COVID-19 is currently considered an inflammatory disease affecting the entire organism. In severe forms, an augmented inflammatory response leads to the fulminant “cytokine storm”, which may result in severe multisystemic end-organ damage. Apart from the acute inflammatory response, it seems that chronic inflammation also plays a major role in the clinical evolution of COVID-19 patients. Pre-existing inflammatory conditions, such as those associated with chronic coronary diseases, type 2 diabetes mellitus or obesity, may be associated with worse clinical outcomes in the context of COVID-19 disease. These comorbidities are reported as powerful predictors of poor outcomes and death following COVID-19 disease. Moreover, in the context of chronic coronary syndrome, the cytokine storm triggered by SARS-CoV-2 infection may favor vulnerabilization and rupture of a silent atheromatous plaque, with consequent acute coronary syndrome, leading to a sudden deterioration of the clinical condition of the patient. This review aims to present the current status of knowledge regarding the link between COVID-19 mortality, systemic inflammation and several major diseases associated with poor outcomes, such as cardiovascular diseases, diabetes and obesity.

Stem cell-derived exosomes - an emerging tool for myocardial regeneration

In participants with stable chest pain referred for invasive coronary angiography, those with a coronary artery calcium score of 0 at CT had very low, while higher scores had increasing occurrence ... Background Coronary artery calcium (CAC) has prognostic value for major adverse cardiovascular events (MACE) in asymptomatic individuals, whereas its role in symptomatic patients is less clear. Pur...

Ischemic stroke is associated with a tremendous economic and societal burden, and only a few therapies are currently available for the treatment of this devastating disease. The main therapeutic approaches used nowadays for the treatment of ischemic brain injury aim to achieve reperfusion, neuroprotection and neurorecovery. Therapeutic angiogenesis also seems to represent a promising tool to improve the prognosis of cerebral ischemia. This review aims to present the modern concepts and the current status of regenerative therapy for ischemic stroke and discuss the main results of major clinical trials addressing the effectiveness of stem cell therapy for achieving neuroregeneration in ischemic stroke. At the same time, as a glimpse into the future, this article describes modern concepts for stroke prevention, such as the implantation of bioprinted scaffolds seeded with stem cells, whose 3D geometry is customized according to carotid shear stress.

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.