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 link between severe forms of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection and cardiovascular diseases has been well documented by various studies that indicated a higher risk of cardiovascular complications in COVID-19 patients, in parallel with a higher risk of mortality in COVID-19 patients with underlying cardiovascular diseases. It seems that inflammation, which is a major pathophysiological substrate for both acute myocardial infarction and severe forms of COVID-19, may play a pivotal role in the interrelation between these two critical conditions, and hypercoagulability associated with SARS-CoV-2 infection could be responsible for acute cardiovascular complications. The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) proved to be independent predictors for prognosis in acute coronary syndromes and systemic inflammatory diseases; therefore, they may be used as independent prognostic markers of disease severity in COVID-19 infection. The aim of this review is to present the most recent advances in understanding the complex link between SARS-CoV-2 infection, inflammation and alteration of blood coagulability and hemorheology, leading to major cardiovascular events.

Iron deficiency and anemia affect approximately half of the chronic heart failure patients and they are associated with increased hospitalization rate, lower functional capacity, lower quality of life, and higher mortality. The exact mechanism of iron deficiency in heart failure patients is still not fully understood. Current guidelines recommend ferritin as the most accurate serum biomarker for the diagnosis of iron deficiency. The use of erythropoiesis-stimulating agents is no longer recommended because of the lack of improvement on mortality or hospital readmission rate, and it was associated with a higher rate of thromboembolic events. Intravenous iron replacement therapy is safe and generally well tolerated, with fewer side effects compared to oral administration. Large randomized studies with ferric carboxymaltose demonstrated its effectiveness and superiority to oral administration, and it was associated with a decreased rate of hospitalization rate and worsening heart failure, and improvement of functional capacity and quality of life. Intravenous iron supplementation for chronic heart failure is strongly recommended by European guidelines. Further studies are needed for a better knowledge of this complex pathology and determination of the long-term safety and effectiveness of iron administration in chronic heart failure patients. .

Recent studies demonstrated that despite restoration of the sinus rhythm, patients with a positive history of atrial fibrillation (AF) are still at risk of thromboembolic events. The primary objective of this study is to identify new imaging-derived biomarkers provided by modern imaging technologies, such as cardiac computed tomography angiography, delayed enhancement magnetic resonance imaging, or speckle tracking echocardiography, as well as hematological biomarkers, associated with the risk of intracavitary thrombosis in patients with AF, in order to identify the imaging-derived characteristics associated with an increased risk of cardioembolic events. Imaging data collected will be post-processed using advanced techniques of computational modeling, in order to fully characterize the degree of structural remodeling and the amount of atrial fibrosis. The primary endpoint of the study is represented by the rate of thromboembolic events. The rate of cardiovascular death, the rate of major adverse cardiovascular events, and the rate of AF recurrence will also be determined in relation to the degree of structural remodeling and atrial fibrosis.

Atrial fibrillation is the most frequent arrhythmia in adults, becoming more frequent with age. Recent clinical studies demonstrated that epicardial fat is linked with atrial fibrillation induction and recurrence. The arrhythmogenic mechanism consists in the fact that the epicardial adipose tissue is metabolically active, inducing local inflammation and enhancing the oxidative stress, which lead to atrial fibrillation as well as atherosclerosis. Having metabolic activity and secreting various anti- and pro-inflammatory biomarkers, the fat surrounding the heart has been linked to the complex process of coronary plaque vulnerabilization. This clinical update aims to summarize the role of epicardial adipose tissue in the pathogenesis, persistence, and severity of atrial fibrillation.