Mitochondria are the source of cellular energy production and are present in different types of cells. However, their function is especially important for the heart due to the high demands in energy which is achieved through oxidative phosphorylation. Mitochondria form large networks which regulate metabolism and the optimal function is achieved through the balance between mitochondrial fusion and mitochondrial fission. Moreover, mitochondrial function is upon quality control via the process of mitophagy which removes the damaged organelles. Mitochondrial dysfunction is associated with the development of numerous cardiac diseases such as atherosclerosis, ischemia-reperfusion (I/R) injury, hypertension, diabetes, cardiac hypertrophy and heart failure (HF), due to the uncontrolled production of reactive oxygen species (ROS). Therefore, early control of mitochondrial dysfunction is a crucial step in the therapy of cardiac diseases. A number of anti-oxidant molecules and medications have been used but the results are inconsistent among the studies. Eventually, the aim of future research is to design molecules which selectively target mitochondrial dysfunction and restore the capacity of cellular anti-oxidant enzymes.

Background Newer antidiabetic drugs, i.e., dipeptidyl peptidase-4 (DPP-4) inhibitors, sodium-glucose cotransporter-2 (SGLT-2) inhibitors, and glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may exert distinct cardiovascular effects. We sought to explore their impact on vascular function. Methods Published literature was systematically searched up to January 2018 for clinical studies assessing the effects of DPP-4 inhibitors, GLP-1 RAs, and SGLT-2 inhibitors on endothelial function and arterial stiffness, assessed by flow-mediated dilation (FMD) of the brachial artery and pulse wave velocity (PWV), respectively. For each eligible study, we used the mean difference (MD) with 95% confidence intervals (CIs) for FMD and PWV. The pooled MD for FMD and PWV were calculated by using a random-effect model. The presence of heterogeneity among studies was evaluated by the I2 statistic. Results A total of 26 eligible studies (n = 668 patients) were included in the present meta-analysis. Among newer antidiabetic drugs, only SGLT-2 inhibitors significantly improved FMD (pooled MD 1.14%, 95% CI: 0.18 to 1.73, p = 0.016), but not DPP-4 inhibitors (pooled MD = 0.86%, 95% CI: -0.15 to 1.86, p = 0.095) or GLP-1 RA (pooled MD = 2.37%, 95% CI: -0.51 to 5.25, p = 0.107). Both GLP-1 RA (pooled MD = −1.97, 95% CI: -2.65 to -1.30, p < 0.001) and, to a lesser extent, DPP-4 inhibitors (pooled MD = -0.18, 95% CI: -0.30 to -0.07, p = 0.002) significantly decreased PWV. Conclusions Newer antidiabetic drugs differentially affect endothelial function and arterial stiffness, as assessed by FMD and PWV, respectively. These findings could explain the distinct effects of these drugs on cardiovascular risk of patients with type 2 diabetes.

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Coronary artery disease is the leading cause of morbidity and mortality worldwide. The most common pathophysiologic substrate is atherosclerosis which is an inflammatory procedure that starts at childhood and develops throughout life. Endothelial dysfunction is associated with the initiation and progression of atherosclerosis and is characterized by the impaired production of nitric oxide. In general, endothelial dysfunction is linked to poor cardiovascular prognosis and different methods, both invasive and non-invasive, have been developed for its evaluation. Ultrasound evaluation of flow mediated dilatation of the branchial artery is the most commonly used method to assessed endothelial function while intracoronary administration of vasoactive agents may be also be used to test directly endothelial properties of the coronary vasculature. Endothelial dysfunction has also been the subject of therapeutic interventions. This review article summarizes the knowledge about evaluation of endothelial function in acute coronary syndromes and stable coronary artery disease and demonstrates the current therapeutic approaches against endothelial dysfunction.

Retinal vein occlusion (RVO) is a common retinal vascular lesion, and a leading cause of visual impairment. Patients with RVO have an increased risk for cardiovascular disease and share multiple common risk factors. In this study, we investigated the endothelial function and arterial stiffness of patients with RVO compared to healthy-control (CL) subjects. We enrolled 40 consecutive patients with RVO and 40 CL subjects. RVO was diagnosed by an ophthalmologist, endothelial function was evaluated by flow mediated dilation (FMD) in the brachial artery, and carotid-femoral pulse wave velocity (PWV) and augmentation index (AIx) of the radial artery were measured to evaluate arterial stiffness and reflected waves, respectively. No significant differences were detected between the studied groups in sex, age, presence of hypertension or dyslipidemia, body mass index, systolic and diastolic blood pressure levels, total cholesterol levels, and smoking habits ( p > 0.05 for all). However, patients with RVO had impaired FMD ( p = 0.002) and increased PWV ( p = 0.004), even after adjustment for several confounders. Both FMD and PWV were also significantly and independently associated with the development of RVO. Furthermore, a significant and positive correlation between PWV and systolic blood pressure existed only in the CL group. Therefore, we have shown that RVO is associated with significant endothelial dysfunction and increased arterial stiffness. Our results strengthen the vascular theory, according to which, systemic endothelial dysfunction and arteriosclerosis play a significant role in the pathogenesis of RVO.

Background: Diabetes mellitus (DM) is on the rise globally. Its prevalence has nearly doubled during the last two decades and it is estimated to affect 8.8% of the global population. Cardiovascular disease (CVD) is the leading cause of death in diabetic population and despite modern anti-inflammatory and cardioprotective therapeutic strategies diabetic patients have at least a twice fold risk of cardiovascular events. Prothrombotic state in DM is associated with multiple determinants such as platelet alterations, oxidative stress, endothelial changes, circulating mediators. Thus, proper antithrombotic strategies to reduce the risk of CVD in this population is critical. Methods: This article reviews the current antiplatelet and anticoagulant agents in the aspect of primary and secondary prevention of CVD in the diabetic population. Results: The use of aspirin may be considered only at high-risk patients in the absence of contraindications. Cangrelor was not inferior to clopidogrel in preventing the composite outcome of CV death, myocardial infraction and revascularization without increasing major bleeding. Triple therapy in the subpopulation with DM significantly reduced the composite primary outcome of CV death, myocardial infraction or repeat target lesion revascularization. That was not the case for stent thrombosis, which was similar in both groups. Importantly, triple therapy did not result in increased bleeding complications, which were similar in both groups. However, cilostazol is linked to various adverse effects (e.g., headache, palpitations, and gastrointestinal disturbances) that drive many patients to withdrawal. Conclusion: In conclusion, DM is a rapidly growing disease that increases the risk of CVD, AF, and CV mortality. Proper antithrombotic strategies to reduce CVD risk in DM is a necessity. Also, new antithrombotic treatments and combination therapies may play a critical role to overcome antiplatelet resistance in DM patients and reduce morbidity and mortality attributed to CVD.

Exercise provides beneficial effects on the primary and secondary prevention of numerous chronic conditions, including cardiovascular disease, diabetes mellitus, and malignancies. Despite its indisputable benefits, exercise can rarely trigger major adverse cardiovascular events such as ventricular arr hythmias, myocardial infarction, or even sudden cardiac arrest in susceptible individuals. Physiological changes that occur during exercise, including increased sympathetic activity and cardiac oxygen requirements, may account for ischemia and trigger ventricular ectopy with eventually adverse outcomes. Tailored preparticipation screening for exercise and sports engagement is fundamental to unveiling underlying pathological conditions. The present review summarizes the overall impact of exercise on cardiovascular health and highlights the recommended prevention strategies.