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Aims To determine the impact of smoking and alcohol exposure during adolescence on arterial stiffness at 17 years. Methods and results Smoking and alcohol use were assessed by questionnaires at 13, 15, and 17 years in 1266 participants (425 males and 841 females) from the ALSPAC study. Smoking status (smokers and non-smoker) and intensity ('high' ≥100, 'moderate' 20-99, and 'low or never' 10 drinks on a typical drinking day)]. Carotid to femoral pulse wave velocity (PWV) was assessed at 17 years [mean ± standard deviation and/or mean difference (95% confidence intervals)]. Current smokers had higher PWV compared with non-smokers (P = 0.003). Higher smoking exposure was associated with higher PWV compared with non-smokers [5.81 ± 0.725 vs. 5.71 ± 0.677 m/s, mean adjusted difference 0.211 (0.087-0.334) m/s, P = 0.001]. Participants who stopped smoking had similar PWV to never smokers (P = 0.160). High-intensity drinkers had increased PWV [HI 5.85 ± 0.8 vs. LI 5.67 ± 0.604 m/s, mean adjusted difference 0.266 (0.055-0.476) m/s, P = 0.013]. There was an additive effect of smoking intensity and alcohol intensity, so that 'high' smokers who were also HI drinkers had higher PWV compared with never-smokers and LI drinkers [mean adjusted increase 0.603 (0.229-0.978) m/s, P = 0.002]. Conclusion Smoking exposure even at low levels and intensity of alcohol use were associated individually and together with increased arterial stiffness. Public health strategies need to prevent adoption of these habits in adolescence to preserve or restore arterial health.

Background: Left ventricular (LV) pacing is unsuccessful in a significant number of patients, mainly due to sub-optimal LV pacing location. Nevertheless, data about the impact of different pacing sites on LV function in intact and ischemic myocardium are scarce. Objectives: To investigate the effect of combinations of alternative LV pacing sites on LV mechanics, in the intact myocardium and after experimental acute anterior myocardial infarction (AMI), in order to define the optimal configuration. Methods: Atrioventricular epicardial pacing at alternative pacing sites was performed in 16 healthy pigs simultaneously, before and after AMI. Hemodynamic parameters together with classic and novel echocardiographic indices were used to evaluate the effect of each pacing combination. Speckle tracking technique using Echo PAC software was used. Results: In intact myocardium, most LV performance variables measured, including deformation parameters were adversely affected during pacing (in all combinations, all variables p 0.05). Conclusions: In intact myocardium, LV function is depressed in comparison to sinus rhythm, in every combination of pacing sites studied. However, during AMI the combination of pacing LV apex lateral wall and LV basal posterior wall managed to maintain the LV function at a level comparable to the sinus rhythm.

Data on the incidence of new onset atrial fibrillation and flutter (AF/f) in patients with acute pericarditis are limited. We sought to determine the incidence and prognostic significance of AF/f in this setting.Between January 2006 and June 2014, consecutive new cases of acute pericarditis were included in two urban referral centres for pericardial diseases. All new cases of AF/f defined as episodes lasting ≥30 s were recorded. Events considered during follow-up consisted of AF/f and pericarditis recurrence, cardiac tamponade, pericardial constriction and death.822 consecutive new cases of acute pericarditis (mean age 53±15 years, 444 men) were analysed. AF/f was detected in 35 patients (4.3%, mean age 66.5±11.3 years, 18 men). Patients with AF/f were significantly older (p=0.017) and presented more frequently with pericardial effusion (p0.001). Arrhythmias developed within 24 h of pericarditis onset in 91.4% of cases, lasted24 h in 25.7% and spontaneously converted in 74.3% of patients. Underlying structural heart disease was present in 17% of AF/f cases. In a 30-month follow-up, patients with history of AF/f at the initial episode had a higher rate of arrhythmia occurrence (34.3% vs 0.9%, p0.001), mostly (75%) within 3 months. No other differences were detected in additional clinical events including haemorrhagic complications in patients receiving oral anticoagulation.The occurrence of AF/f in acute pericarditis identifies a predisposed population to AF/f with a high recurrence risk (about 35%): in these patients, pericarditis may act as an arrhythmic trigger and oral anticoagulation should be seriously considered according to guidelines.

Background: Hypertension (HT) is an important risk factor for cardiovascular disease and might precipitate pathology of the aortic valve. Objective: To investigate the association of HT with aortic dysfunction (including both aortic regurgitation and stenosis) and the impact of antihypertensive treatment on the natural course of underlying aortic disease. Methods: We performed a systematic review of the literature for all relevant articles assessing the correlation between HT and phenotype of aortic disease. Results: Co-existence of HT with aortic stenosis and aortic regurgitation is highly prevalent in hypertensive patients and predicts a worse prognosis. Certain antihypertensive agents may improve haemodynamic parameters (aortic jet velocity, aortic regurgitation volume) and remodeling of the left ventricle, but there is no strong evidence of benefit regarding clinical outcomes. Renin-angiotensin system inhibitors, among other vasodilators, are well-tolerated in aortic stenosis. Conclusion: Several lines of evidence support a detrimental association between HT and aortic valve disease. Therefore, HT should be promptly treated in aortic valvulopathy. Despite conventional wisdom, specific vasodilators can be used with caution in aortic stenosis.

Background: The failing heart is characterized by a depleted metabolic energy reserve and the up-regulation of several molecular mechanisms leading to cardiac hypertrophy, inflammation, fibrosis, angiogenesis, and apoptosis. Dietary or non-dietary supplementation of vitamins could potentially benefit energy balance. Objective: The objective of the present study was to evaluate all available information on vitamins supplementation in patients with chronic HF for possible beneficial effect on metabolic, inotropic, chronotropic and hemodynamic indices. Method: We searched MEDLINE via Pubmed by using the following terms: “chronic heart failure” OR “cardiomyopathy” AND "vitamins", “vitamin A”, “B complex vitamins”, "vitamin C", "ascorbic acid", “vitamin D”, “retinol”, “vitamin E”, “thiamine“, “riboflavin”, “niacin”, “pyridoxine”, “cobalamin”, “folate”, “pantothenic acid”, “biotin”, “tocopherol” and combinations of them. Results: Data regarding supplementation of micronutrients in HF for most vitamins were sparse, and the inference about cardiovascular outcomes was obscured by the heterogeneity of studies, high inherent morbidity, and mortality of this group of high-risk patients, limited sample sizes in certain studies, unclear design and lack of head to head comparisons. Most vitamins in human trials failed to establish survival, or robust beneficial effect and mostly indirect favorable evidence is derived from patients with deficiencies of certain micronutrients rather that the ad hoc supplementation of them. Conclusion: While vitamins and micronutrients are promising compounds for optimizing myocardial metabolism and homeostasis in HF, additional randomized clinical trials of larger scale are warranted to demonstrate the benefits of their supplementation in this high risk group of patients.

Heart failure (HF) consists the fastest growing clinical cardiac disease. HF patients are categorized on the basis of underlying left ventricular ejection fraction (LVEF) into HF with preserved EF (HFpEF), reduced LVEF (HFrEF), and mid-range LVEF (HFmrEF). While LVEF is the most commonly used surrogate marker of left ventricular (LV) systolic function, the implementation of two-dimensional echocardiography in estimating this parameter imposes certain caveats on current HF classification. Most importantly, LVEF could fluctuate in repeated measurements or even recover after treatment, thus blunting the borders between proposed categories of HF and enabling upward classification of patients. Under this prism, we sought to summarize possible procedures to improve systolic function in patients with HFrEF either naturally or by the means of pharmacologic and non-pharmacologic treatment and devices. Therefore, we reviewed established pharmacotherapy, including beta-blockers, inhibitors of renin–angiotensin–aldosterone axis, statins, and digoxin as well as novel treatments like sacubitril–valsartan, ranolazine, and ivabradine. In addition, we assessed evidence in favor of cardiac resynchronization therapy and exercise training programs. Finally, innovative therapeutic strategies, including stem cells, xanthine oxidase inhibitors, antibiotic regimens, and omega-3 polyunsaturated fatty acids, were also taken into consideration. We concluded that LVEF is subject to changes in HF after intervention and besides the aforementioned HFrEF, HFpEF, and HFmrEF categories, a new entity of HF patients with recovered LVEF should be acknowledged. An improved global and refined LV function assessment by sophisticated imaging modalities and circulating biomarkers is expected to render HF classification more accurate and indicate patients with viable—yet dysfunctional—myocardium and favorable characteristics as the ideal candidates for LVEF recovery by individualized HF therapy.

Background/Introduction: Risk stratification in chronic heart failure (HF) remains a challenge. Renal function and B-natriuretic peptide (BNP) might confer predictive value towards long-term mortality in HF patients after an acute coronary syndrome (ACS). Methods: From May 2006 to March 2009, 1,000 consecutive patients who were hospitalized with ACS diagnosis were enrolled in the study. In 2016, the 10-year follow-up (2006 -2016) was performed in 745 participants. GFR was evaluated through the MDRD formula. HF phenotype was defined according to baseline ejection fraction (EF); HF with reduced EF (i.e.

Aim: The investigation of the association between total arterial compliance (C-T)-estimated by a novel technique-with left ventricular mass (LVM) and hypertrophy (LVH). Our hypothesis was that C-T may be better related to LVM compared to the gold-standard regional aortic stiffness. Within the frame of the ongoing cross-sectional study "SAFAR," 226 subjects with established hypertension or with suspected hypertension underwent blood pressure (BP) assessment, carotid-to-femoral pulse wave velocity (cf-PWV), and echocardiographic measurement of LVM. LVM index (LVMI) was calculated by the ratio of LVM to body surface area. C-T was estimated by a previously proposed and validated formula: C-T = 36.7 /cf-PWV2 [ml/mmHg]. LVMI was related to age (r = 0.207, p = 0.002), systolic BP (r = 0.248, p < 0.001), diastolic BP (r = 0.139, p = 0.04), mean BP (r = 0.212, p = 0.002), pulse pressure (r = 0.212, p = 0.002), heart rate (r = -0.172, p = 0.011), cf-PWV (r = 0.268, p < 0.001), and C-T (r = -0.317, p < 0.001). The highest correlation was observed for CT that was significantly stronger than the respective correlation of cf-PWV (p < 0.001). In multivariate analysis, C-T was a stronger determinant, compared to cf-PWV, of LVMI and LVH. It remains to be further explored whether C-T has also a superior prognostic value beyond and above local or regional (segmental) estimates of pulse wave velocity.

Renin–angiotensin system (RAS) inhibition may exert beneficiary pleiotropic effects on heart hemodynamics in hypertensive patients. We aimed to assess these effects on coronary flow reserve (CFR) and left ventricular (LV) filling pressure after acute and long-term treatment. Thirty-nine patients (48.4±6.8 years) with newly diagnosed, never-treated essential arterial hypertension were consecutively recruited from an outpatient hypertension clinic. CFR in the left anterior descending artery and the ratio of mitral inflow E wave to the averaged mitral annulus tissue velocity of the E waves (E/e' ratio), as an estimate of LV filling pressure, were assessed by Doppler echocardiography. In the acute phase of the study, consecutive eligible patients were assigned to receive po Quinapril (Q) 20 mg (n=15) or Losartan (L) 100 mg (n=14) or no treatment (n=10) and were reexamined 2 h post treatment. In the chronic phase of the study, the patients were reevaluated after 1 month on the assigned treatment. During the acute phase, CFR (P=0.005) was significantly improved in the RAS inhibition as compared with the control group, independently of blood pressure (BP) changes. The E/e' ratio was also marginally improved (P=0.053), but this effect was more pronounced in patients with E/e' ratio>8 (P=0.005). CFR and E/e' ratio were also improved after 1 month of treatment, particularly in responders after the acute phase. In hypertensive patients, RAS inhibition acutely improved CFR and E/e' ratio independently of BP changes. An acute positive response in these parameters was closely related to sustained improvement after 1 month of single-drug treatment.

The metabolic dysfunction accompanying the polycystic ovary syndrome (PCOS) may increase the risk of hypertension and cardiovascular disease (CVD). Although menopause per se may be an additional risk factor of CVD, the association between PCOS in postmenopausal women and cardiovascular risk has not been adequately investigated. We aimed to evaluate the effect of PCOS on markers of subclinical atherosclerosis in nondiabetic postmenopausal women.This cross-sectional study included 286 postmenopausal women with intact ovaries. PCOS phenotype was defined if three of the following were present: insulin resistance, current hyperandrogenism or history of clinical androgen excess, history of infertility, central obesity and history of irregular menses. Traditional CVD risk factors, as well as indices of arterial structure (intima-media thickness, atheromatous plaques presence) and function [flow-mediated dilation, pulse wave velocity (PWV), augmentation index] were compared between women with a PCOS phenotype and the rest of the sample, who served as controls.Women with the PCOS phenotype (N=43) had higher SBP and triglycerides and lower high-density lipoprotein (HDL)-cholesterol than controls. Mean values of PWV differed significantly between PCOS cases and controls (9.46±1.74 vs. 8.60±1.51 m/s, P=0.001, univariate). Multivariate regression analysis showed that the PCOS phenotype, age and SBP were the only independent predictors of PWV.Arterial stiffness is increased in asymptomatic, nondiabetic women with a putative PCOS phenotype, independently of age, BMI or blood pressure. This might present one mechanism through which PCOS increases the risk of CVD and hypertension later in life.

Several studies have examined the association of the PvuII polymorphism of the estrogen receptor alpha gene with the risk of stroke. Data linking the polymorphism with the severity and outcome of cerebrovascular disease are lacking. In this study, we evaluated 285 postmenopausal Caucasian patients suffering an acute stroke, hospitalized in two tertiary hospitals over a period of 2 years, and searched for associations between the PvuII polymorphism and the one-month outcome and the neurological severity on admission. The prevalence of CC genotype was 21%, CT 50% and TT 29%. Estradiol levels were higher with increasing frequencies of the C allele (p = 0.04). There was no difference in the short-term functional outcome and mortality and the neurological severity on admission among the three genotypes. We did not find a significant association of the PvuII polymorphism with intracerebral hemorrhage and classical stroke risk factors. An association of the CC genotype with venous thromboembolism history was recorded (p 0.05). There was no association between the PvuII polymorphism and stroke severity and short-term outcome in the studied female stroke population. It is possible that the long-term estrogenic action, reflected by the genetic polymorphism, is not a major determinant of disease severity and prognosis in older age.

Postmenopausal women are at increased risk for progression of arteriosclerosis and hypertension. Recent cross-sectional evidence suggests that high normal circulating prolactin levels may accelerate vascular ageing in menopause. Postmenopausal women (n=201) were consecutively recruited from a Menopause Clinic and re-evaluated in at least one follow-up visit within the next 3 years. Baseline circulating prolactin levels were measured while both baseline and follow-up vascular and biochemical measurements were performed. Endothelial function was assessed by flow-mediated dilation (FMD), aortic stiffness by pulse-wave velocity (PWV) and arterial wave reflections by applanation tonometry. Baseline prolactin significantly correlated with lower FMD at follow-up (P=0.005). After multivariable adjustment for age, follow-up time, blood pressure (BP), body mass index, smoking and medication, this correlation remained significant (P=0.003). In addition, baseline circulating prolactin levels were independently associated with changes in mean BP (β=0.131, P=0.021), peripheral diastolic BP (β=0.169, P=0.004) and new-onset hypertension (OR=1.235, P=0.001). Owing to significant interaction between baseline prolactin and age for changes in PWV over time (P=0.036), a subgroup analysis based on median age was performed. This analysis revealed that in women younger than 55 years, prolactin was an independent predictor of changes in PWV over time (P=0.008). In conclusion, high normal circulating prolactin levels predict changes in haemodynamic indices and worsening endothelial function in healthy postmenopausal women. Particularly in young postmenopausal women, prolactin predicts accelerated arterial stiffening.

Environmental factors constitute an important but underappreciated risk factor towards the development and progression of cardiovascular disease (CVD). Environmental exposure to variable pollutants is implicated in the derangement or propagation of adverse pathophysiological processes linked with atherosclerosis, including genetic, hemodynamic, metabolic, oxidative and inflammation parameters. However, no data exist on environmental pollution in rural or semi-rural areas. Therefore, the purpose of the “Corinthia” study is to examine the impact of environmental pollution in indices of cardiovascular morbidity and mortality in a cross-sectional and longitudinal design. The Corinthia study began in October 2015 and is planned to recruit 1,500 individuals from different regions of Corinthia country with different environmental exposures to pollutants and different patterns of soil/ground and/or air pollution until December 2016. Baseline measurements will include lifestyle measurements, anthropometric characteristics and a comprehensive cardiovascular examination. The follow-up is planned to extend prospectively up to 10 years and this study is anticipated to provide valuable data on the distinct impact of soil and air pollution on early markers of atherosclerosis and cardiovascular disease and on the overall impact of environment pollution to cardiovascular morbidity and mortality. (C) 2016 Hellenic Cardiological Society. Publishing services by Elsevier B.V.

The possible effects of sesame oil on hemodynamics are unknown. The aim of the study was to investigate the acute and long-term effects of sesame oil on hemodynamic responses in hypertensive men. The authors enrolled 30 hypertensive men in a two-phase study. In the first phase, patients consumed 35 g of either sesame oil or control oil. Central and peripheral blood pressure, pulse wave velocity, augmentation index (AI), C-reactive protein, tumor necrosis factor α, malonydealdehyde, and total antioxidant capacity (TAC) were assessed at fast and 2 hours postprandially. In the second phase, patients consumed 35 g of either sesame oil or control oil daily for 2 months. The above-mentioned parameters were assessed before and following 15, 30, and 60 days of oil consumption. Sesame oil decreased central and peripheral diastolic pressures 1 hour postprandially (P=.006). Fifteen days of sesame oil intake decreased peripheral systolic blood pressure (P=.016) and heart rate-corrected AI75 (P=.017) and increased TAC (P=.007). This is the first study to demonstrate a favorable acute and long-term effect of sesame oil on hemodynamics in hypertensive men. Further research is warranted to establish the potential protective role of sesame oil.

Although long-term weight gain has been associated with cardiovascular risk and intima-media thickening (IMT), no sufficient data exist on possible associations of such weight changes with more advanced stages of subclinical atherosclerosis. Moreover, the value of self-reported weight changes, a more practical approach to assess long-term history in adiposity status, is still a matter of debate. In this longitudinal study, long-term changes in BMI and overweight status were assessed in 106 healthy young adults (age 40.5 ± 1.1 years, 60 males). These were a subgroup of adolescent school students who had originally been examined in 1983 initially aiming to assess cardiovascular risk factor prevalence. Markers of early (carotid IMT) and advanced (presence of plaques in the carotid and femoral arteries and ankle-brachial index, ABI) subclinical atherosclerosis were measured in all individuals. By multivariate analysis, among other risk factors, IMT and the presence of plaques were independently determined by BMI change, while a low ABI was also determined by changes in overweight status. An adverse long term adiposity profile change (≥ +4 kg/m(2) and/or change into overweight/obese status from normal weight since adolescence) incrementally determined a low ABI over current risk factors. Self-reported and actual BMI changes were correlated (r = 0.587) but their means significantly differed, while the former significantly correlated with IMT only (P = 0.032). In conclusion, an adverse long term adiposity status change was more prominently associated with advanced subclinical atherosclerosis and particularly low ABI. These results also suggest that the utility of self-reported weight changes may be limited in primary prevention practice.

Background and Purpose— Limited data exist concerning obesity and survival in patients after acute stroke. The objective of this study was to investigate the association between obesity and survival in patients with acute first-ever stroke. Methods— Patients were prospectively investigated based on a standard diagnostic protocol over a period of 16 years. Evaluation was performed on admission, at 7 days, at 1, 3, and 6 months after discharge, and yearly thereafter for up to 10 years after stroke. The study patients were divided into 3 groups according to body mass index (BMI): normal weight (2 ), overweight (25–29.9 kg/m 2 ), and obese (≥30 kg/m 2 ). Overall survival during follow-up was the primary end point. The secondary end point was the overall composite cardiovascular events over the study period. Results— Based on our inclusion criteria, 2785 patients were recruited. According to BMI, 1138 (40.9%) patients were of normal weight, 1113 (41.0%) were overweight, and 504 (18.1%) were obese. NIHSS score on admission (mean, 11.28±8.65) was not different among the study groups. Early (first week) survival in obese (96.4%; 95% CI, 94.8%–97.9%) and overweight patients (92.8%; 95% CI, 91.2%–94.4%) was significantly higher compared to that of normal-weight patients (90.2%; 95% CI, 88.4%–92.0%). Similarly, 10-year survival was 52.5% (95% CI, 46.4%–58.6%) in obese, 47.4% (95% CI, 43.5%–51.3%) in overweight, and 41.5% (95% CI, 39.7%–45.0%) in normal-weight patients (log-rank test=17.7; P Conclusions— Based on BMI estimation, obese and overweight stroke patients have significantly better early and long-term survival rates compared to those with normal BMI.

Increased wave reflection is an independent factor associated with cardiovascular diseases, risk, and mortality. The influence of the menstrual cycle on wave reflections and particularly on the reproducibility of their measurement has never been examined. The aim of the present study was to examine the reproducibility and variability of wave reflection indices in premenopausal healthy women during their menstrual cycle. Thirty-two women were examined at 3 phases of their menstrual cycle: days 1 to 2 (menstrual phase), days 6 to 14 (late follicular), and days 4 to 7 after ovulation (early luteal phase). Applanation tonometry of the radial artery and aortic pulse wave analysis were performed for the calculation of augmentation pressure, augmentation index, and timing of reflected waves. Reproducibility of these measures was evaluated by intraclass correlation coefficient and Bland-Altman analysis, whereas ANOVA was performed to assess their variability during the menstrual cycle. The SD of augmentation index differences between repeated measurements within the menstrual cycle ranged from 7.6% to 9.9%. Bland-Altman analysis indicated no evidence of systemic bias and no trend for the reproducibility of measurements to vary with their underlying mean value. Intraclass correlation coefficient indicated a moderate reproducibility of augmentation index and augmentation pressure (>0.80) and a rather low reproducibility for timing of reflected waves (0.43). Mean augmentation pressure, augmentation index, and timing of reflected waves did not vary significantly during the menstrual cycle (ANOVA). Measurement of wave reflections at the same phase of the menstrual cycle or statistical adjustment could be suggested for optimal study design and data interpretation.

Objective— The extent to which atherosclerosis is accelerated in chronic inflammatory diseases is not established. We compared preclinical atherosclerosis in rheumatoid arthritis with diabetes mellitus, a known coronary heart disease equivalent. Methods and Results— Endothelial function, arterial stiffness, carotid intima-media thickness, and analysis of atheromatous plaques were examined in 84 rheumatoid arthritis patients without cardiovascular disease versus healthy controls matched for age, sex, and traditional cardiovascular disease risk factors, as well as in 48 diabetes patients matched for age, sex, and disease duration with 48 rheumatoid arthritis patients. Rheumatoid arthritis duration associated with arterial stiffening, whereas disease activity associated with carotid plaque vulnerability. All markers of preclinical atherosclerosis were significantly worse in rheumatoid arthritis compared to controls, whereas they did not differ in comparison to diabetes despite a worse cardiovascular risk factor profile in diabetics. Both diseases were associated independently with increased intima-media thickness; rheumatoid arthritis, but not diabetes, was independently associated with endothelial dysfunction. Conclusions— Preclinical atherosclerosis appears to be of equal frequency and severity in rheumatoid arthritis and diabetes of similar duration with differential impact of traditional risk factors and systemic inflammation. Cardiovascular disease risk factors in rheumatoid arthritis may need to be targeted as aggressively as in diabetes.

Hyperprolactinemia has been associated with endothelial dysfunction and an adverse cardiovascular risk profile, possibly as a result of the vasoconstrictive properties of prolactin. In this cross-sectional study, we examined the hypothesis that prolactin contributes to the increased cardiovascular risk occurring in early menopause by studying apparently healthy women without hyperprolactinemia. Prolactin serum levels were measured by immunoassay in 76 women aged 54.4±4.9 years in menopause for 4.9±2.8 years, and possible correlations with traditional cardiovascular risk factors and surrogate markers of preclinical atherosclerosis, arterial stiffening, and endothelial and microcirculatory function were examined. Positive correlations between prolactin serum levels and arterial blood pressure, but no other traditional risk factors, were found. Prolactin also correlated with central aortic systolic ( r =0.337; P =0.002) and diastolic ( r =0.272; P =0.012) blood pressures and pulse wave velocity ( r =0.264; P =0.02), a marker of aortic stiffness, but not with endothelial or microcirculatory function or carotid intima-media thickness. By multivariate regression analysis, prolactin levels determined, independent of traditional risk factors, both blood pressures and aortic stiffness. Notably, prolactin correlated with European Society of Cardiology HeartScore ( r =0.364; P =0.002), a composite index that predicts 10-year cardiovascular mortality. Prolactin levels >8.0 ng/mL had 100% sensitivity to predict a high peripheral blood pressure. Prolactin may play a role in accelerated arteriosclerosis in early menopause by affecting central/peripheral blood pressure and arterial stiffness. In contrast, no correlation was observed with other risk factors or surrogate markers of atherosclerosis. Prospective studies to assess whether prolactin is an additional hormone increasing cardiovascular risk are warranted.

Introduction: The impact of diet on atherosclerosis progression is well established. However, the independent predictive value of unhealthy diet in the prognosis and severity of coronary artery disease (CAD) has not been definitely confirmed and clinicians often ignore how to incorporate it in clinical practice. Hypothesis: Dietary patterns may impact CAD severity. Methods: In this cohort study we included 188 consecutive symptomatic stable CAD patients. The diagnosis of CAD was based on coronary angiography and patients were categorized as having severe CAD and non-severe CAD. The diagnosis of severe CAD was based on the presence of either left main coronary artery disease (stenosis≥50%), or three-vessel coronary artery disease, or two-vessel coronary artery disease marked by stenosis of the proximal left anterior descending artery ≥70%. Among several demographics and clinical characteristics all subjects were tested with a validated semi quantitative food frequency questionnaire. Results: Concerning baseline demographic characteristics there was no difference between subjects with severe CAD and non-severe CAD while, the prevalence of severe CAD was higher in current smokers compared to non-smokers. Principal component analysis revealed 8 distinct dietary patterns. The first component-western dietary pattern (increased intake of fat, red meat and carbohydrates and minimal consumption of fruits vegetables and green leafy)- was predictive of severe CAD (AUC:0.73, 95% CIs:0.64-0.83, p Conclusion: The unhealthy western type of diet is associated with the severity and extent of coronary artery lesions in patients with stable CAD. These findings highlight the importance of accessing dietary patterns when calculating cardiovascular risk and to take into consideration dietary habits in the management of cardiovascular patients.

Introduction: Resistant hypertension is related to sympathetic overdrive and arterial stiffening, while there are scarce data whether metabolic syndrome further potentiates sympathetic activity and vascular abnormalities in this setting. Hypothesis: The aim of this study was to assess the effect of the metabolic syndrome on muscle sympathetic nerve activity (MSNA) and arterial stiffness in resistant hypertensive patients. Method: We studied 24 patients with resistant hypertension [age: 58±10 years, 15 males, office blood pressure (BP): 178/94±15/12 mmHg, 24-hour BP: 149/84±15/11 mmHg, under 4.2±0.5 drugs] that underwent transthoracic echocardiographic study and blood sampling for assessment of the metabolic profile. Metabolic syndrome was defined according to the Adult Treatment Panel III criteria and arterial stiffness was evaluated on the basis of carotid to femoral pulse wave velocity (PWV). In all participants sympathetic drive was assessed by MSNA estimations based on established methodology (microneurography). Results: Resistant hypertensive patients with metabolic syndrome (n=11) compared to those without (n=13) exhibited higher waist circumference (108.1±5.4 vs 94.6±9.2 cm, p=0.001), fasting glucose (131.8±2.9 vs 94.6±2.1 mg/dl, p Conclusions: In resistant hypertensive patients, metabolic syndrome is associated with high MSNA and PWV levels. These findings support that metabolic syndrome further deteriorates sympathetic activity and arterial stiffening characterizing resistant hypertension.

Background Increased arterial stiffness (AS) might be one significant acute mediator of the well-attested association between female depression and cardiovascular disease. Methods We tested this hypothesis in an inpatient sample of 20 drug-free women undergoing a new clinically severe major depressive episode of recent onset with an adequately matched mentally healthy control group. Patients' clinical (Hamilton Depression Rating Scale) and vascular (Pulse–Wave–Velocity, PWV) assessments were performed both before the initiation and after the completion of their six-week antidepressant treatment. Results Although initially patients exhibited significantly higher PWV values than controls, this was decreased and reached comparable levels to controls after treatment completion. Moreover, full-responders exhibited significantly greater vascular improvement than their partial-responders counterparts and the magnitude of their amelioration was strongly associated with the magnitude of their clinical improvement. Limitations Our sample-size was small and patients' follow-up short. Conclusions Our findings provide support to the hypothesis that current severe major depressive episode in women leads acutely to aggravation of arterial stiffness, reversible however upon timely and effective antidepressant treatment.

OBJECTIVE To assess the association of common polymorphisms involved in lipoprotein oxidation, platelet activation, and cholesterol and homocysteine metabolism with subclinical atherosclerosis and indices of endothelial function and arterial elasticity in healthy postmenopausal women. DESIGN The study investigated 84 healthy postmenopausal women recruited from the Menopause Clinic of the 2nd Department of Obstetrics and Gynecology, University of Athens, Aretaieion Hospital. The following polymorphisms were genotyped: apolipoprotein B 3500, apolipoprotein E (E2/E3/E4), cholesterol 7 alpha-hydroxylase A-204C (CYP A-204C), cholesterol ester transfer protein B1/B2, glycoprotein IIIa leu33pro, integrin beta 3 PLA1/PLA2, plasminogen activator inhibitor 1 4G/5G, paraoxonase 1 gln192 arg, and methylenetetrahydrofolate reductase ala222val. Ultrasound examination aimed to assess the presence of atherosclerotic plaque and to measure intima-media thickness in the carotid and femoral arteries and to estimate the augmentation index, brachial flow-mediated dilatation, and radial and femoral pulse-wave velocity. RESULTS The cholesterol 7 alpha-hydroxylase A-204C polymorphism was positively associated with the presence of atherosclerotic plaque (P = 0.004) and carotid and femoral intima-media thickness (P = 0.047 and P = 0.025, respectively). CONCLUSIONS The CYP A-204C polymorphism was positively associated with subclinical atherosclerosis in healthy postmenopausal women. It remains to be clarified whether the presence of these polymorphisms may be valuable in assessing the inherent risk among postmenopausal women.