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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 < 101 μg/L) regarding age, male gender, smoking habits, family history of CAD or history of a previous myocardial infarction, diabetes mellitus, arterial hypertension, hyperlipidemia, duration of CAD and treatment with relevant medication. Importantly, subjects with Lp-PLA2 values in the highest tertile, had significantly reduced FMD values compared to the middle and lower tertile (4.43 ± 2.37% vs. 4.61 ± 1.97% vs. 5.20 ± 2.52% respectively, 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 < 101 μg/L. A linear regression analysis showed that 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 < 0.001] independently of cofounders like gender, age, diabetes mellitus, arterial hypertension, dyslipidemia, smoking habits, family history of CAD, history of previous myocardial infarction, serum glucose, circulating lipid levels, duration of CAD, antihypertensive medication, antidiabetic drugs, statin therapy and treatment with β-blockers. 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. [ABSTRACT FROM AUTHOR]

Background: The clustering of arterial stiffness with microvascular disease (MD) and their effects on the clinical outcome of patients with type 2 diabetes (T2D) remains not fully clarified. Methods: In a prospective study of 414 patients with T2D, we investigated the prognostic value of arterial stiffness and MD for clinical outcomes. Participants were assessed for the presence of MD (ie diabetic retinopathy, nephropathy and neuropathy) and arterial stiffness by pulse wave velocity (PWV) and followed‐up for a median of 30 (range 1‐60) months. The primary endpoint of the study was the composite endpoint of major adverse cardiovascular events, that is, cardiovascular and non‐cardiovascular mortality and non‐fatal myocardial infarction/stroke. Results: A total of 146 (35.3%) patients had evidence of MD at baseline. In cox regression models, MD and PWV were independently associated with the composite clinical endpoint; for MD hazard ratio (HR), 3.24, 95%CI, 1.10‐9.54, P=.032, and for PWV HR, 1.20, 95%CI, 1.06‐1.36, P=.004) after adjustment for traditional risk factors, and enhanced risk discrimination and reclassification. The subgroup of patients with MD and high PWV was associated with increased incidence of the composite clinical endpoint (20.9% vs 1.8% in those with no MD & low PWV, P=.001). Importantly, absence of MD at baseline was associated with no mortality events during the follow‐up period. PWV at baseline was not associated with MD progression during follow‐up. Conclusions: These findings support that screening for arterial stiffness and MD in the routine clinical assessment of patients with T2D may enhance prognostication and cardiovascular risk reclassification. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

Abstract: Background: Arterial stiffness and vascular calcification significantly contribute to coronary atherosclerosis progression. The prognostic value of increased arterial stiffness and vascular calcification in subjects with stable coronary artery disease (CAD) after percutaneous coronary intervention(PCI) is currently under question. Materials and Methods: We randomly enrolled 262 patients with stable CAD 1 month after successful PCI. Carotid‐femoral pulse wave velocity (PWV) was measured as a well‐established index of central aortic stiffness. Osteoprotegerin (OPG) plasma levels were measured as a biomarker of vascular calcification. Patients were followed up prospectively up to 52 months. The primary endpoint was the composite of death from cardiovascular causes, myocardial infarction, stroke or hospitalization for cardiovascular causes. Results: During the follow‐up period, 48 patients presented the primary composite endpoint. Subjects who presented the primary endpoint, compared to subjects free of cardiovascular events, had significantly increased PWV (9.45 ± 2.19 m/s vs 8.73 ± 2.07 m/s, P = .04) and OPG levels (4.21 ± 2.19 pmol/L vs 3.18 ± 1.74 pmol/L, P = .003). Survival analysis indicated that PWV predicted adverse cardiac events MACE (Hazard ratio = 1.29 95%CI: 1.07‐1.57, P = .008) independently from confounders such as age, sex, smoking habits, ejection fraction, extent of coronary artery disease, hypertension and diabetes mellitus. Interestingly, for every increase in pulse wave velocity by 1 m/s, there is an anticipated increase in the risk of major adverse cardiovascular event (MACE) by 29%. Conclusions: These findings extend the current knowledge concerning the role of arterial stiffness as powerful biomarkers in cardiovascular disease. Measurement of PWV might have a role in ascertaining prognosis and managing treatment in patients with stable CAD after PCI. [ABSTRACT FROM AUTHOR]

Ocular involvement occurs in sarcoidosis (Sar) patients mainly in the form of uveitis. This study was designed to determine if uveitis in Sar patients is associated with vascular impairment. We enrolled 82 Sar patients and 77, age and sex matched, control subjects (Cl). Sar patients were divided into those with ocular sarcoidosis (OS) and those without ocular sarcoidosis (WOS). Endothelial function was evaluated by flow-mediated dilation (FMD). Pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections. Although there was no significant difference in sex, age and mean arterial pressure, patients with OS compared to WOS patients and Cl subjects had impaired FMD (p < 0.001), increased AIx (p = 0.02) and increased PWV (p = 0.001). Interestingly, impaired FMD in Sar patients was independently, from possible covariates (age, sex, smoking habits, arterial hypertension, dyslipidemia), associated with increased odds of ocular involvement (odds ratio = 1.69, p = 0.001). More precisely ROC curve analysis revealed that FMD had a significant diagnostic ability for the detection of OS (AUC = 0.77, p < 0.001) with a sensitivity of 79% and a specificity of 68% for an FMD value below 6.00%. To conclude in the present study we have shown that ocular involvement in Sar patients is associated with impaired endothelial function and increased arterial stiffness. These results strengthen the vascular theory which considers uveitis a consequence of vascular dysfunction in Sar patients and reveals a possible clinical importance of the use of endothelial function tests. [ABSTRACT FROM AUTHOR]

Background In the present study, we evaluated the association of platelet reactivity with vascular function in patients after percutaneous coronary intervention receiving clopidogrel treatment. Methods We enrolled 150 patients with stable CAD receiving clopidogrel regimen (75 mg/d), 1 month after percutaneous coronary intervention. Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as an index of arterial wave reflections. High on treatment platelet reactivity (HPR) was evaluated using VerifyNow Assay. VerifyNow reports its results in P2Y12 reaction units (PRU), and the diagnostic cutoff value is 230 PRU. Patients were evaluated prospectively up to 24 months. The primary end point was a composite of death from cardiovascular causes, nonfatal major cardiovascular events and hospitalization for cardiovascular causes. Results There was no difference in the basic clinical and demographic characteristics between subjects with HPR and non-HPR. Subjects with high on treatment platelet reactivity and PRU > 230 had significantly increased PWV (8.81 ± 2.25 m/s vs. 7.69 ± 1.95 m/s, p = 0.001) and AIx (25.27 ± 8.67% vs. 20.87 ± 10.57%, p = 0.04) compared to subjects with PRU ≤ 230. PWV was also associated with PRU (r = 0.23, p = 0.02). HPR was associated with significantly increased risk of primary end point [HR = 5.38, 95%CI:(1.15, 26.04), p = 0.03]. Conclusions Increased platelet reactivity is associated with impaired arterial stiffness in patients after percutaneous coronary intervention receiving clopidogrel treatment, highlighting another clinical factor implicated in individual platelet response to antiplatelet therapy. Moreover, increased platelet reactivity is associated with adverse outcome in these patients. [ABSTRACT FROM AUTHOR]

BACKGROUND Smoking is associated with impaired vascular function. Concord grape juice (CGJ), a rich source of flavonoids, can modify cardiovascular risk factors. Endothelial function and arterial stiffness are surrogate markers of arterial health. We examined the impact of CGJ on arterial wall properties in healthy smokers. METHODS We studied the effect of a 2-week oral treatment with CGJ in 26 healthy smokers on 3 occasions (day 0 (baseline), day 7, and day 14) in a randomized, placebo-controlled, double-blind, crossover study. Measurements were taken before (pSm), immediately after (Sm0), and 20 minutes after (Sm20) cigarette smoking. Endothelial function was evaluated by flow-mediated dilation (FMD) of the brachial artery. Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. RESULTS Compared with placebo, treatment with CGJ resulted in a significant improvement in pSm values of FMD (P = 0.02) and PWV (P = 0.04). At baseline, smoking decreased FMD in both the CGJ group (P < 0.001) and the placebo group (P < 0.001). Compared with placebo, CGJ treatment prevented the acute smoking-induced decrease in FMD on day 7 (P = 0.02) and day 14 (P < 0.001). Moreover, at baseline, smoking induced a significant elevation in PWV in both the CGJ group (P = 0.02) and the placebo group (P = 0.04). Treatment with CGJ prevented the smoking-induced elevation in PWV on day 7 (P = 0.003) and day 14 (P < 0.001). CONCLUSIONS CGJ consumption improved endothelial function and vascular elastic properties of the arterial tree in healthy smokers and attenuated acute smoking-induced impairment of arterial wall properties. [ABSTRACT FROM AUTHOR]

Background: Osteopontin (OPN) and osteoprotegerin (OPG) have recently emerged as key factors in both vascular remodeling and development of atherosclerosis. Arterial stiffness has an independent predictive value for cardiovascular events. We evaluate the relationship between OPG, OPN serum levels and vascular function in coronary artery disease (CAD) patients. Methods: The study population was consisted of 409 subjects (280 with CAD and 129 without CAD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. OPG and OPN levels were measured, as markers of vascular remodeling and calcification, by ELISA. Gensini score was used to evaluate the extent of CAD. Results: CAD patients, compared to those without CAD, had higher OPG (3.91±1.87pmol/l vs. 2.88±1.32pmol/l, p<0.001) and logOPN levels (1.81±0.18ng/ml vs. 1.71±0.24ng/ml, p<0.001) and impaired PWV (8.94±2.21m/s vs. 8.28±1.91m/s, p=0.006). Furthermore, PWV was associated with serum OPG levels (r=0.19, p<0.001) and with serum logOPN levels (r=0.10, p=0.049). Multivariate linear regression analysis revealed that increased OPG (p=0.013) and logOPN (p=0.006) levels are associated with 3‐vessel CAD and Gensini score (p=0.04 for OPG and p=0.09 for OPN), independently of other known cardiovascular risk factors. Conclusion: The present study revealed that serum OPG and OPN levels are positively associated with arterial stiffness, and with the extent of CAD. These preliminary results suggest that OPG and OPN levels are significantly correlated with vascular function contributing to the pathogenesis of atherosclerosis in CAD. Further studies are needed to explore the mechanisms of action of OPG and OPN in CAD. [ABSTRACT FROM AUTHOR]

Abstract: Background: Smoking is associated with endothelial dysfunction and arterial stiffness. Supplementation of omega-3 PUFAs is associated with better prognosis. Aim of this study was to evaluate the effects of omega-3 polyunsaturated fatty acids (PUFAs) supplementation on smoking-induced impairment of arterial function. Methods: We studied the effect of a 12weeks oral treatment with 2gr/day of omega-3 PUFAs in 20 healthy smokers on three occasions (day0:baseline, day28 and day84). The study was carried out on two separate arms (omega-3 fatty acids and placebo), according to a randomized, placebo-controlled, double-blind, cross-over design. Measurements were carried out before (pSm), immediately and 20min after cigarette smoking. Endothelial function was evaluated by flow-mediated dilation (FMD) of the brachial artery. Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections. Circulating levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and plasminogen activator inhibitor-1 (PAI-1) were measured. Results: Compared with placebo, omega-3 PUFAs treatment resulted in a significant improvement in pSm values of FMD (p<0.05), AIx (p<0.001) and PWV (p<0.01). Although, acute cigarette smoking decreased FMD and caused an increase in AIx and PWV, omega-3 PUFAs treatment blunted the acute smoking-induced impairment of FMD (p<0.001), AIx (p<0.05) and PWV (p<0.05) and significantly decreased levels of TNFα (p<0.05) and IL-6 (p=0.01) and increased levels of PAI-1 (p=0.05). Conclusions: Omega-3 PUFAs improved endothelial function and the elastic properties of the arterial tree in healthy smokers, with a parallel anti-inflammatory effect. [Copyright &y& Elsevier]

BackgroundSarcoidosis is an inflammatory disease, which may affect vascular function. The study was designed to assess the impact of sarcoidosis on endothelial function and arterial stiffness.MethodsEighty-seven sarcoidosis patients and eighty-seven matched healthy subjects (Cl) were included in the study. Sarcoidosis patients were divided into two groups. Group 1 included patients never treated and group 2 included patients receiving cortisone treatment. Endothelial function was evaluated by flow-mediated dilatation (FMD). Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AI75) as a measure of arterial wave reflections. Serum levels of soluble intercellular adhesion molecule-1 and tumor necrosis factor-α (TNF-α), were measured.ResultsIn the totality of the population, sarcoidosis patients had significantly lower FMD (P < 0.01) and significantly higher AI75 (P < 0.05). There was also a significant difference, between group 1, and Cl in FMD and AI75, but there was no difference between group 2 and Cl in FMD and AI75. AI75 values were significantly correlated with serum levels of intercellular adhesion molecule-1 (ICAM-1) (r = 0.370, P < 0.01) and TNF-α (r = 0.219, P = 0.049).ConclusionsIn the present study, we have shown that sarcoidosis patients have impaired endothelial function and increased arterial stiffness. Sarcoidosis patients on cortisone treatment had no differences compared to controls on the vascular parameters. Moreover, there was a significant correlation between inflammatory process and vascular function impairment. These findings indicate that sarcoidosis patients have impaired vascular function and increased inflammatory status, which may improve with cortisone treatment.American Journal of Hypertension (2011). doi:10.1038/ajh.2011.30 [ABSTRACT FROM AUTHOR]

Soluble suppression of tumorigenesis-2 (sST2) has been introduced as a marker associated with heart failure (HF) pathophysiology and status. Endothelial dysfunction is a component underlying HF pathophysiology. Therefore, we examined the association of arterial wall properties with sST2 levels in patients with HF of ischemic etiology. We enrolled 143 patients with stable HF of ischemic etiology and reduced left ventricular ejection fraction (LVEF) and 77 control subjects. Flow-mediated dilation (FMD) was used to evaluate endothelial function and pulse wave velocity (PWV) to assess arterial stiffness. Although there was no significant difference in baseline demographic characteristics, levels of sST2 were increased in HF compared to the control (15.8 (11.0, 21.8) ng/mL vs. 12.5 (10.4, 16.3) ng/mL; p < 0.001). In the HF group, there was a positive correlation of sST2 levels with age (rho = 0.22; p = 0.007) while there was no association of LVEF with sST2 (rho = −0.119; p = 0.17) nor with PWV (rho = 0.1; p = 0.23). Interestingly, sST2 was increased in NYHA III [20.0 (12.3, 25.7) ng/mL] compared to patients with NYHA II (15.0 (10.4, 18.2) ng/mL; p = 0.003) and inversely associated with FMD (rho = −0.44; p < 0.001) even after adjustment for possible confounders. In patients with chronic HF of ischemic etiology, sST2 levels are increased and are associated with functional capacity. There is an inverse association between FMD and sST2 levels, highlighting the interplay between the dysfunctional endothelium and HF pathophysiologic mechanisms. [ABSTRACT FROM AUTHOR]

The article discusses the development of diabetic retinopathy (DR) and its link to endothelial dysfunction and arterial stiffness. Topics include diabetic microvascular complications, irreversible blindness, and the atherosclerotic progression in patients manifesting insulin resistance. Other topics include type 2 diabetes mellitus (T2DM), the Early Treatment Diabetic Retinopathy Study (ETDRS), and diabetes-related structural and compositional alterations to the ocular basement membranes.

Abstract: Objectives: Metabolic syndrome (MetS) is associated with adverse cardiovascular events, and impaired vascular function. In this study we evaluated the effects of omega-3 polyunsaturated fatty acids (PUFAs) supplementation on vascular function, inflammatory and fibrinolytic process in subjects with MetS. Methods: We studied the effect of a 12 weeks oral treatment with 2 g/day of omega-3 PUFAs in 29 (15 male) subjects (mean age 44 ± 12 years) with MetS on three occasions (day0: baseline, day 28 and day 84). The study was carried out on two separate arms (PUFAs and placebo), according to a randomized, placebo-controlled, double-blind, cross-over design. The diagnosis of MetS was based on the guidelines of Adult Treatment Panel III definition. Endothelial function was evaluated by flow-mediated dilation (FMD) of the brachial artery. Carotid-femoral pulse wave velocity (PWV) was measured as an index of aortic stiffness. Serum levels of interleukin-6(IL-6) and plasminogen activator inhibitor-1(PAI-1) were measured by ELISA. Results: Treatment with PUFAs resulted in a significant improvement from day 0 to 28 and 84 in FMD and PWV (p < 0.001 for all). Nevertheless, treatment with placebo resulted in no significant changes in FMD (p = 0.63) and PWV (p = 0.17). Moreover, PUFAs treatment, compared to placebo, decreased IL-6 levels (p = 0.03) and increased PAI-1 levels (p = 0.03). Finally, treatment with PUFAs resulted in a significant decrease in fasting triglyceride levels from day 0 to 28 and 84 (p < 0.001) and in serum total cholesterol levels (p < 0.001). Conclusions: In subjects with MetS, treatment with omega-3 PUFAs improved endothelial function and arterial stiffness with a parallel antiinflammatory effect. [Copyright &y& Elsevier]

The study of arterial properties in patients with aortic valve stenosis who undergo transcatheter aortic valve implantation (TAVI) remains challenging and results so far seem equivocal. We sought to investigate the acute and long-term effect of TAVI on arterial stiffness and wave reflections. We enrolled 90 patients (mean age 80.2 ± 8.1 years, 50% males) with severe symptomatic aortic stenosis undergoing TAVI. Arterial stiffness was assessed by carotid-femoral and brachial-ankle pulse wave velocity (cfPWV and baPWV). Augmentation index corrected for heart rate (AIx@75), central pressures and subendocardial viability ratio (SEVR) were assessed with arterial tonometry. Measurements were conducted at baseline, after TAVI and at 1 year. Immediately after TAVI there was an increase in arterial stiffness (7.5 ± 1.5 m/s vs 8.4 ± 1.7 m/s, p =.001 for cfPWV and 1773 ± 459 vs 2383 ± 645 cm/s, p <.001 for baPWV) that was retained at 1 year (7.5 ± 1.5 m/s vs 8.7 ± 1.7 m/s, p <.001 and 1773 ± 459 cm/s vs 2286 ± 575, p <.001). Post-TAVI we also observed a decrease in AIx@75 (32.2 ± 12.9% vs 27.9 ± 8.4%, p =.016) that was attenuated 1 year later (32.2 ± 12.9% vs 29.8 ± 9.1%, p =.38), and an increase in SEVR (131.2 ± 30.0% vs 148.4 ± 36.1%, p =.002), which remained improved at 1 year (131.2 ± 30.0% vs 146.0 ± 32.2%, p =.01). After TAVI the arterial system exhibits an increase of stiffness in response to the acute relief of the obstruction, which is retained in the long term. • After transcatheter aortic valve implantation (TAVI) the arterial system exhibits a loss of compliance in response to the acute relief of the obstruction that aortic valve stenosis (AVS) poses, which is established in the long term. • Both the stable and the pulsatile component of the arterial system were studied, in a large sample with the longest follow-up so far. • Vascular biomarkers could assist in the risk-stratification as well as in the follow-up of these patients and even serve as therapeutic targets. [ABSTRACT FROM AUTHOR]

Cardiotoxicity restricts anthracycline and trastuzumab treatment of Human Epidermal Growth Factor Receptor 2 positive early breast cancer. Endothelial dysfunction and arteriosclerosis are significant cardiovascular risk factors. We studied the effect of anthracycline-based chemotherapy, with or without trastuzumab, on endothelium and arteriosclerosis in patients with breast cancer. In this case-control study, 52 women with breast cancer and 104 women without breast cancer were examined longitudinally up to 15 months following (in the breast cancer group) initiation of chemotherapy. Arterial stiffness was evaluated through pulse wave velocity (PWV), while endothelial function via flow-mediated dilatation (FMD) at baseline (T0), 3 (T1), 6 (T2), and 15 (T3) months later. There was no difference between subjects with breast cancer and control in PWV and FMD at baseline. Longitudinally, participants with breast cancer exhibited considerable impairment of PWV and FMD compared to the control group (p for interaction <0.001 for both parameters). In breast cancer patients, there was a significant increase from T0 to T3 in PWV (7.43 ± 1.68 m/s vs. 8.18 ± 2.00 m/s, p = 0.01) and decrease in FMD (6.95 ± 2.86% vs. 5.03 ± 2.83%, p = 0.006). The addition of trastuzumab in the treatment did not have any effect on PWV (p = 0.74) or FMD (p = 0.91). In patients with breast cancer, there is progression of endothelial dysfunction and arteriosclerosis up to 15 months following initiation of anthracycline-based chemotherapy. Trastuzumab has no additive effect on endothelial function or arterial stiffness. [Display omitted] [ABSTRACT FROM AUTHOR]

Introduction: Cardiac performance depends on optimum ventriculoarterial coupling which is impaired in patients with heart failure (HF). Galectin-3 is a mediator of myocardial fibrosis and remodeling and is associated with clinical status in patients with chronic HF. We examined the association of arterial stiffness with galectin-3 levels in patients with HF of ischemic etiology. Methods: We consecutive enrolled 40 subjects with stable ischemic HF and reduced ejection fraction. Central aortic stiffness was evaluated non-invasively by measurement of carotid-femoral pulse wave velocity (PWV). Among other factors, serum levels of galectin-3 and b-type natriuretic peptide (BNP) were measured in blood samples. Results: The median values of galectin-3 in our study population was 12.9 (10.8-18.7) ng/ml and the mean value of PWV in our study population was 9.31±2.79 m/sec. There was significant association of Galectin-3 levels with age (r=0.48, p=0.003) with creatine clearance (r=-0.66, p<0.001) and with BNP levels (r=0.36, p=0.05). Importantly there was a significant association of Galectin-3 levels with pulse wave velocity (r=0.37, p=0.03) and patients with PWV above the median had also significant increase levels of galectin-3 compare to patients with lower values of PWV [16.1(11.8-25.2) ng/ml vs. 12.1(10.5-14) ng/ml, p=0.03] Conclusions: In the present study we found that there is an association of arterial stiffness and PWV with galectin-3 levels in patients with chronic HF of ischemic etiology. These findings imply an additive alternative pathway driving arterial stiffening and myocardial remodeling in HF which give insight into the mechanism determining prognosis and clinical status of patients with HF. [ABSTRACT FROM AUTHOR]

Introduction: Pseudoexfoliative glaucoma (PEX) is a type of glaucoma characterized by the secretion of a grey-white, fibrogranular material in several tissues. Microparticles are shed membrane vesicles released from a variety of cell types in response to cellular activation or apoptosis and correlate with the pathogenesis of cardiovascular diseases. Endothelial MPs may be used as biomarkers of endothelial function. Hypothesis: We evaluated the role of endothelial dysfunction, arterial stiffness and systemic inflammation in patients with PEX compared to patients with Primary open angle glaucoma (POAG) and control subjects as well as the possible pathophysiologic role of a specific microparticle profile associated with endothelial damage. Methods: We enrolled 29 subjects with PEX, 57 subjects with POAG and 44 control subjects. Endothelial function was evaluated by flow-mediated dilation (FMD). Pulse wave velocity (PWV) was measured as an index of aortic stiffness and augmentation index (AIx) as a measure of arterial wave reflections. Growth differentiation factor-15 (GDF-15) and intercellular adhesion molecule1 (ICAM1) were measured to evaluate systemic inflammatory status. Total circulating MPs and EMPs were isolated and analysed by flow cytometry, utilizing specific labels for EMPs (CD 144+) and Annexin V staining for phospatidylserine bearing- MPs (AnnexinV + MPs). Results: There was a linear impairment in FMD (p=0.005), PWV (p=0.007) and Aix (p=0.02) and a stepwise increase in GDF-15 (p=0.001) and sICAM-1 levels (p=0.08) between the three study groups (control, POAG, PEX). Interestingly, the PEX subjects expressed greater levels of total circulating MPs (Annexin V+) [1698 (1199-5894) MPs/μL vs. 1641 (1470-2705) MPs/μL. vs 493 (417-1512) MPs/μL, p=0.004] and EMPs (CD144+)[1412 (645-1760) MPs/μL3vs 1380 (498-2496) MPs/μL vs 34 (184-870) MPs/μL, p<0.001] compared to POAG and control subjects. Conclusion: Pseudoexfoliative glaucoma is associated with impaired endothelial function, arterial wall properties and vascular inflammation with a parallel increase in EMPs. Our findings indicate the significant role of endothelial damage in the progress of glaucomatous disease especially in subjects with pseudoexfoliative glaucoma. [ABSTRACT FROM AUTHOR]