Search

Endothelial dysfunction is regarded as the initial lesion in the development of atherosclerosis. Endocan, previously called endothelial cell-specific molecule 1 (ESM-1), is a new candidate immunoinflammatory marker that may be associated with cardiometabolic risk factors. Therefore, we assessed serum levels of endocan in newly diagnosed patients with untreated essential hypertension (HT). A total of 18 patients with HT and 23 normotensive control participants were included in the study. Serum endocan levels, carotid intima-media thickness (cIMT), and high-sensitivity C-reactive protein (hsCRP) were measured. Serum endocan levels were significantly higher in the HT group (P < .001). In patients with HT, serum endocan levels correlated positively with cIMT and hsCRP (r = .551, P < .001 and r = .644, P < .001, respectively). Our findings suggest that circulating endocan levels represent a new marker in patients with essential HT. Endocan may be a surrogate endothelial dysfunction marker and may have a functional role in endothelium-dependent pathological disorders., (© The Author(s) 2013.)

Antihypertensive agents may, even within the same class, exert variable effects on arterial stiffness variables. Nebivolol could have a better impact than atenolol on arterial stiffness, by increasing the bioavailability of endothelium-derived nitric oxide. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) increase plasma renin activity (enhancing the production of angiotensin II via non-ACE-related pathways) whereas aliskiren does not, potentially affecting central hemodynamics differently. We compared the effects of two renin-angiotensin-aldosterone system (RAAS) inhibitors (quinapril and aliskiren) and 2 beta-blockers (atenolol and nebivolol) on arterial stiffness variables. Treatment-naïve patients (n = 72; 68.1% males; age, 47.6 ± 10.6 years) with uncomplicated stage I-II essential hypertension were randomly assigned to quinapril, aliskiren, atenolol, or nebivolol for 10 weeks. Central systolic and diastolic blood pressure (BP), central pulse pressure (PP), augmentation index (AIx), and pulse wave velocity (PWV) were measured at baseline, 2, and 10 weeks. The same measurements were performed in 20 normotensive subjects (65.0% males; age, 40.0 ± 8.9 years). Peripheral and central systolic and diastolic BP, peripheral PP, and PWV were significantly and similarly reduced by all agents. However, PWV continued to decline between the second and last visit in patients on quinapril and aliskiren but did not change in those on nebivolol or atenolol. Central PP and AIx decreased in patients on quinapril, aliskiren, and nebivolol but did not change in those taking atenolol. The decrease in central PP and AIx did not differ between patients on quinapril, aliskiren, and nebivolol. Despite similar reductions in peripheral BP, atenolol is less effective than nebivolol and RAAS inhibitors in improving central pulsatile hemodynamics. Aliskiren exerts similar effects on markers of arterial stiffness as quinapril. The clinical relevance of these differences remains to be established., (Copyright © 2014 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.)

Objective: The aim of this meta-analysis was to investigate whether statin therapy is associated with blood pressure (BP)-lowering in patients with or without hypertension., Background: The beneficial effects of statins on the cardiovascular system may in part be related to effects beyond lipid-lowering. It has been suggested that statins may reduce BP; however the available data are still ambiguous and often conflicting., Methods: Data from Scopus, PubMed, Web of Science, and the Cochrane Central Register of Controlled Trials for the years 1966-January 2012 were searched for studies that investigated the effect of statins on BP in normotensive or in hypertensive subjects. We included all randomized controlled clinical trials that investigated this effect. Changes in systolic and diastolic BP were the key outcomes of interest., Results: The final analysis included 18 trials and 5628 subjects (4692 normotensive and 936 hypertensive patients) randomized to receive either statins or placebo. The weighted mean difference of systolic (∆SBP) and diastolic blood pressure (∆DBP) in normotensive patients for the 11 statin trials included were 0.03 (95% CI: -0.95-1.02; p = 0.95) and -0.28 (95% CI: -0.80-0.24; p = 0.29), respectively. For hypertensive patients treated with statins (8 trials) the weighted mean difference of ∆SBP and ∆DBP were 1.45 (95% CI: -0.49-3.39; p = 0.14) and -1.32 (95% CI: -3.93-1.28; p = 0.32) respectively., Conclusions: Despite previous suggestions statin therapy in normotensive or hypertensive patients does not lead to significant reductions in systolic or diastolic BP., (Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.)

Even though hydrochlorothiazide (HCTZ) and chlorthalidone are frequently considered interchangeable antihypertensive agents, they appear to differ both in their blood pressure lowering efficacy and in their effects on the lipid profile and on serum potassium, uric acid and glucose levels. More importantly, in randomized controlled trials, chlorthalidone was equally or more effective than other antihypertensive agents in cardiovascular risk reduction whereas treatment with HCTZ yielded conflicting results. Although there are no randomized trials comparing the effects of these two agents on cardiovascular events, retrospective data from the Multiple Risk Factor Intervention Trial suggest that chlorthalidone might reduce cardiovascular morbidity more than HCTZ. However, current guidelines do not consistently recommend one or the other and it remains to be established which one is the diuretic of choice.

Biomarkers should have high sensitivity, specificity, reproducibility, be cost-effective, and provide incremental predictive or diagnostic utility over standard risk factors or tests. Despite numerous studies investigating biomarkers in heart failure (HF), there are only a few that predict HF in hypertensive patients. This article summarizes data from numerous studies concerning possible biomarkers of HF in hypertensive patients such as: serum uric acid (SUA), interleukins, monocyte chemoattractant protein one (MCP-1), cardiotrophin-1 (CT-1), carboxy-terminal propeptide of procollagen type I (PICP), type I collagen telopeptide (CITP) and N-terminal propeptide of type III procollagen (PIIINP), metalloproteinases (MMPs), B-type natriuretic peptide (BNP) and its derivatives, glycoprotein CA125 and cystatin C. Early detection of patients of increased risk of hypertensive heart disease may result in early implementation of effective preventive strategies. Therefore, there is need to identify newer biomarkers, if they can improve risk prediction, identifying patients, in which earlier or more aggressive intervention will improve clinical outcomes.

Arterial stiffness is an independent predictor of cardiovascular (CV) morbidity and mortality in patients with hypertension, as well as a potential therapeutic target. There is increasing awareness that the pulsatile hemodynamics (central blood pressure [CBP], pulse pressure [PP], wave reflections [augmentation index or AIx] and pulse wave velocity [PWV]) may provide better insight into the pathophysiology of CV disorders and target organ damage related to hypertension. Different antihypertensive drugs produce diverse effects on arterial stiffness variables, despite similar effects on peripheral (brachial) blood pressure. Identifying the pharmacologic interventions that can improve arterial stiffness ('de-stiffening' treatment) is a promising field of research.

Most patients on dialysis are hypertensive and their blood pressure (BP) control is often poor. Renalase is preferentially expressed in proximal tubules, but it is also present in glomeruli and distant tubules, as well as in cardiomyocytes, liver, and skeletal muscle. It had been proposed that renalase had a flavin adenine dinucleotide (FAD)-binding domain and that FAD was an essential cofactor for its stability and monoamine oxidase activity. It was reported that renalase, secreted by the kidney and circulating in the blood, degraded catecholamines and might play a role in the regulation of sympathetic tone and BP. It has been also proposed that renalase-coding gene is a novel susceptibility gene for essential hypertension and its variations may influence BP. In addition, polymorphisms of the renalase gene in hemodialysed patients were associated with hypertension. However, several unresolved and controversial issues still remain such as how to measure renalase and its physiological activity. Furthermore, there are few data on possible activators and/or inhibitors of renalase. We are at the very beginning of solving the problem of whether renalase is a causative factor of hypertension in kidney disease or just an innocent bystander. Therefore, more research is needed to establish whether renalase can become a useful therapeutic target.

Aims: The metabolic syndrome (MetS) is associated with increased risk of cardiovascular disease (CVD) and diabetes mellitus (DM). Several definitions of MetS have been proposed. The aim of the present study was to estimate and compare the prevalence of MetS according to the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III), American Heart Association-National Heart Lung and Blood Institute (AHA-NHLBI), International Diabetes Federation (IDF) and the more recent Joint Interim Statement (JIS) definitions in patients attending a hypertension clinic., Methods: The records of patients referred to the hypertension clinic at the University Hospital (Heraklion, Crete) from January 2001 to June 2009 were screened retrospectively. A total 384 patients (146 men) were included in the study., Results: The prevalence of MetS according to the IDF and JIS definitions was significantly higher compared with that of the NCEP ATP III in both genders (IDF: P = .009 and P = .002, JIS: P = .002 and P = 0.001 for men and women, respectively); this was the case for the AHA-NHLBI definition only among women (P = .03). All MetS components differed significantly (P from < .0001 to .02) between patients with and without MetS for all definitions., Conclusions: The prevalence of MetS varies considerably depending on the definition used in a hypertensive population in a Mediterranean country. These differences will influence risk assessment.

Objectives: To investigate the inter-relationships of osteoprotegerin (OPG) with albumin to creatinine ratio (ACR) and asymmetric dimethylargine (ADMA) in hypertensive patients., Methods: In 198 untreated non-diabetic hypertensive patients [130 males, mean age=51.5 years, office blood pressure (BP)=152/98 mmHg] ACR values and OPG and ADMA levels were determined., Results: Based on the median value of OPG distribution (5.03 pmol/l) patients with high (n=101) compared with those with low OPG values (n=97) had greater 24-h systolic BP (152±5 versus 137±7 mmHg, p<0.0001), ACR [25.3 (5-190) versus 17.3 (5-92) mg/g, p=0.003) and ADMA [0.62 (0.58-0.68) versus 0.57 (0.48-0.62) μmol/l, p=0.001), independently of confounding factors. Multiple regression analyses revealed that ADMA (b=0.388, p<0.0001), 24-h systolic BP (b=0.228, p=0.01) and ACR (b=0.470, p<0.0001) were independent predictors of OPG (R2=0.398, p<0.0001)., Conclusions: In hypertensive patients, high OPG levels are accompanied by pronounced albuminuria and endothelial dysfunction, as reflected by raised ADMA levels. Furthermore, the independent associations of OPG with ACR and ADMA, suggests a link between OPG and the progression of diffuse hypertensive vascular damage.

Introduction: An enlarged left atrium is associated with increased risk for stroke. However, there are controversies regarding how left atrial size should be measured., Material and Methods: Echocardiography and carotid artery ultrasound were performed in 120 patients with essential hypertension (HT group) and in 64 hypertensive patients admitted with a first-ever ischemic stroke (HT-stroke group). Left atrial size was measured as antero-posterior diameter (LAD) and as left atrial volume (LAV) and indexed to body surface area (LADi/LAVi). All patients were in sinus rhythm and without mitral valve disease., Results: In the HT-stroke group, LAVi and LADi were significantly larger as compared with the HT group (P ≤ 0.03 for all). In bivariate correlations, larger left atrial size was associated with higher SBPs and DBPs and significant carotid artery stenosis both in HT and HT-stroke groups (all P < 0.05). In multivariate logistic regression analysis, stroke was associated significantly with larger LAVi [odds ratio (OR) 1.73, 95% confidence interval (CI) 1.06-2.65]; left ventricular mass index (OR 1.11, 95% CI 1.03-1.21); significant carotid artery stenosis (OR 1.09, 95% CI 1.03-1.24); and any carotid artery stenosis (OR 1.07, 95% CI 1.03-1.14). Analysis of receiver operating characteristic curves revealed that LAVi was the best left atrial measurement for prediction of stroke (OR 0.77, 95% CI 0.70-0.84)., Conclusion: In hypertensive patients, a first-ever ischemic stroke was associated with larger left atrial size, left ventricular mass index and internal carotid artery stenosis. LAVi was the left atrial measurement most closely associated with ischemic stroke.

Introduction: The blood pressure (BP) J-curve debate has lasted for over 30 years and we still cannot definitively answer all the questions. However, recent studies suggest that BP should be reduced carefully in patients with hypertension and coronary artery disease. BP should not fall below 110 - 115/70 - 75 mmHg, because this may be associated with more cardiovascular events., Areas Covered: A retrospective analysis of the INVEST Trial and the results of the BP arm of the ACCORD Trial shows that care is needed in patients with hypertension and diabetes. Although the ACCORD BP Trial suggests important benefits connected with the significant reduction of stroke in patients being treated intensively, it also shows the lack of advantage of such therapy on each main and other additional endpoints. The ACCORD Trial also confirmed the increased risk of adverse events that might appear when intensive treatment was used in this group of patients., Expert Opinion: Most available studies were observational and randomized trials (BBB, HOT, ACCORD BP), do not have or have lost their statistical power and were inconclusive. Further studies are therefore needed to provide definitive conclusions on the subject. In the meantime, it seems that in high-risk patients with hypertension, it is necessary to carefully select those who might suffer adverse events and those who may benefit from intensive BP lowering.

Antihypertensive agents exert different effects on insulin sensitivity, lipids and haemostasis. However, most studies assessing these effects were small and short-term yielding conflicting results. Moreover, it has not been established whether the impact of antihypertensive drugs on insulin sensitivity, lipids, thrombosis and fibrinolysis adds to or attenuates vascular risk reduction. On the other hand, new onset type 2 diabetes mellitus (T2DM) appears to be more frequent in patients treated with β-blockers and diuretics, whereas angiotensin converting enzyme inhibitors and angiotensin receptor blockers might reduce the risk for T2DM and calcium channel blockers have a neutral effect. Therefore, the risk of developing T2DM should be considered when selecting an antihypertensive agent. This review discusses the differential effects of antihypertensive drugs on insulin sensitivity, lipids and haemostasis and considers their association with vascular risk.

Hypertension is a major contributor to vascular morbidity and mortality. Endocrine hypertension (EH) refers to secondary hypertension caused by specific endocrine abnormalities. The significance of EH is that the identification of the underlying disorder and its management may lead to partial or complete normalization of blood pressure. When EH is suspected thorough investigation with biochemical and imaging testing are necessary to establish or exclude mineralocorticoid, catecholamine, glucocorticoid, thyroid, parathyroid or growth hormone disorders as well as rare hereditary syndromes. In addition, it is important to differentiate benign from malignant tumors. The present review provides an update on the pathophysiology and clinical presentation of EH. We also discuss the diagnostic work-ups and therapeutic strategies.

Background: Statins are the first-line drug therapy in the treatment of hypercholesterolemia. The beneficial clinical impact of statins on the cardiovascular system results not only from their lipid-lowering action but also from other effects. Recently, it has been suggested that statins can reduce blood pressure, especially in hypertensive patients., Aim: The role of the hypotensive action of statins and other mechanisms which reduce cardiovascular risk in hypertensive patients are discussed in this review., Methods: Electronic databases searched were [MEDLINE (1966 - February 2009), EMBASE and SCOPUS (1965 - February 2009), DARE (1966 -- February 2009)]. Additionally, abstracts from national and international cardiovascular meetings were studied to identify unpublished studies. The main data search terms were: blood pressure, hypertension, hypercholesterolemia and statins., Findings: At present, it is difficult to unequivocally assess the impact of statins on blood pressure. However, according to most authors, the impact of statins on the decrease in BP is slight, but significant, especially among patients with hypertension.

Endothelial dysfunction plays an important role in the pathogenesis of hypertension. Other risk factors of atherosclerosis also affect its development. The aim of the study was to assess nitric oxide metabolites concentration (nitrites and nitrates No(x)) and endothelin (ET-1) in plasma and cyclic 3,5-guanosine monophosphate (cGMP) in 24 h-urine collection in patients with noncomplicated hypertension without risk factors of atherosclerosis and in hypertensive patients with coronary artery disease (CAD). Sixty-eight subjects were included in the study (44 men, 24 women), aged 47 +/- 76 years, allotted into four groups: I - controls (18 clinically healthy subjects); II - 12 subjects with hypertension without risk factors of atherosclerosis; III - 16 subjects with hypertension and risk factors of atherosclerosis; and IV - 22 subjects with hypertension and CAD. Plasma NO(x) concentration was determined using the Greiss method, plasma ET-1 by ELISA, and urine cGMP using the immunoenzymatic method. Plasma NO(x) concentration was 14.00 +/- 6.88 micromol/L in group I, in group II - 18.62 +/- 5.84 micromol, in group III - 9.96 +/- 4.72 micromol/L, and in group IV - 8.78 +/- 3.72 micromol/L. Statistically significant differences were between groups I and III (p < 0.05) and I and IV (p < 0.04) and groups II and III (p < 0.01) and II and IV (p < 0.01). The concentration of cGMP in 24 h urine collection was in group I - 40 +/- 24 pmol/L; in group II - 54 +/- 41 pmol/L; in group III - 38 +/- 32 pmol/L; and in group IV - 42 +/- 36 pmol/L. There were no significant differences between the groups. Plasma ET-1 concentration was 3.86 +/- 0.52 pg/mL in group I, in group II - 4.05 +/- 0.71 pg/mL, in group III - 4.22 +/- 0.79 pg/mL and in group IV - 4.38 +/- 0.75 pg/mL. Statistically significant differences were between group I and III (p < 0.05), I and IV (p < 0.03), and between group II and IV (p < 0.04). Endothelial dysfunction was not found in hypertensive patients without a family history of cardiovascular diseases and without other risk factors of atherosclerosis. Deterioration of endothelial function was observed in patients with hypertension with risk factors of atherosclerosis. It was most pronounced in those with CAD.

The aim of our study was to investigate the role of dyslipidemia on red blood cell sodium-lithium countertransport activity in healthy and hypertensive individuals. A total of 128 Caucasian individuals, aged 20 to 60 years old, were divided into 4 groups: dyslipidemic/ hypertensive, dyslipidemic/normotensive, normolipidemic/hypertensive, and normolipidemic/ normotensive (controls). Sodium-lithium countertransport activity was determined based on the Canessa et al method. Sodium-lithium countertransport activity was significantly higher in all patient groups compared with controls (P < .001) and similar in the 3 patient groups. Sodium-lithium countertransport activity was significantly and positively associated with triglyceride levels (P < .001), body mass index (P < .001), total cholesterol levels (P = .001), and systolic (P = .001) and diastolic blood pressure (P = .001). In multivariate regression analysis, triglycerides made the largest contribution to sodium-lithium countertransport variation among the variables tested (R(2) = 0.273). Our results suggest that dyslipidemia affects sodium-lithium countertransport activity independently of essential hypertension and even to a greater extent than hypertension.

The aim of this prospective, randomised, open-label, blinded-end point study was to compare the efficacy and safety of eplerenone versus spironolactone in patients with bilateral idiopathic hyperaldosteronism (IHA). After a 2-week washout period, 34 patients with IHA were assigned to receive either spironolactone 25 mg b.i.d. (n = 17) or eplerenone 25 mg b.i.d. (n = 17) for 24 weeks. If the patients' blood pressure (BP) was not < 140/90 mmHg, the doses were gradually increased up to 400 mg for spironolactone and 200 mg for eplerenone. If the patients' BP remained uncontrolled, a daily dose of hydrochlorothiazide 12.5 mg was added at week 16. The primary outcome was the percentage of patients with BP < 140/90 mmHg at 16 weeks (i.e., with aldosterone antagonist monotherapy). The patients' BP was normalised in 13 out of 17 (76.5%) and 14 out of 17 (82.4%) patients in the spironolactone and eplerenone groups, respectively (p = 1.00). Systolic BP decreased more rapidly with eplerenone. Serum potassium levels were normalised (> 3.5 mmol/l) in all patients at 4 weeks. Mild hyperkalaemia was observed in two patients receiving 400 mg of spironolactone and in three patients receiving 150 mg of eplerenone. Two patients presented with bilateral painful gynaecomastia at the end of week 16 while receiving 400 mg of spironolactone. Switching spironolactone to 150 mg of eplerenone daily resulted in resolution of gynaecomastia and also maintained BP control. At the end of the study, 19 patients were on eplerenone and 15 were on spironolactone. However, this did not affect the primary end point, because the switch from spironolactone to eplerenone (in two patients) occurred at the end of week 16. It was concluded that eplerenone was as effective as spironolactone in reducing BP in patients with IHA. The risk of mild hyperkalaemia was similar with both drugs.

The metabolic syndrome (MetS) is a strong predictor of cardiovascular morbidity and mortality, as well as new Type 2 diabetes. MetS consists of visceral obesity, elevated blood pressure, impaired glucose metabolism, atherogenic dyslipidaemia (elevated triglycerides and low levels of high-density lipoprotein cholesterol), as well as other metabolic abnormalities. The underlying pathophysiology seems to be largely, but not uniquely, attributable to insulin resistance. Existing antihypertensive drugs were designed to lower blood pressure rather than to modify the metabolic abnormalities associated with hypertension. This review considers the role of renin-angiotensin system inhibition and especially the use of angiotensin receptor blockers (ARBs) in the treatment of hypertension in MetS. There are differences among ARBs. Among them is the uricosuric effect of losartan. Furthermore, telmisartan may function as a partial agonist of the peroxisome proliferator-activated receptor-gamma (PPAR-gamma).

The beneficial effect of antihypertensive treatment on the risk of major vascular events is well established. Several trials comparing older and newer drugs in the treatment of primary hypertension suggested that it is the blood pressure achieved, rather than choice of the drug that determines most of the primary outcomes. Beta-blockers have been widely used to treat hypertension and are still recommended as first-line drugs in guidelines. However, recent meta-analyses of trials (either placebo-controlled or using drug comparisons) involving atenolol (a popular beta-blocker), have cast doubt on the suitability of atenolol as a first-line antihypertensive drug. We consider the mechanisms which might be responsible for the inferiority of atenolol in preventing vascular morbidity and mortality in patients with primary hypertension. This knowledge may help design drugs that are not only more effective in achieving blood pressure targets but that also markedly decrease vascular events.

The influence of hypertension, and its treatment, on circulating lipid and fibrinogen (Fib) concentrations in patients with essential hypertension was investigated. The lipid profile and Fib levels were measured in 353 patients (131 men) with essential hypertension. Their median age was 60 years (range: 18-85 years). All patients had normal results from liver, renal, and thyroid function tests. There were 162 patients (45.9%) who were not receiving antihypertensive treatment. Of the remaining patients, 117 were taking 'lipid-hostile' beta-blockers, thiazide diuretics) antihypertensives and 74 were taking 'lipid-neutral' (angiotensin-converting enzyme inhibitors, calcium channel blockers, angiotensin-II receptor blockers) agents. Patients who were taking 'lipid-hostile' antihypertensive drugs had significantly higher plasma Fib concentrations when compared with those taking 'lipid-neutral' antihypertensives or those not receiving antihypertensive treatment. These differences were not attributable to established factors that influence plasma Fib levels, since when smokers and patients with diabetes mellitus and/or vascular disease were excluded, the difference remained significant. In addition, in these more homogeneous groups, patients receiving 'lipid-neutral' treatment had significantly higher serum high-density lipoprotein (HDL) cholesterol levels when compared with both those taking 'lipid-hostile' antihypertensives and untreated ones. There were no significant differences in the other lipid variables, independently of the presence/absence or the type of antihypertensives. These results suggest that antihypertensive drugs have additional effects, beyond lowering blood pressure, on other vascular risk factors, like Fib and HDL. These effects may depend on the type of drug used.

It is well established that hypertension and the more traditional anti-hypertensive drugs are associated with erectile dysfunction (ED). There is evidence showing that two antihypertensive drugs--doxazosin and losartan--have a positive effect on erectile function. Therefore these drugs may decrease the incidence of ED in patients who need treatment for hypertension. Doxazosin and/or losartan can also be beneficial in patients who develop ED after starting treatment with other antihypertensive drugs. These options could, in turn, ensure better compliance and blood pressure control. A fall in the overall cost of treatment will also be anticipated if there is a reduced need for drugs prescribed for ED in patients with hypertension.

Quercetin, the most abundant dietary flavonol, has antioxidant effects in cardiovascular disease, but the evidence regarding its effects on blood pressure (BP) has not been conclusive. We assessed the impact of quercetin on BP through a systematic review and meta-analysis of available randomized controlled trials. We searched PUBMED, Cochrane Library, Scopus, and EMBASE up to January 31, 2015 to identify placebo-controlled randomized controlled trials investigating the effect of quercetin on BP. Meta-analysis was performed using either a fixed-effects or random-effect model according to I(2) statistic. Effect size was expressed as weighted mean difference (WMD) and 95% CI. Overall, the impact of quercetin on BP was reported in 7 trials comprising 9 treatment arms (587 patients). The results of the meta-analysis showed significant reductions both in systolic BP (WMD: -3.04 mm Hg, 95% CI: -5.75, -0.33, P=0.028) and diastolic BP (WMD: -2.63 mm Hg, 95% CI: -3.26, -2.01, P500 mg/day. Further studies are necessary to investigate the clinical relevance of these results and the possibility of quercetin application as an add-on to antihypertensive therapy.

The associations of egg consumption with total, coronary heart disease (CHD), and stroke mortality are poorly understood. We prospectively evaluated the link between total, CHD, and stroke mortality with egg consumption using a randomly selected sample of U.S. adults. Next we validated these results within a meta-analysis and systematic review of all available prospective results. We assessed the mean of cardiometabolic risk factors across the intake of eggs. We made the analysis based on data from the National Health and Nutrition Examination Surveys (NHANES; 1999-2010). In NHANES, vital status through December 31, 2011, was ascertained. Cox proportional hazard regression models were used to relate baseline egg consumption with all-cause and cause-specific mortality. PubMed, Scopus, Web of Science, and Google Scholar databases were also searched (up to December 2017). The DerSimonian-Laird method and generic inverse variance methods were used for quantitative data synthesis. Overall, 23,524 participants from NHANES were included (mean age of 47.7 years; 48.7% were men). Across increasing the intake of eggs, adjusted mean levels of cardiometabolic risk factors worsened. Adjusted logistic regression showed that participants in the highest category of egg intake had a greater risk of diabetes (T2DM; 30%) and hypertension (HTN; 48%). With regard to total and CHD mortality, multivariable Cox regression in a fully adjusted model showed no link in males and females. In males, egg intake had a reverse (66%) association with stroke mortality, while this link was not significant among females. The results of pooling data from published prospective studies also showed no link between CHD and total mortality with egg consumption, whereas we observed a reverse (28%) association between egg intake and stroke mortality. These findings were robust after sensitivity analysis. According to our findings, egg intake had no association with CHD and total mortality, whereas was associated with lower risk of mortality from stroke. Egg consumption was associated with T2DM, HTN, C-reactive protein, and markers of glucose/insulin homeostasis. If confirmed in clinical trials (causation), this information may have applications for population-wide health measures. Key teaching points No link between total and CHD mortality with eggs intake in males and females. In males, egg intake had a reverse association with stroke mortality, while this link was not significant among females. The results of pooling data from published prospective studies also showed no link between CHD and total mortality with egg consumption, whereas we observed a reverse association between egg intake and stroke mortality. [ABSTRACT FROM AUTHOR]

A growing number of studies suggest that diet and renal function are related. However, little is known about the link between both whole grain (WG) and refined grain (RG) consumption and kidney function parameters. Thus, we investigated the association of WG and RG with urinary albumin to creatinine ratio (ACR) and prevalent chronic kidney disease (CKD). Data from participants of the National Health and Nutrition Examination Surveys (NHANES) from 2005 to 2010 were collected. Estimated glomerular filtration rate (eGFR) was calculated by the CKD Epidemiology Collaboration equation. Survey design and sample weights were taken into consideration for statistical analyses. Finally, we included 16 325 participants from NHANES, 6·9 % of whom had prevalent CKD. In models adjusted for age, sex, race, fasting blood glucose, blood pressure, adiposity, hypertension and diabetes status, mean eGFR significantly increased across increasing quartiles of WG (Q1: 88·2 v. Q4: 95·4 ml/min per 1·73 m2, P <0·001), whereas it significantly decreased across increasing quartiles of RG (Q1: 97·2 v. Q4: 88·4 ml/min per 1·73 m2, P <0·001). Furthermore, serum uric acid levels and ACR significantly decreased across quartiles of WG (both P <0·001). In multivariable-adjusted logistic regression models, the likelihood of prevalent CKD was 21 % lower in the highest WG quartile compared with the lowest one. In conclusion, our results shed light on the beneficial impact of WG on kidney function and CKD, whereas RG is adversely associated with eGFR. [ABSTRACT FROM AUTHOR]

Abstract: The metabolic syndrome (MetS) is a cluster of risk factors including insulin resistance, dyslipidemia and hypertension which are also relevant for the development of chronic kidney disease (CKD). It has proven difficult to elucidate whether the renal dysfunction in MetS is due to the MetS itself or the individual risk factors. For example, obesity – which is also part of the MetS – may enhance the risk of renal dysfunction development probably through mechanisms associated with renal hyperfiltration, hyperperfusion and focal glomerulosclerosis. Insulin resistance also promotes kidney disease by worsening renal hemodynamics. In patients with MetS, tubular atrophy, interstitial fibrosis, and arteriolar sclerosis indicating the presence of vascular damage, have also been described. As yet, there has been little evidence that preventing or treating symptoms of the MetS protects patients from renal impairment. [Copyright &y& Elsevier]

It is well recognized that the proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, including atherosclerosis and hypertension. We have previously shown that among extracellular signal-regulated protein kinases (ERKs), the 42- and 44-kDa isoforms (ERK½) participate in the cellular mitogenic machinery triggered by several VSMCs activators, including insulin (INS) and thrombin (Thr). However, understanding of the intracellular signal transduction pathways involved is incomplete. This review considers the recent findings in INS and Thr signaling mechanisms that modulate the proliferation of VSMCs with particular emphasis on the ERK½ signaling pathway, an important mediator of VSMCs hypertrophy and vascular disease. Moreover, because the ERK½ pathway have been acknowledged as an important mediator of VSMCs hypertrophy, ERK ½ is identified as a key target for novel therapeutic interventions to minimize irreversible tissue damage associated with hypertension and atherosclerosis. [ABSTRACT FROM AUTHOR]

Several studies have shown that angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers are useful in the treatment of hypertension, cardiovascular disease, chronic heart failure, and some types of nephropathy. In this context, dual renin-angiotensin system blockade with both angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers may be more effective than treatment with each agent alone. Many clinical trials have demonstrated the beneficial effect of this combined treatment on proteinuria, hypertension, heart failure, and cardiovascular events. Moreover, these studies demonstrated that dual renin-angiotensin system blockade is generally safe and well tolerated. Long-term studies are under way to confirm these effects and also investigate the effectiveness of dual renin-angiotensin system blockade on cerebrovascular disease and prevention of type 2 diabetes mellitus. These studies are expected to define the optimal use of combination treatment in everyday clinical practice. This review considers the most important clinical trials that evaluated the effect of dual renin-angiotensin system blockade on blood pressure, heart failure, and renal function. [ABSTRACT FROM AUTHOR]

There is convincing evidence that the prevalence of erectile dysfunction is increased among men with ischaemic heart disease. This association may be attributed to the fact that both erectile dysfunction and ischaemic heart disease share similar risk factors (e.g. hypertension, dyslipidaemia, diabetes and smoking). Nitric oxide (NO) activity is adversely affected, in penile and vascular tissue, by these risk factors. It is therefore not surprising that a defect in NO activity is thought to play a role in the pathogenesis of both erectile dysfunction and ischaemic heart disease. We consider this evidence and propose that defective NO activity provides a unifying explanation for the association between these two conditions. Further research in this area may improve our understanding of the pathogenesis of cardiovascular diseases as a whole. [ABSTRACT FROM PUBLISHER]

The article presents an overview of the relationship between peripheral artery disease and HIV infection. Medical and health behavior factors which medical personnel must consider when treating peripheral artery disease in HIV-positive patients and HIV-positive patients who also have type two diabetes are examined.

Research has led to effective treatment regimes for erectile dysfunction (ED). Convincing evidence links vascular risk factors (hypertension, diabetes mellitus, hyperlipidaemia and smoking) with ED. This association is not surprising since the corpus cavernosum is a modified vascular tissue. This review presents a brief account of the aetiology, diagnosis and treatment of ED. There is a need to raise awareness of this condition and to make appropriate treatment available to patients. [ABSTRACT FROM PUBLISHER]

No abstract available [ABSTRACT FROM AUTHOR]

• Albumin transports drugs and substances, maintains oncotic pressure and physiological function • Albumin also serves as a strong predictor of cardiovascular (CV) risk in several groups of patients • Hypoalbuminemia increases all-cause and CV mortality in patients with or without comorbidities • Compared with hypoalbuminemia, normalized albumin levels before discharge lowers mortality risk • When albumin is combined with other risk factors (uric acid or CRP), the prognostic value is enhanced Albumin, the most abundant circulating protein in blood, is an essential protein which binds and transports various drugs and substances, maintains the oncotic pressure of blood and influences the physiological function of the circulatory system. Albumin also has anti-inflammatory, antioxidant, and antithrombotic properties. Evidence supports albumin's role as a strong predictor of cardiovascular (CV) risk in several patient groups. Its protective role extends to those with coronary artery disease, heart failure, hypertension, atrial fibrillation, peripheral artery disease or ischemic stroke, as well as those undergoing revascularization procedures or with aortic stenosis undergoing transcatheter aortic valve replacement, and patients with congenital heart disease and/or endocarditis. Hypoalbuminemia is a strong prognosticator of increased all-cause and CV mortality according to several cohort studies and meta-analyses in hospitalized and non-hospitalized patients with or without comorbidities. Normalization of albumin levels before discharge lowers mortality risk, compared with hypoalbuminemia before discharge. Modified forms of albumin, such as ischemia modified albumin, also has prognostic value in patients with coronary or peripheral artery disease. When albumin is combined with other risk factors, such as uric acid or C-reactive protein, the prognostic value is enhanced. Although albumin supplementation may be a plausible approach, its efficacy has not been established and in patients with hypoalbuminemia, priority is focused on diagnosing and managing the underlying condition. The CV effects of hypoalbuminemia and relevant issues are considered in this review. Large cohort studies and meta-analyses are tabulated and the physiologic effects of albumin and the deleterious effects of low albumin are pictorially illustrated. [ABSTRACT FROM AUTHOR]

To estimate the prevalence of cardiovascular (CV) disease and CV risk factors among Polish patients. A nationwide cross-sectional study, LIPIDOGRAM2015, was carried out in Poland in the 4th quarter of 2015 and 1st and 2nd quarters of 2016; 438 primary care physicians enrolled 13,724 adult patients that sought medical care in primary health care practices. Nearly 19% of men and approximately 12% of women had cardiovascular disease (CVD). Over 60% of the recruited patients had hypertension (HTN), >80% had dyslipidaemia and <15% of patients were diagnosed with diabetes (DM). All of these disorders were more frequent in men. In 80% of patients the waist circumference exceed norm for the European population. Less than half of the patients were current smokers or had smoked in the past. Patients with CVD had significantly higher blood pressure and glucose levels but lower low density lipoprotein-cholesterol level. The prevalence of CVD and CV risk factors among patients in Poland is high. CVD is more common in men than in women. The most common CV risk factors are excess waist circumference, dyslipidaemia and HTN. Family physicians should conduct activities to prevent, diagnose early and treat CVD in the primary health care population. Image 1 • LIPIDOGRAM2015 is a nationwide cross-sectional study on the prevalence of CVD and CV risk factors in Poland. • The most common CV risk factors are excess waist circumference, dyslipidaemia and HTN. • Among primary care patients, CVD was present in 19% of men and 12% of women. [ABSTRACT FROM AUTHOR]

Background: We investigated the relationship between complications development and estimated glomerular filtration rate (eGFR), in a cohort of type 2 diabetes mellitus (T2DM) outpatients. Methods: This observational study considered 1284 T2DM outpatients, who had been followed-up for 4.5 ± 1.6 years. eGFR was estimated using Chronic Kidney Disease Epidemiology Collaboration equation. The independent relationship between development of complications and clinical data was evaluated, and hazard ratio (HR) by Cox regression analysis calculated. Results: Mean age of the population was 66.8 ± 10.4 years mean serum creatinine and eGFR were 1.05 ± 0.36 mg/dl and 71.6 ± 21.6 ml/min/1.73 m2, respectively. Complications including death (14.2% of the whole population) were recorded in 504 subjects (39.3%). Patients with complications were older and more frequently male with history of hypertension, coronary heart disease, congestive heart disease, retinopathy, nephropathy and had higher levels of glycated hemoglobin. At Cox regression analysis, eGFR was the major risk factor for development of complications, and the HR increased according with lower eGFR (HR 1.53 and 1.86, for eGFR < 45 and < 30 ml/min/1.73 m2, respectively) Conclusions: In our cohort of T2DM outpatients, a reduced eGFR was associated with an increased risk of complications development. [ABSTRACT FROM AUTHOR]