The 2019 novel coronavirus, known as severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) or coronavirus disease 2019 (COVID-19), is causing a global pandemic. The virus primarily affects the upper and lower respiratory tracts and raises the risk of a variety of non-pulmonary consequences, the most severe and possibly fatal of which are cardiovascular problems. Data show that almost one-third of the patients with a moderate or severe form of COVID-19 had preexisting cardiovascular comorbidities such as diabetes mellitus, obesity, hypertension, heart failure, or coronary artery disease. SARS-CoV2 causes hyper inflammation, hypoxia, apoptosis, and a renin–angiotensin system imbalance in a variety of cell types, primarily endothelial cells. Profound endothelial dysfunction associated with COVID-19 can be the cause of impaired organ perfusion that may generate acute myocardial injury, renal failure, and a procoagulant state resulting in thromboembolic events. We discuss the most recent results on the involvement of endothelial dysfunction in the pathogenesis of COVID-19 in patients with cardiometabolic diseases in this review. We also provide insights on treatments that may reduce the severity of this viral infection.

Metabolomics, the research area studying chemical processes involving metabolites, finds its utility in inflammasome biomarker discovery, thus representing a novel approach for cardiometabolic syndrome pathogeny acknowledgements. Metabolite biomarkers discovery is expected to improve the disease evolution and outcome. The activation of abundantly expressed NLRP3 inflammasome represents the background process of the diabetes mellitus disturbances like hyperglycemia and insulin resistance, as well as for myocardial cell death and fibrosis, all of them being features characteristic for cardiometabolic syndrome. Many molecules like troponins, brain natriuretic protein (BNP), ST2/IL-33, C-reactive protein (CRP), TNF, IL-1β, and IL-18 cytokines have been already examined as molecular markers for diagnosing or predicting different cardiac disturbances like myocardial infarction, heart failure, or myocarditis. In addition, metabolomics research comes with new findings arguing that NLRP3 inflammasome becomes a promising molecular tool to use for clinical and therapeutical management providing new targets for therapies in cardiometabolic syndrome. Inflammasome markers analyses, along with other molecular or genetic biomarkers, will result in a better understanding of cardiometabolic syndrome pathogenesis and therapeutic targets. Screening, diagnostic, and prognostic biomarkers resulted from inflammasome biomarker research will become standard of care in cardiometabolic syndrome management, their utility becoming the first magnitude.

The present study aimed to investigate the association between apolipoprotein B (Apo B) and classical features associated with clinical or subclinical atherosclerosis. A total of 811 adult patients from the general Romanian population, included in the national SEPHAR registry on hypertension, were divided into two groups based on Apo B value (low versus high Apo B with a cut-off established at 130 mg/dL) and subsequently into four subgroups according to the cut-offs recommended by the 2021 ESC Guidelines on Cardiovascular Disease Prevention. In all patients, lipid profile, uric acid, full blood count and presence of significant carotid plaques were assessed. Apo B levels were positively correlated with proatherogenic lipids (total cholesterol, triglycerides and LDL-cholesterol, p < 0.0001) and negatively correlated with HDL cholesterol (all p < 0.05). In comparison with patients with low Apo B levels, those with elevated Apo B levels more frequently presented significant carotid plaques (17% vs. 19% vs. 28% vs. 46%, p < 0.0001). Univariate regression analysis identified a strong association between the level of uric acid and increased value of Apo B in the four subgroups (uric acid 4.8 +/− 1.3 vs. 5 +/− 1.6 vs. 5.1 +/− 1.5 vs. 5.8 +/− 1.6, r = 0.2, p < 0.0001). The results of this nationwide registry on hypertension in Romania indicate that high Apo B may be considered as a risk factor for CVD, promoting atherosclerosis and associated with increased expression of classical markers of clinical or subclinical CVD.

Cardiovascular (CV) risk assessment charts are useful in establishing a patient therapeutic plan, but the most commonly used charts have essential limitations when applied to special populations. Our aim was to determine whether the Systematic Coronary Risk Evaluation (SCORE) chart underestimates the CV risk in young patients with ankylosing spondylitis (AS) and to promote the necessity of new risk assessment models. We conducted a prospective study in Constanta County, Romania including 70 consecutive patients ≤50 years of age, previously diagnosed with AS, without a history of established CV disease, diabetes mellitus and chronic kidney disease. We estimated the CV risk using SCORE based on total cholesterol, applied for a high‑risk population, such as the Romanian population. Estimation of CV risk was also conducted with the relative risk (RR) chart, considering the following variables: smoking, systolic blood pressure and total cholesterol. The majority of patients (n=46, 65.71%) had low risk according to the SCORE chart and only 24 (34.28%) were found to have moderate CV risk; none of them with high or very high CV risk. Ten patients (21.74%) of the 46 who were considered to have a low risk based on the SCORE system presented with carotid plaques. Twelve patients (50%) of the remaining 24 with moderate CV risk were found to have carotid plaques. According to 2016 ‘European Society of Cardiology’ (ESC) guidelines, 22 of all 70 patients were at high/very high CV risk due to the presence of carotid plaques. Comparing the RR chart with carotid plaque detection, only 4 out of 30 (13.3%) patients with RR=1 had carotid plaques; the frequency was higher in those with RR>1. Our results attested that the SCORE system underestimates the risk in patients with carotid plaques. Carotid ultrasound provided a more heightened sensitivity of the RR chart. C‑reactive protein (CRP) >3 mg/dl is associated with RR>1, making this chart a better CV risk predictive system in this particular category of patients.

An elevated level of total plasma homocysteine has been associated with a higher risk of atherosclerosis and coronary heart disease. The aim of our research was to study the relation between homocysteine and myocardial infarction (MI) in young patients. We conducted a case‑control study in Constanţa County, Romania including 61 patients, divided in two groups. The first group, the MI group, consisted of 28 patients, male (67.9%) and female (32.1%) aged less than 45 years who were consecutively admitted to the Intensive Coronary Care Unit of the Emergency County Hospital of Constanţa from September 1, 2017 to August 31, 2018 (12 months), with an established diagnosis of first acute MI. The second group, the control group, included 33 patients, male (75.8%) and female (24.2%) aged less than 45 years, with cardiovascular risk factors and/or stable angina pectoris that were consecutively addressed for ambulatory cardiac evaluation at the Outpatient Clinic of Emergency County Hospital of Constanţa during the same period. Fasting plasma homocysteine was determined in both groups, within 24 h after MI onset, respectively after first cardiac exam in the controls. High homocysteine was statistically confirmed to be a risk factor in the study group, especially in association with smoking, chronic kidney disease (CKD), and to a lesser extent with diabetes mellitus (DM) and hypertension. Data analysis was performed using IBM SPSS Statistics 23. The procedures used included descriptive statistics, parametric statistical tests (Independent sample t‑test), non‑parametric statistical tests [Chi‑square test of the association, with the evaluation of odds ratio (OR)]; the significance level used in the analysis (P‑value) was 0.05. After adjusting for variables, our study results pointed out a strong association between plasma homocysteine and first acute MI among young patients, emphasising plasma homocysteine as a possible risk factor for myocardial infarction.