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Cardiovascular disease (CVD) remains the main cause of death in patients with type 2 diabetes (T2D). Although hyperuricemia has been associated with multiple CV complications, it is not officially recognized as a target parameter for CVD risk reduction.To systematically review the literature in order to determine whether treating hyperuricemia with allopurinol in patients with T2D reduces CVD risk.A thorough literature search in the PubMed, CENTRAL, and EMBASE databases from inception to August 2022 was performed. After application of selection criteria, 6 appropriate studies were identified.Detailed analysis of the data derived indicated that there is an association between allopurinol treatment and CV benefits, resulting in a reduced risk of CVD events and mortality rates. This association can be attributed mainly to the reduction of inflammation and oxidative burden, as well as to the improvement of glycemic and lipid profiles.This systematic review provides evidence that allopurinol may reduce CVD risk in patients with T2D. Randomized, placebo-controlled trials should be performed in order to confirm these findings and identify specific subgroups of patients who will benefit most.

Abstract: Cardiovascular disease remains the main cause of human morbidity and mortality in developed countries. Microparticles (MPs) are small vesicles originating from the cell membrane as a result of various stimuli and particularly of biological processes that constitute the pathophysiology of atherosclerosis, such as endothelial damage. They form vesicles that can transfer various molecules and signals to remote target cells without direct cell-to-cell interaction. Circulating microparticles have been associated with cardiovascular diseases. Therefore, many studies have been designed to further investigate the role of microparticles as biomarkers for diagnosis, prognosis, and disease monitoring. To this concept, the pro-thrombotic and atherogenic potential of platelets and endothelial-derived MPs have gained research interest, especially concerning accelerated atherosclerosis and triggering as well as prognosis of an acute coronary syndrome. MPs, especially those of endothelial origin, have been investigated in different clinical scenarios of heart failure and in association with left ventricular loading conditions. Finally, most cardiovascular risk factors present unique features in the circulating MPs population, highlighting their pathophysiologic link to cardiovascular disease progression. In this review article, we present a synopsis of the biogenesis and characteristics of microparticles, as well as the most recent data concerning their implication in cardiovascular settings.

Cardiovascular disease (CVD) remains the leading cause of death worldwide, representing a major health, social, and economic issue. Thyroid disorders are very common and affect10% of the adult population in total. The aim of this review is to describe the physiologic role of thyroid hormones on cardiovascular system, to present cardiovascular manifestations in patients with thyroid disorders, emphasizing in molecular mechanisms and biochemical pathways, and to summarize current knowledge of treatment options. Thyroid hormone receptors are located both in myocardium and vessels, and changes in their concentrations affect cardiovascular function. Hyperthyroidism or hypothyroidism, both clinical and subclinical, without the indicated therapeutical management, may contribute to the progression of CVD. According to recent studies, even middle changes in thyroid hormones levels increase cardiovascular mortality from 20% to 80%. In more details, thyroid disorders seem to have serious effects on the cardiovascular system via plenty mechanisms, including dyslipidemia, hypertension, systolic and diastolic myocardial dysfunction, as well endothelial dysfunction. On top of clinical thyroid disorders management, current therapeutics focus on younger patients with subclinical hypothyroidism and elderly patients with subclinical hyperthyroidism.

Background: In recent years much research has been devoted to the deployment of biomarkers in the field of heart failure. Objectives: To study the potential of post-transcriptional regulation by microRNAs on the diagnosis, management and therapy of heart failure. Methods: Literature search focus on the role of microRNAs in heart failure. Results: MicroRNAs are expressed and regulated in the course of the pathological manifestations of heart failure (HF). This wide and uncharted area of genetic imprints consisting of small non-coding RNA molecule is upregulated and released into the bloodstream from organs under certain conditions and or stress. The use of genetically based strategies for the management of HF has gained great interest in the field of biomedical science because they can be used as biomarkers providing information regarding cardiac status and function. They also appear as promising tools with therapeutic potential because of their ability to induce changes at the cellular level without creating alterations in the gene sequence. In addition, with the advances in genomic sequencing, quantification and synthesis in technologies of microRNAs identification as well as the growing knowledge of the biology of miRNAs and their involvement in HF, it is expected to favorably affect the prognosis of HF patients. Conclusion: MicroRNAs are involved in the regulation of multibiological processes involved in the progress of heart failure. More studies are needed to achieve a clinical valuable implementation of microRNAs in the management of HF.

Heart failure (HF) is nowadays classified as HF with reduced ejection fraction (HFrEF), HF with mildly reduced EF (HFmrEF), and HF with preserved EF (HFpEF). Endothelial dysfunction (assessed by flow-mediated dilatation [FMD]), increased arterial stiffness (assessed by carotid-femoral pulse-wave velocity [PWV]), and galectin-3, a biomarker of myocardial fibrosis, have been linked to major adverse cardiovascular events (MACE) in patients with ischemic HF.In this study we prospectively enrolled 340 patients with stable ischemic HF. We assessed the brachial artery FMD, carotid-femoral PWV, and galectin-3 levels, and patients were followed up for MACE according to EF group.Interestingly, the FMD values exhibited a stepwise improvement according to left ventricular ejection fraction (LVEF) (HFrEF: 4.74 ± 2.35% vs. HFmrEF: 4.97 ± 2.81% vs. HFpEF: 5.94 ± 3.46%, p = 0.01), which remained significant after the evaluation of possible confounders including age, sex, cardiovascular risk factors, and number of significantly stenosed epicardial coronary arteries (b coefficient: 0.990, 95% confidence interval: 0.166-1.814, p = 0.019). Single-vessel coronary artery disease (CAD) was more frequent in the group of HFpEF (HFrEF: 56% vs. HFmrEF: 64% vs. HFpEF: 73%, p = 0.049). PWV did not display any association with LVEF. Patients who presented MACE exhibited worse FMD values (4.51 ± 2.35% vs. 5.32 ± 2.67%, p = 0.02), and the highest tertile of galectin-3 was linked to more MACEs (36% vs. 5.9%, p = 0.01).Flow-mediated dilatation displayed a linear improvement with LVEF in patients with ischemic HF. Deteriorated values are associated with MACE. Higher levels of galectin-3 might be used for risk stratification of patients with ischemic HF.

Background: Concerns of elevated cardiovascular risk with some anti-diabetic medications warranted trials on the cardiovascular outcome to demonstrate cardiovascular safety of newly marketed anti-diabetic drugs. Although these trials were initially designed to evaluate safety, some of these demonstrated significant cardiovascular benefits. Purpose of Review: We reviewed the cardiovascular and safety outcomes of novel antidiabetic agents in patients with type 2 diabetes and established cardiovascular disease or at high risk of it. We included the outcomes of safety trials, randomized controlled trials, meta-analysis, large cohort studies, and real-world data, which highlighted the cardiovascular profile of DPP-4is, GLP-1RAs and SGLT-2is. Summary: Although DPP-4is demonstrated non-inferiority to placebo, gaining cardiovascular safety, as well market authorization, SGLT-2is and most of the GLP-1RAs have shown impressive cardiovascular benefits in patients with T2D and established CVD or at high risk of it. These favorable effects of novel antidiabetic agents on cardiovascular parameters provide novel therapeutic approaches in medical management, risk stratification and prevention.

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.

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.

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.

Background Lipoprotein-associated Phospholipase A2 (Lp-PLA2), can exert proinflammatory as well as proatherogenic properties on the vascular wall. The current study sought to evaluate the influence of high Lp-PLA2 levels on indices of arterial wall properties in patients with stable coronary artery disease (CAD). Methods Three hundred seventy-four consecutive patients with stable CAD (mean age 61 ± 11 years, 89% males) were enrolled in this single-center cross-sectional study. Flow-mediated dilation (FMD) was used to assess endothelial function and augmentation index (AIx) of the central aortic pressure was used to assess reflected waves. ELISA was used to determine Lp-PLA2 serum levels. Results After dividing the participants in 3 equal groups based on the tertiles of circulating Lp-PLA2 values, no significant differences were demonstrated between those in the 3rd tertile with Lp-PLA2 values > 138 μg/L, in the 2nd tertile with Lp-PLA2 values between 101 and 138 μg/L and in the 1st tertile (Lp-PLA2 values P = 0.03). Patients in the highest tertile of Lp-PLA2 values had significantly higher AIx values (24.65 ± 8.69% vs. 23.33 ± 9.65%, P = 0.03), in comparison to the lowest tertile, with Lp-PLA2 values 138 μg/L negatively correlated to FMD [b = − 0.45 (95% CI: − 0.79 – -0.11), P = 0.01] and AIx values [b = 1.81 (95% CI: 0.57–3.05), P Conclusions Elevated Lp-PLA2 levels relate to endothelial dysfunction and arterial stiffness in patients with stable CAD independently from classical risk factors for CAD, statin use, antihypertensive treatment, and duration of the disease.

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.

Cardiovascular disease (CVD) remains the predominant cause of human morbidity and mortality in developed countries. Currently, microRNAs have been investigated in many diseases as well-promising biomarkers for diagnosis, prognosis, and disease monitoring. Plenty studies have been designed so as to elucidate the properties of microRNAs in the classification and risk stratification of patients with CVD and also to evaluate their potentials in individualized management and guide treatment decisions. Therefore, in this review article, we aimed to present the most recent data concerning the role of microRNAs as potential novel biomarkers for cardiovascular disease.

We systematically reviewed the literature regarding the impact of dipeptidyl peptidase-4 inhibitors (DPP-4i) on vascular function, including endothelial function and arterial stiffness, as predictors of atherosclerosis progression and cardiovascular disease in patients with type 2 diabetes mellitus (T2DM). We searched PubMed in order to identify clinical trials that investigated the effect of DPP-4i on vascular function in patients with T2DM when compared with placebo. Although 168 articles were initially found, only 6 studies (total 324 patients) investigated the effect of DPP-4i in comparison with placebo, specifically linagliptin and sitagliptin, and satisfied the inclusion criteria. There are scarce data to indicate that linagliptin may enhance endothelial function and exert a slight beneficial effect on arterial wall properties. Sitagliptin seems to have a neutral effect on these variables. Further trials are needed to elucidate the topic. The standards of reporting were in accordance with the PRISMA guidelines.

Background Arterial stiffness flags increased cardiovascular disease risk in type 2 diabetes mellitus (T2DM) patients. There is limited data on how novel anti-diabetic agents affect arterial stiffness. Purpose To investigate the effects of novel anti-diabetic agents on arterial stiffness in T2DM patients. Patients and methods We enrolled 64 consecutive patients under stable antidiabetic therapy who did not achieve therapeutic targets. Subjects were assessed to receive an additional antidiabetic agent to optimize glucose control; dipeptidyl peptidase-4 inhibitor (DPP4i, n=14), glucagon like peptide-1 receptor agonist (GLP1RA, n=21), sodium/glucose cotransporter-2 inhibitor (SGLT2i, n=21) or long-acting insulin (n=8). Glycosylated hemoglobin (HbA1c) as well as carotid-femoral pulse wave velocity (PWV) and augmentation index (Alx) were measured (as indices of arterial stiffness) were measured at baseline and 3 months after treatment intensification. Results There were no differences between the study groups in traditional risk factors, or baseline HbA1c, PWV and Alx levels (p=NS for all). All groups achieved better glycemic control in terms of HbA1c values between baseline and follow-up (for DPP4i: 7.4±0.2% vs 6.7±0.2%, for GLP1RA: 8.3±0.2% vs 6.9±0.1%, for SGLT2i: 7.5±0.1% vs 6.7±0.1% and for insulin 9.8±0.5% vs 7.7±0.4%, p Conclusions These preliminary data provide evidence that treatment intensification -particularly with GLP1RA, and SGLT2i- benefits vascular properties, a finding which could partly explain the positive findings of recent randomized clinical trails in this field. Acknowledgement/Funding None

Background Patients with type 2 diabetes mellitus (T2DM) are at higher risk for thrombotic events. Platelet function may be used to assess prothrombotic state in patients with cardiovascular disease. Purpose We aimed to investigate whether the administration of novel antidiabetic agents influence platelet function in TDM2 patients. Patients and methods We 60 enrolled consecutive patients with T2DM, on stable antidiabetic therapy, who did not achieve therapeutic targets. Subjects were assessed to receive an additional anti-diabetic agent; dipeptidyl peptidase-4 inhibitor (DPP4i, n=14), glucagon like peptide-1 receptor agonist (GLP1RA, n=24), sodium/glucose cotransporter-2 inhibitor (SGLT2i, n=22). Platelet reactivity was measured with PFA-200 collagen/epinephrine (c-EPI) and PFA-200 collagen/ADP (c-ADP) closure time. Glycosylated hemoglobin (HbA1c), c-EPI and c-ADP were assessed at baseline and 3 months after treatment intensification. Results There was no difference between the study groups regarding gender, age, hypertension, dyslipidemia, smoking, Hba1c and CADP or CEPI (p=NS for all) at baseline. All groups achieved better glycemic control in terms of HbA1c values between baseline and follow-up (for DPP4i: 7.4±0.2% vs 6.7±0.2%, for GLP1RA: 8.3±0.2% vs 6.9±0.1%, for SGLT2i: 7.5±0.1% vs 6.7±0.1% and for insulin 9.8±0.5% vs 7.7±0.4%, p Conclusion Antiplatelet treatment prevents thrombotic risk in T2DM patients receiving novel antidiabetics. The effects of novel antidiabetics on platelet reactivity -as well as any distinct class properties- merits further investigation. Acknowledgement/Funding None

Background: Arterial stiffness is a well-established surrogate marker of vascular properties in patients with type 2 diabetes mellitus (DM2). We aimed to investigate whether optimization of DM2 therapy with novel antiglycemic agents additional to metformin, may improve arterial wall properties. Methods: We enrolled 99 consecutive patients (male gender=63.3%) receiving metformin and still not achieving the therapeutic targets. Subjects were assigned to age and sex matched equal groups (n=33/group) of an additional antiglycemic agent; either DPP-4i, SGLT2i (n=28) or GLP-1 agonists. Applanation tonometry was used to assess non-invasively augmentation index (AIx) and aortic pulse wave velocity (PWV) as a measure of arterial stiffness at baseline and at 3-month follow-up. Among other demographics data, hemoglobin A1c (HbA1c) was measured. Results: There was no difference for male gender (p=0.10) or age (64.92 ± 8.30 years, p=0.27) between the 3 study groups. Interestingly, baseline values improved significantly after SGLT2i and DPP-4i administration both for PWV (11.46 ± 2.77 vs. 9.83 ± 2.19 m/s and 10.89 ± 2.35 vs. 9.68 ± 1.77 m/s respectively, p=0.01 for both) and AIx (28.81 ± 8.55 vs. 25.82 ± 7.40 and 27.91 ± 13.05 vs. 24.91 ± 12.70 respectively, p=0.01 for both), when compared to those at follow-up time. In contrast, GLP-1A administration decreased PWV (12.82 ± 3.00 m/s at baseline vs. 11.67 ± 2.77 m/s during follow-up, p Conclusion: The optimization of DM2 treatment with SGLT2i, DPP-4i or GLP-1A, added to metformin, not only helps to achieve better glycemic control but significantly ameliorates arterial stiffness indices and achieves therapeutic targets in patients with DM2. Disclosure G. Siasos: None. E. Bletsa: None. P.K. Stampouloglou: None. K. Batzias: None. S.A. Paschou: None. A. Antonopoulos: None. V. Tsigkou: None. N. Gouliopoulos: None. S. Mazaris: None. E. Oikonomou: None. A. Thanopoulou: None. M. Politou: None. A. Vryonidou: None. D. Tousoulis: None. N. Tentolouris: None.

Background: Patients with type 2 diabetes mellitus (DM2) exert a higher risk for thrombotic events. Platelet reactivity may be used to assess prothrombotic state in patients with cardiovascular disease. We aimed to investigate whether the administration of novel antiglycemic agents may influence platelet reactivity in these patients. Methods: We enrolled 99 patients (male=63.3%) receiving metformin for DM2 who did not achieve therapeutic targets under current treatment. Subjects were assigned to age and sex matched groups (n=33 per group) of an additional antiglycemic agent; either DPP-4 inhibitor, SGLT2 inhibitor or a GLP-1 agonist. Platelet reactivity was measured with PFA-200 assay; collagen/epinephrine (CEPI) and collagen/ADP closure time (CADP) were calculated in seconds and HbA1c at baseline and at 3 months. Results: There was no difference for male gender (p=0.10) or age (64.92 ± 8.30 years, p=0.27) between the study groups. All patients achieved better glycemic control in terms of HbA1c values between baseline and follow-up (7.78% vs. 6.92% for DPP-4, 7.52% vs. 6.73% for SGLT2 and 8.19% vs. 6.85% for GLP-1, p Conclusion: The addition of DPP-4 or GLP-1 to metformin influences platelet reactivity and achieves better glycemic control in DM2 patients, providing further insights in the pathophysiology of DM2. Disclosure G. Siasos: None. E. Bletsa: None. P.K. Stampouloglou: None. K. Batzias: None. A. Antonopoulos: None. S.A. Paschou: None. V. Tsigkou: None. N. Gouliopoulos: None. S. Mazaris: None. G. Vogiatzi: None. S. Tsalamandris: None. E. Oikonomou: None. M. Zaromytidou: None. M. Politou: None. A. Vryonidou: None. A. Thanopoulou: None. N. Tentolouris: None. D. Tousoulis: None.

Background: Arterial stiffness is a prominent macrovascular complication in patients with type 2 diabetes mellitus (DM2). Antiplatelet therapy is the cornerstone of CVD therapy. There is little evidence about the influence of antiglycemic agents on arterial wall properties and prothrombotic state. Methods: We enrolled 80 consecutive patients (males=64.4%), aged 64.19 ± 8.82 years receiving either metformin plus another antiglycemic agent such as sulphonylureas, DPP-4i, GLP-1 agonists, insulin, or metformin alone (n=16 per group). Applanation tonometry was used to assess aortic pulse wave velocity (PWV) as a measure of arterial stiffness. Platelet reactivity was measured with PFA-200, collagen/epinephrine (CEPI) and PFA-200 collagen/ADP closure time (CADP). Results: There was no difference between the study groups regarding gender, age, hypertension, dyslipidemia, smoking, PWV, CADP or CEPI (p=NS for all). When conducting a separate analysis between patients receiving aspirin (AS), dual antiplatelet therapy (DAPT) and those without antiplatelet therapy (nAPT), we observed that nAPT patients exerted significantly lower CEPI values (134.42 ± 40 s for nAPT vs. 170.36 ± 64 s for AS vs. 178.90 ± 74 s for DAPT, p=0.03). PWV was 10.96 ± 2.54 m/s for nAPT vs. 11.20 ± 2.88 m/s for AS vs. 10.82 ± 2.76 m/s for DAPT (p=0.9). Within-group analysis showed that CEPI values were significantly reduced in nAPT under sulphonylureas (121 s vs. 243 s vs. 262 s for nAPT, AS and DAPT respectively, p=0.02) or GLP-1 (138 s vs. 203 s vs. 168 s for nAPT, AS and DAPT respectively, p=0.05). Additionally, we found an inverse, linear association between CEPI and PWV (rho= -0.45, p=0.02) and CADP and PWV (rho= -0.04, p=0.05) in nAPT patients alone. Conclusion: Increased prothrombotic state is associated with impaired arterial wall elastic properties. Antidiabetic and antiplatelet treatment interactions may regulate the relationship between arterial stiffness and thrombosis in patients with DM2. Disclosure G. Siasos: None. P.K. Stampouloglou: None. K. Batzias: None. S.A. Paschou: None. A. Antonopoulos: None. V. Tsigkou: None. N. Gouliopoulos: None. M. Zaromytidou: None. S. Mazaris: None. E. Oikonomou: None. S. Tsalamandris: None. G. Vogiatzi: None. A. Thanopoulou: None. A. Vryonidou: None. M. Politou: None. D. Tousoulis: None. N. Tentolouris: None.

Patients with type 2 diabetes (T2D) are at high risk for thrombotic events. Platelet reactivity may be used to assess prothrombotic status. We investigated whether administration of novel antidiabetic agents may alter platelet reactivity in patients with T2D. We enrolled 54 consecutive male

Lipoprotein-associated Phospholipase A2 (Lp-PLA2), has inflammatory and atherogenic effect on vasculature. Hence, we examine the impact of high Lp-PLA2 levels on endothelial function and arterial stiffness of patients with coronary artery disease (CAD). We enrolled 374 patients with stable CAD.

Retinal vein occlusion (RVO), the second most common retinal vascular lesion, is divided in central retinal vein occlusion (CRVO) and branch retinal vein occlusion (BRVO), and is regarded a significant cause of visual impairment. RVO patients have an increased risk for cardiovascular disease and

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.

Arterial stiffness is a well-established surrogate marker of vascular properties and arterial dysfunction in patients with type 2 diabetes mellitus (DM2). We aimed to investigate whether optimization of DM2 therapy with, additional to metformin, novel antiglycemic agents may improve arterial wall

Arterial stiffness is considered a surrogate marker of arterial dysfunction in type 2 diabetes mellitus (DM2). Antiplatelet therapy is the cornerstone of cardiovascular disease therapy. There exists little evidence about the influence of antiglycemic agents on arterial wall properties and