Increased alcohol consumption has been associated with CVD risk. Subclinical arterial damage (SAD) precedes the onset of cardiovascular disease (CVD), and allows early identification and study of the pathophysiology of CVD. Reliable, noninvasive vascular biomarkers are available for the early detection of SAD and reclassification of CVD risk. To investigate the association of alcohol consumption with multiple SAD biomarkers and central hemodynamics in a large sample of Greek adults with CVD risk factors.

This cross-sectional study was conducted with 938 participants (43.5% men) and collected data on SAD biomarkers, central hemodynamics, and dietary intake. Multiple linear regression analysis was performed according to sex after adjusting for several confounders. In men, alcohol consumption of 20-30g/d was positively associated with mean, diastolic, and peripheral systolic blood pressure (BP). The consumption of >30g/d was positively associated with the augmentation index. In women, no statistically significant associations were found between alcohol consumption and BP or SAD indices. No statistically significant associations were found between alcohol consumption and arterial compliance or distensibility in both sexes.

In men even a small deviation from the current recommendation for alcohol consumption is associated with both higher BP indices and pressure wave reflections. The absence of association in women might be due to very low alcohol intake, even in the high consumption group. Liraglutide More studies are needed to verify our findings and establish the above associations in each sex.

In men even a small deviation from the current recommendation for alcohol consumption is associated with both higher BP indices and pressure wave reflections. The absence of association in women might be due to very low alcohol intake, even in the high consumption group. More studies are needed to verify our findings and establish the above associations in each sex.

Studies have reported that nut consumption is potentially beneficial in preventing cardiovascular disease. However, data are insufficient regarding the association between nut consumption and left ventricular hypertrophy (LVH).

In the Kangbuk Samsung Health Study, the participants were 34,617 men and 12,257 women who completed a food-frequency questionnaire for nut consumption and received echocardiography. Nut consumption was evaluated only for peanuts, pine nuts, and almonds defining 15g as one serving/servings dose. Multivariable adjusted odds ratio (OR) and 95% confidence interval (CI) for LVH were evaluated according to the consumption frequency of one serving dose of nut. The frequency of nut consumption was categorized into five groups (<1/month, 1/month-1/week, 1-2/week, 2-4/week, and ≥4/week). The subgroup analysis was conducted by dividing the participants into the following two groups the nonhypertensive/nondiabetic group and hypertensive or diabetic group. In women, nut consumption ≥2/week had the lower multivariable adjusted OR and 95% CI for LVH (2-4/week 0.46 [0.26-0.81] and ≥4/week 0.48 [0.25-0.92]) when compared with nut consumption<1/month. This association was identically observed in the subgroup analysis for women without hypertension and diabetes mellitus (DM) and women with hypertension or DM. However, men did not show the significant association.

In women, nut consumption ≥2/week was associated with the decreased probability of LVH. Further research studies should investigate whether the beneficial effect of nut consumption on LV structure results in better cardiovascular prognosis.

In women, nut consumption ≥2/week was associated with the decreased probability of LVH. Further research studies should investigate whether the beneficial effect of nut consumption on LV structure results in better cardiovascular prognosis.

Cardiovascular disease is the main cause of death worldwide, but the collective efforts to prevent this pathological condition are directed exclusively to individuals at higher risk due to hypercholesterolemia, hypertension, obesity, diabetes. Recently, vitamin D deficiency was identified as a risk factor for cardiovascular disease in healthy people, as it predisposes to different vascular dysfunctions that can result in plaque development and fragility. In this scenario, the fundamental aim of the study was to reproduce a disease model inducing vitamin D deficiency and atheromatosis in ApoE

mice and then to evaluate the impact of this vitamin D status on the onset/progression of atheromatosis, focusing on plaque formation and instability.

In our murine disease model, vitamin D deficiency was achieved by 3 weeks of vitamin D deficient dietalong with intraperitoneal paricalcitol injections, while atheromatosis by western-type diet administration. Under these experimental conditions, vitamin D deficient mice developed more unstable atheromatous plaques with reduced or absent fibrotic cap. Since calcium and phosphorus metabolism and also cholesterol and triglycerides systemic concentration were not affected by vitamin D level, our results highlighted the role of vitamin D deficiency in the formation/instability of atheromatous plaque and, although further studies are needed, suggested a possible intervention with vitamin D to prevent or delay the atheromatous disease.

The data obtained open the question about the potential role of the vitamins in the pharmacological treatments of cardiovascular disorders as coadjutant of the primary drugs used for these pathologies.

The data obtained open the question about the potential role of the vitamins in the pharmacological treatments of cardiovascular disorders as coadjutant of the primary drugs used for these pathologies.

Diabetes is one of the most important risk factors and comorbidities of ischemic stroke. Endoplasmic reticulum stress (ERS) is considered to be the major injury mechanism of ischemic stroke with diabetes. Studies have found that incretin can inhibit ERS in ischemia-reperfusion injury of the liver and heart. We aimed to explore the effects of GLP-1/GIP double agonist DA3-CH and GLP-1 single agonist liraglutide on ERS and apoptosis in diabetic rats with cerebral ischemia-reperfusion injury.

72 Sprague-Dawley (SD) male rats were randomly divided into 4 groups ① blank group (Sham group, n=18); model group (Saline group, n=18); DA3 treatment group (DA3 group, n=18); liraglutide treatment group (Lir group, n=18). The Sham group was not given any treatment and was only raised in the same environment as the other groups. The remaining 3 groups used STZ-induced diabetes models. After the successful membrane formation of diabetes, DA3-CH and liraglutide (10mmol/kg, once-daily for 14 days) were injected intraperitoneally.