity-matched population. However, no statistically significant association was found between the history of COVID-19 and the severity of coronary stenosis based on CAD-RADS and CAC score. We found that the history of COVID-19 might be associated with coronary atherosclerosis assessed via CCTA.

The potential role of SARS-CoV-2 infection in acute coronary syndrome and type 2 myocardial infarction (T2MI): Intertwining spread.

Coronavirus disease 2019 (COVID-19) is a novel pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It has been shown that SARS-CoV-2 infection-induced inflammatory and oxidative stress and associated endothelial dysfunction may lead to the development of acute coronary syndrome (ACS). Therefore, this review aimed to ascertain the link between severe SARS-CoV-2 infection and ACS. ACS is a spectrum of acute myocardial ischemia due to a sudden decrease in coronary blood flow, ranging from unstable angina to myocardial infarction (MI). Primary or type 1 MI (T1MI) is mainly caused by coronary plaque rupture and/or erosion with subsequent occlusive thrombosis. Secondary or type 2 MI (T2MI) is due to cardiac and systemic disorders without acute coronary atherothrombotic disruption. Acute SARS-CoV-2 infection is linked with the development of nonobstructive coronary disorders such as coronary vasospasm, dilated cardiomyopathy, myocardial fibrosis, and myocarditis. Furthermore, SARS-CoV-2 infection is associated with systemic inflammation that might affect coronary atherosclerotic plaque stability through augmentation of cardiac preload and afterload. Nevertheless, major coronary vessels with atherosclerotic plaques develop minor inflammation during COVID-19 since coronary arteries are not initially and primarily targeted by SARS-CoV-2 due to low expression of angiotensin-converting enzyme 2 in coronary vessels. In conclusion, SARS-CoV-2 infection through hypercytokinemia, direct cardiomyocyte injury, and dysregulation of the renin-angiotensin system may aggravate underlying ACS or cause new-onset T2MI. As well, arrhythmias induced by anti-COVID-19 medications could worsen underlying ACS.

Study of common hypertriglyceridaemia genetic variants and subclinical atherosclerosis in a group of women with SLE and a control group.

OBJECTIVE: SLE is associated with increased cardiovascular risk (CVR). High serum concentrations of triglyceride-rich lipoproteins and apolipoprotein B-rich particles constitute the characteristic dyslipidaemia of SLE. METHODS: A cross-sectional study was conducted to study the relationship between genetic variants involved in polygenic hypertriglyceridaemia, subclinical atherosclerosis and lipoprotein abnormalities. 73 women with SLE and 73 control women age-matched with the case group were recruited (age range 30-75 years). Serum analysis, subclinical atherosclerosis screening studies for the detection of plaque, and genetic analysis of the APOE, ZPR1, APOA5 and GCKR genes were performed. RESULTS: Triglyceride concentrations and the prevalence of hypertension, dyslipidaemia and carotid atherosclerosis were higher in women with SLE than in the control group. Multivariate logistic regression showed that CC homozygosity for the GCKR rs1260326 gene (OR=0.111, 95% CI 0.015 to 0.804, p=0.030) and an increase of 1 mmol/L in triglyceride concentrations were associated with a greater risk of carotid plaque in women with SLE (OR=7.576, 95% CI 2.415 to 23.767, p=0.001). CONCLUSIONS: GCKR CC homozygosity (rs1260326) and serum triglyceride concentrations are independently associated with subclinical carotid atherosclerosis in women with SLE. Subclinical carotid atherosclerosis is also more prevalent in these women compared with the control group. The study of GCKR rs1260326 gene variants may contribute to more precise assessment of CVR and modulation of the intensity of lipid-lowering treatment in patients with SLE.