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Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide production. The purpose of this study was to assess the correlation between ADMA and treadmill stress test outcome parameters with known prognostic value, in patients with intermediate risk for coronary artery disease (CAD).Study participants were referred for treadmill exercise stress test (EST) due to symptoms of suspected CAD. Participants with prior history of CAD, cerebrovascular events, peripheral artery disease, systemic inflammatory disease or use of anti-inflammatory agents were excluded. ADMA levels were measured before EST.The study prospectively enrolled 209 individuals (165 males, aged 58.1±10.9). A significant negative correlation was detected between ADMA and maximal exercise time (r=-0.556, p0.001), metabolic equivalents (METs) (r=-0.555, p0.001) and Duke treadmill score (DTS) (r=-0.347, p0.001). Subjects who exercised to ≥10 METs (n=114) had lower ADMA levels than those who achieved7 METs (n=30) (0.58±0.06 vs 0.87±0.08μmol/L, p0.001), and those with DTS5 (n=63) had higher ADMA (0.75±0.19 vs 0.64±0.15μmol/L, p0.001) compared to those with DTS ≥5 (n=146). In multivariable analysis, ADMA remained an independent predictor of DTS (R(2)=0.210; beta=-10.5; 95% confidence interval -14.9 to -6.2; adjusted p0.001) and METs (R(2)=0.500; beta -8.5; 95% confidence interval -9.7 to -6.0; adjusted p0.001) after adjustment for age, BMI, gender, diabetes, smoking status, dyslipidemia, hypertension and family history of premature CAD.ADMA is correlated to EST parameters with proven prognostic value. This implies that ADMA itself might be a useful prognosticator in patients with suspected CAD.

Heart failure (HF) is a complex heterogeneous syndrome with immune, metabolic and neurohumoral mechanisms interacting and leading to gradual heart contractility impairment. From the first study-to correlate inflammation with HF, inflammation biomarkers have been the subject of intense inquiry in patients with various forms of HF. Chronic HF (CHF) is strongly associated with inflammation in terms of pathogenesis, progression, severity and prognosis. Inflammatory mediators participate in CHF pathophysiology in various ways like exerting direct impact on cardiac myocytes, fibroblasts and β-adrenergic receptors leading to hypertrophy, fibrosis and impaired cardiac contractility, respectively, or inducing apoptosis by stimulation of the proper genes. The anti-inflammatory effects of classical heart failure therapeutic strategies such as ACEI and b-blockers are rather conflicting. Whether novel immunomodulating and anti-inflammatory therapeutic approaches should be added to existing therapies in order to ensure additional benefit to HF patients is under investigation. In this review, we summarize the pathophysiological link between inflammatory processes and CHF, focusing on the role of novel and traditional inflammatory biomarkers and highlighting novel anti-inflammatory therapeutic strategies.

Background Fibrinogen is a coagulation/inflammatory biomarker strongly associated with atherogenesis. Data have reported that the genetic variability on fibrinogen chains may affect the atherosclerotic process and the risk of coronary artery disease (CAD). We examined the combined effects of the G455A and the G58A fibrinogen genetic polymorphisms on prothrombotic profile, endothelial function and the risk of CAD in a Caucasian population. Methods We recruited 422 patients with angiographically documented CAD and 277 controls matched for age and gender. The two polymorphisms were genotyped by polymerase chain reaction and restriction endonuclease digestion. Fibrinogen and D-Dimers levels, as well as factors' (f) V, X activity were measured by standard coagulometry techniques. Endothelial function was assessed by the flow mediated dilatation (FMD) of the brachial artery. Results The two polymorphisms had no significant effect on the risk for CAD. Although the 58AA subjects had not significantly different levels of fibrinogen compared with the 58GG + GA in both groups (p = NS), we importantly found that the 455AA homozygosity was associated with increased fibrinogen levels not only in the control group (p = 0.035), but also in the CAD group (p < 0.001) compared to the G allele carriers. Moreover, both the 58AA (p = 0.016) and 455AA homozygotes (p = 0.022) presented with higher levels of D-Dimers in the CAD group. Interestingly, the 455AA homozygotes had increased fV activity in the CAD group (p = 0.048). However, no significant effects were observed on fX activity and FMD. Conclusions Both fibrinogen polymorphisms are capable to modify the atherosclerotic process via their effects on the coagulation cascade. © 2013 Elsevier Ireland Ltd.

Objectives The study objectives were to identify predictors of outcome in patients with inflammatory dilated cardiomyopathy (DCMi). Methods From 2004 to 2008, 55 patients with biopsy-proven DCMi were identified and followed up for 58.2±19.8 months. Predictors of outcome were identified in a multivariable analysis with a Cox proportional hazards analysis. The primary endpoint was a composite of death, heart transplantation and hospitalization for heart failure or ventricular arrhythmias. Results For the primary endpoint, a QTc interval >440msec (HR 2.84; 95% CI 1.03–7.87; p = 0.044), a glomerular filtration rate (GFR) 440msec, a GFR

Introduction: Hypertension (HTN) and diabetes mellitus (DM) are associated with atherosclerosis and affect coagulation and inflammation. Hypothesis: We aimed to investigate the role of fibrinogen genetic variants (rs180070 and rs2070011) on coagulation and inflammation in patients with combined DM and HTN. Methods: 744 subjects (HTN and DM) were enrolled in our study. Fibrinogen polymorphisms were determined by PCR-RFLP technique. Fibrinogen, interleukin-6 (IL-6), high sensitivity C-reactive protein (hsCRP) CD40L, D-dimers and factors V, X activity were measured with appropriate laboratory methods. Results: In HTN patients, hsCRP levels were higher in the group of patients with higher fibrinogen levels compared to patients with lower and intermediate fibrinogen levels [0.28(0.12-0.42) vs 0.17(0.04-0.38) vs 0.18 (0.09-0.39), p=0.032)]. In addition, we found a significant effect of the rs180070 polymophism on IL-6 levels among HTN and DM. In HTN, IL-6 levels were higher in AA homozygotes of the rs180070 compared to all other genotypes (AG or GG) (4.96±0.69 vs 3.7±0.2, p=0.046). Similarly, DM patients homozygotes for the A allele (rs180070) had higher IL-6 levels (6.72±0.99 vs 4.01±0.35, p=0.016). In multivariable analysis, the only independent predictor of IL-6 levels in DM was the AA genotype [β(SE): 0.216 (1.76), P = 0.047]. In hypertensives, AA (rs180070) homozygosity was the only adjusted independent predictor of IL-6 levels [β(SE): 0.151 (0.642), P = 0.032]. Subgroup analysis of HTN and DM patients did not reveal any differences of CD40L levels in the presence of AA genotype (rs180070) (p=0.919 for DM and p=0.144 for HTN). We did not observe any significant change in IL-6 or CD40L levels with the presence of the AA genotype of the rs2070011 among the studied subgroups. Finally, we found that the AA homozygosity (rs180070) was associated with increases D-dimer levels in both DM and HTN (DM: 741.6±109,4 vs 487.3±35.6, p=0.028, HTN 623.3±79.6 vs 388.6±23.5, p=0.048). Conclusions: The AA homozygosity (rs180070) was associated with higher IL-6 levels and CD40L. We demonstrated for the first time, that the AA homozygosity (rs180070) is associated with increased D-dimer levels. These were also associated with higher fibrinogen levels.

Introduction: Smoking is a well known risk factor for coronary artery disease (CAD). Moreover, controversial data suggest that the -174 G/C polymorphism on Interleukin-6 (IL-6) gene promoter (rs1800795) may represent an early marker of inflammatory activation, closely related to the initiation and evolution of atherosclerosis. However, no data exist concerning a combined effect of smoking and this IL-6 genetic variant on several aspects of inflammation and thrombosis, endothelial function and the presence of CAD. Methods: 646 subjects (361 non smokers) were subjected to appropriate genotyping. Endothelial function was assessed by the flow mediated dilatation (FMD) of brachial artery. IL-6 (pg/ml), Tumor Necrosis Factor-a (TNF-a) (pg/ml), high sensitivity CRP (hsCRP) (mg/l) and D-dimers (μg/l) were measured with appropriate methods. Results: An increased incidence of CAD was found among the carriers of the allele C, compared to GG homozygotes, (OR:1.59, CI:1.26-2.93, p=0.032) in smokers, while a decreased incidence was observed in non smokers (OR:0.42, CI:0.26-0.68, p Conclusions: The C allele of rs1800795 exerts a synergistic effect on smoking resulting to a significantly increased risk for CAD. This action is mediated by inflammatory and thrombotic mechanisms as well as by the impairment of endothelial function.

Objective : Endothelial function is an independent predictor of prognosis in heart failure (HF) subjects. Statins, beyond their lipid lowering role, exert beneficial effect in patients with atherosclerosis. In the present study we examined the impact of low and intermediate dose atorvastatin treatment on endothelial function, bone marrow-derived endothelial progenitor cells (EPC) mobilization and inflammatory status according to HF patient status. Methods : We studied the effect of 4 weeks administration of atorvastatin in 26 patients with ischemic HF. The study was carried out on two separate arms, one with atorvastatin 40 mg/d and one with atorvastatin 10 mg/d (randomized, double-blind, cross-over design). The number of circulating CD34(+)/CD133(+)/KDR(+) EPCs was evaluated by flow cytometry. Endothelial function was evaluated by flow mediated dilation (FMD) in the brachial artery. Serum levels of tumor necrosis factor alpha (TNF-α) were measured by ELISA. Results : Treatment with atorvastatin 40 mg/d significantly increased circulating EPC ( p = 0.002), FMD ( p = 0.001) and reduced TNF-α ( p = 0.01) compared to baseline. Similarly, treatment with atorvastatin 10 mg/day increased circulating EPC ( p = 0.01), FMD ( p = 0.08) and reduced TNF-α ( p = 0.01) compared to baseline. Interestingly, with 40 mg/day atorvastatin treatment the increase in EPC was higher in subjects categorized as NYHA class II compared to subjects categorized as NYHA class III ( p = 0.03). Conclusions : Our results confirmed the distinct impact of atorvastatin treatment on the restoration of endothelial function due to EPC mobilization in ischemic HF subjects. Moreover, these findings provide the potential clinical significance of EPC status monitoring to individualize treatment in HF subjects.

The vascular endothelium not only is a single monolayer of cells between the vessel lumen and the intimal wall, but also plays an important role by controlling vascular function and structure mainly via the production of nitric oxide (NO). The so called "cardiovascular risk factors" are associated with endothelial dysfunction, that reduces NO bioavailability, increases oxidative stress, and promotes inflammation contributing therefore to the development of atherosclerosis. The significant role of endothelial dysfunction in the development of atherosclerosis emphasizes the need for efficient therapeutic interventions. During the last years statins, angiotensin-converting enzyme inhibitors, angiotensin-receptor antagonists, antioxidants, beta-blockers and insulin sensitizers have been evaluated for their ability to restore endothelial function (Briasoulis et al., 2012). As there is not a straightforward relationship between therapeutic interventions and improvement of endothelial function but rather a complicated interrelationship between multiple cellular and sub-cellular targets, research has been focused on the understanding of the underlying mechanisms. Moreover, the development of novel diagnostic invasive and non-invasive methods has allowed the early detection of endothelial dysfunction expanding the role of therapeutic interventions and our knowledge. In the current review we present the available data concerning the contribution of endothelial dysfunction to atherogenesis and review the methods that assess endothelial function with a view to understand the multiple targets of therapeutic interventions. Finally we focus on the classic and novel therapeutic approaches aiming to improve endothelial dysfunction and the underlying mechanisms.

Recent data consider inflammatory biomarkers and waist hip ratio (WHR) index prognostic agents of advanced atherosclerosis. C- reactive protein (CRP) contributes to the pathogenesis of type 2 diabetes mellitus (T2DM). However, the impact of common polymorphisms of inflammatory genes on the

Background: Adiponectin is an adipokine with an important role in cardiovascular system conferring anti-inflammatory and anti-atherogenic effects. Two common single nucleotide polymorphisms (SNP) on adiponectin gene, rs2241766 and rs1501299, have been associated with insulin resistance and diabetes mellitus risk however their effects on cardiovascular risk remain unclear. We examined the impact of rs2241766 and rs1501299 on circulating adiponectin levels, endothelial function and cardiovascular disease risk. Methods: We recruited in total 594 subjects; 462 patients with angiographically confirmed coronary artery disease (CAD) and 132 controls matched for age and gender. rs2241766 and rs1501299 were genotyped by polymerase chain reaction and restriction endonuclease digestion. Serum adiponectin levels were determined by enzyme-linked immunosorbent assay. Endothelial function was assessed by the flow mediated dilatation (FMD) of the brachial artery. Results: rs2241766 had no effects on circulating adiponectin levels or FMD. In subjects without CAD, carriers of the T/T alleles at rs1501299 had lower adiponectin levels (p = 0.001) and impaired endothelial function (p < 0.05). After multivariate adjustment none of the SNPs had any effect on CAD risk. However, carriers of the T allele at rs1501299 were at increased myocardial infarction (MI) risk, independently of classic risk factors (OR = 2.558 [95%CI = 1.587-4.123], p = 0.0001). The number of T alleles in both SNPs was strongly associated with MI history (p = 0.0001). Conclusions: rs1501299 polymorphism of adiponectin gene affects circulating adiponectin levels and endothelial function in subjects without CAD. Presence of the T variant at rs1501299 on adiponectin gene is independently associated with increased myocardial infarction risk. © 2012 Elsevier Ireland Ltd. All rights reserved.

The role of diabetes mellitus (DM) in cardiovascular disease is well established and currently is considered as an equivalent of coronary artery disease. Studies have also reported that DM is associated with the prevalence of occlusive carotid artery disease (AD) [1] as well as the grade carotid artery stenosis [2]. In addition, DM is related to impaired renal function via several mechanisms [3]. During the last years novel data have arisen for the role of genetics in the initiation and progression of carotid AD [4–8] as well as for impaired renal function [9,10]. However, scarce data exist regarding genetic polymorphisms in patients with diabetes mellitus and their role in carotid artery disease and renal function. Thus, in the present study we examined the potential role of a single nucleotide polymorphism (SNP) on C-reactive protein (CRP) gene in the onset of carotid AD and impaired renal function in patients with diabetes mellitus type 2. Our study population consisted of 430 patients with DM2 (documented for carotid AD or not). Subjects were characterized as patients with DM2 if fasting plasma glucose levels were ≥126 mg/dl, or 2-hour post glucose loading plasma levels were ≥200 mg/d according to the American Diabetes Association [11]. Carotid artery disease was evaluated based on history of transient ischemic attack or stroke, important degree of carotid stenosis in Doppler ultrasonography or blowing existence or interventional procedure of carotid revascularization. Subjects were considered to have systemic hypertension if their systolic and/or diastolic blood pressure was ≥140 and/or ≥90 mmHg on two different occasions. Moreover subjects were considered to have systemic hypertension if they were currently being treated with anti-hypertensive drugs or when a significant history of hypertension was present [12]. Subjects were considered to have dyslipidemia if total cholesterol levels ≥200 mg/dl were revealed in biochemical tests or if they were already treated with antihyperlipidemic agents [13]. Current smokers were regarded as subjects smoking 1–10 cigarettes/day for at least the last year [14]. In the exclusion criteriawe included any acute or chronic inflammatory disease, malignancies, and renal or liver failure. Glomerular filtration rate (GFR) was measured by the appropriate formula. The studywas approvedby the institutional ethics committees, and an informed consent was given by all the participants. Venous blood samples were centrifuged at 3500 rpm at 4 °C for 15 min, and plasma or serum was collected and stored at −80 °C until assayed. Serum concentrations of lipids were determined by using colorimetric enzymatic method in a Technicon automatic analyzer RA

OBJECTIVE: To investigate the effects of atorvastatin on endothelial function and low-grade systemic inflammation in subjects with successful surgery for aortic coarctation repair (SCR). DESIGN: Open-label study. SETTING: Outpatients visiting the adult congenital heart disease department of our hospital. PATIENTS: 34 young people with SCR. INTERVENTIONS: Patients with SCR received atorvastatin 10 mg/day (n=17) or no treatment (n=17) for 4 weeks. At baseline and at 4 weeks, endothelial function was assessed by flow-mediated dilatation (FMD) of the right brachial artery, and blood samples were obtained. Serum levels of interleukin (IL) 1b, IL-6 and soluble vascular cell adhesion molecule-1 (sVCAM-1) were determined by ELISA. MAIN OUTCOME MEASURES: Effects of treatment on FMD and serum levels of IL-1b, IL-6 and sVCAM-1. RESULTS: FMD in the atorvastatin group was significantly improved after 4 weeks (from 6.46±0.95% to 11.24±1.38%, p

BACKGROUND: Nitric oxide synthase (NOS) inhibitor asymmetrical dimethylarginine (ADMA) is synthesized by the methylation of arginine as part of the methionine/homocysteine cycle. However, the mechanisms regulating ADMA synthesis in hypertension are unclear. METHODS: We investigated the role of ADMA and antioxidants in endothelial dysfunction during methionine-induced homocysteinemia in hypertensives. Thirty-nine hypertensives and forty-nine normotensive controls underwent methionine loading (100 mg methionine/kg BW), after being randomized to receive vitamin C (2 g) and E (800 IU) or placebo. Endothelium-dependent dilation (EDD) was evaluated by plethysmography (baseline and 4-h post-methionine loading (4-h PML)). RESULTS: Hypertensives had higher homocysteine at baseline (P < 0.001) and 4-h PML (P < 0.05), whereas methionine increased homocysteine in all groups. EDD was decreased in both vitamins and placebo groups in controls (P < 0.01 for both) and vitamins- and placebo-treated hypertensives (P < 0.05 and P < 0.01, respectively). In controls, ADMA was increased in both vitamin- and placebo groups (P < 0.01 for both) at 4-h PML. Hypertensives had higher ADMA at baseline (P < 0.01 vs. normotensive) and remained unchanged at 4-h PML (P = NS in placebo and vitamins treated). CONCLUSIONS: ADMA is elevated in hypertensives but remains unchanged after methionine loading, suggesting that ADMA plays an important role in endothelial dysfunction in hypertensives, but it is not responsible for homocysteine-induced endothelial dysfunction in these patients.

It is well established that matrix metalloproteinases (MMPs) contribute to the degradation of the extracellular matrix of coronary plaque and contribute to the thinning of the fibrous cap. As a result, the atheromatous plaque becomes unstable and prone to rupture with consequent clinical manifestations including acute coronary syndromes. Moreover, genetic polymorphisms of MMPs have been found to be associated with the concentration of circulating MMPs, and over the past decade, considerable efforts have been devoted to explore the relationships between MMPs polymorphisms and myocardial infarction risk among various populations. However, existing studies have yielded inconsistent results. Some observations have suggested that genetic variation that affects the expression of MMPs may contribute to the occurrence of myocardial infarction, whereas others reported no support for an association of MMPs polymorphisms with myocardial infarction susceptibility. Furthermore, the interpretation of these studies has been complicated by the use of different populations or different control sources. Therefore, further studies are required to evaluate the role of matrix metalloproteinases and especially the associated genetic polymorphisms in cardiovascular disease.

T cells are involved in the process of endothelial dysfunction contributing to plaque destabilization [1] and several studies have shown that the predominant population of T cells that infiltrates atherosclerotic plaques is CD4+ T cells [2]. An increased number of CD4+ T cells have already been found in the peripheral blood of patients presenting with acute coronary syndromes [3]. Particularly, a subset of CD4+ T cells characterized by a loss of the CD31 molecule seems to have a crucial role in plaque destabilization and thrombotic complications. Furthermore, an increased number of CD4+ T lymphocytes characterized by a defective cell surface expression of CD28 have been detected in patients with unstable angina (UA). CD4+CD28null T cells were found to expand in the peripheral blood of patients with UA and infiltrate unstable coronary plaques, where they undergo clonal expansion, probably due to their activation by specific antigens [4]. Therefore, we aimed to investigate whether CD4+CD31null and CD4+CD28null T cell subpopulations contribute to vascular function in patients with UA. We enrolled 61 patients with UA admitted to our Coronary Care Unit with UA Braunwald's class IIIB and 23 healthy individuals without overt cardiovascular disease who were screened in our outpatients' clinic for cardiovascular prevention. Endothelial function was evaluated by estimating the flow-mediated dilation (FMD) in the brachial artery, while flow cytometry was used to determine both the number of T-cells present as well as the frequencies of the various T-cell subsets of interest. We have found that endothelial function was significantly impaired in patients with UA compared to healthy controls (4.76 ± 0.24 vs 8.4 ±0.52, p b 0.001, Fig. 1A), while further analysis among the genders of the 2 groups did not reveal any significant differences in FMD (p = 0.631 for males and p= 0.767 for females). Similarly, FMD was not age related. More specifically, after dividing patients into two subgroups according to age, using as a cut-off point the age of 60 years, we observed no significant differences (p = 0.453 and p = 0.562 respectively). Importantly, we have shown that T cell population as marked by CD4+ was elevated in UA patients compared to healthy controls (42.07 ± 1.58 vs 35.43 ± 3.1, p = 0.046). Interestingly, a significant difference was detected between the two groups when the T cell subpopulation CD4+CD31null was examined. A significant increase of these circulating cells were found in the UA group (37.33 ± 1.5 vs 28.98 ± 3.1, p = 0.016, Fig. 1B). Similarly, UA patients presented with a significantly elevated frequency of CD4+CD28null T cells (9.49 ± 0.69 vs 6.69 ± 1.19, p = 0.018, Fig. 1C). However, no significant difference between groups was observed in the frequency

Background: Marfan syndrome is characterised by high risk of aortic dissections and increased cardiovascular risk. However, the impact of Marfan syndrome on endothelial function and arterial stiffness is unclear, while the role of matrix metalloproteinases is unknown. We examined the impact of Marfan syndrome on the elastic properties of the arterial tree, and vascular endothelial function, and we evaluated the potential role of matrix metalloproteinases in these effects. Methods: The study population consisted of 17 subjects with Marfan syndrome, aged 26.6±2.3 years old, with BMI 20.5±1.03Kg/m2 and 22 healthy individuals matched for gender, age (26.4±0.78 years old, p=NS) and BMI (22.4±0.86 Kg/m2). Arterial stiffness was evaluated by measuring carotid-femoral pulse wave velocity (PWV), while augmentation pressure and augmentation index (AIx) were also determined, as measures of arterial wave reflections. Endothelial function was evaluated by determining flow mediated dilation (FMD) in the brachial artery while matrix metalloproteinase 9 (MMP-9) levels were determined by ELISA. Results: Patients with Marfan syndrome had significantly lower pulse pressure in the radial artery (41.0±1.07mmHg) compared to controls (51.3±4.4mmHg). In addition, patients had higher AIx (17.6±2.4%) and augmentation pressure (5.44±0.65mmHg) compared to controls (7.72±3.43% and 2.41±1.14mmHg respectively, p Conclusions: Marfan syndrome is associated with increased MMP-9 levels, as well as with elevated augmentation index and augmentation pressure compared to healthy individuals, matched for age, gender and body mass index. Moreover, flow-mediated dilation is also impaired in these subjects. These findings suggest that Marfan syndrome directly affects the elastic properties and endothelial function of the arterial tree, with matrix metalloproteinases being important mediators in the pathophysiology of this syndrome.

It is well established that hypertension (HTN) and diabetes mellitus (DM) are strongly associated with coronary artery disease (CAD). In addition, controversial data exist related to the role of fibrinogen genetic variants in atherosclerosis-CAD. Therefore, we examined the effects of the rs180070

Arterial stiffening is associated with the incidence of stroke however little is known about its relationship with cerebral microvascular damage. Retinal arterioles provide important information on cerebral microvascular function thus we sought to investigate the relationship of retinal alterations

Introduction: Stroke related with catheterization was devastating complications after procedures. The rates of stroke range from 0.1-0.4% according to previous studies. Stroke was taken only as new neurological complications, therefore clinically unapparent cerebral embolisms were not taken into account. Diffusion weighted magnetic resonance imaging (DW-MRI) is very high sensitive tools for detecting acute cerebral ischemic lesions. Due to improvements of catheter design and approach, catheterization-related cerebral infarctions are expected to decrease, whereas this may be counterbalanced by increased risk profile of patients who undergo catheterization. Objectives: We aimed to examine the current prevalence and risk factors of symptomatic and asymptomatic catheterization-related cerebral infarctions by DW-MRI. Methods: We retrospectively analyzed 84 patients who underwent 1237 diagnostic and interventional catheterization procedures through the aortic arch conducted within 2010 and 2011 in our hospital and who obtained the MRI within 14 days a catheterization. Results: Ten patients who developed symptoms and 3 patients were finally diagnosed as stroke, which was defined as any neurological deficits lasting over 24 hours. The remaining 74 patients were asymptomatic and underwent MRI for various other reasons, including the assessment before coronary artery bypass graft (35%), valvular surgery (18%) or aortic repair (6.8%). The MRI revealed a fresh cerebral infarction in 22 of 74 asymptomatic patients (29.7%). Patients with cerebral infarction underwent longer procedures (mean SEM, 17.1 1.7 minutes vs. 22.7 2.4 minutes, p

Patients with stable angina pectoris are characterized by increased levels of thrombotic and inflammatory biomarkers including fibrinogen, interleukin 6 (IL-6) and sCD40L. However, it is unclear, whether fibrinogen genetic variability could modify these processes in those patients. Thus, we