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Background: Although flow-mediated vasodilation (FMD) of brachial artery and carotid intima-media thickness (IMT) are important surrogate markers in the process of atherosclerosis, information about relationship between both markers is insufficient. In the present study, we assessed extensively the relationship in patients with coronary artery disease (CAD)., Methods: The values of brachial FMD and carotid ultrasonography findings in 159 patients (67±8 years, 130 males) with angiographically verified CAD were retrospectively analyzed., Results: In all patients, mean carotid IMT tended to be correlated with FMD, although the correlation was not statistically significant (R=-0.149, P=0.061). Maximum IMT was not correlated with the FMD (R=0.053, P=0.508). In addition, carotid artery diameter was significantly correlated with the FMD (R=0.290, P=0.0002). Prevalence of high IMT value (≥1.0 mm) was higher in the abnormal FMD group (4%>; N.=67), compared with the normal FMD group (≥7%; N.=24; P<0.05). Carotid artery diameter was larger in abnormal FMD group, compared with both groups of normal FMD (P<0.01) and borderline FMD (4-7%; N.=68) (P<0.01). In all patients, receiver operating characteristics analysis demonstrated that cut-off value of FMD to predict the prevalence of ischemic stroke was 3.7% (AUC=0.735, P<0.001). The cut-off value of maximum IMT was 1.9 mm, but was not significant (AUC=0.522, P=0.829)., Conclusions: Brachial FMD and carotid IMT would be different in clinical significance as a surrogate marker for pathophysiology of atherosclerotic disease.

Coronary artery disease (CAD) is caused by a thrombotic occlusion or spasm of the coronary artery. Association of genetic variants with susceptibility to CAD has been reported in various populations, but the association should be replicated in other populations to establish the role of genetic variants in CAD. We conducted a case-control study with a total of 1480 CAD cases and 2115 controls from two East Asian populations, Japanese and Korean, to validate the associations of CAD with eight single nucleotide polymorphisms (SNPs) in eight loci, which were identified from large-scale whole-genome association studies in Europeans or East Asians. Among the tested SNPs, one SNP in BRAP (rs11066001) showed a significant association in allele frequency distribution with CAD in both the Japanese (Odds ratio (OR)=1.63, 95% confidence interval (CI); 1.41-1.89, P=5.0 x 10(-11), corrected P (Pc)=4.0 x 10(-10)) and Korean populations (OR=1.68, 95% CI; 1.41-2.00, P=6.5 x 10(-9), Pc=5.2 x 10(-9)), and a meta-analysis showed a significant association in the East Asian populations (OR=1.65, 95% CI; 1.48-1.85, P=1.8 x 10(-18), Pc=1.4 x 10(-17)), whereas no evidence of association was found for the other SNPs. In addition, a combined analysis of BRAP and another CAD locus on 9p21 suggested that these loci had a synergistic role in the susceptibility. Failure to replicate the association with the other SNPs, which were reported in the European populations, suggested that their contributions to CAD were not large enough to be readily captured in the East Asian populations.

Coronary artery disease (CAD) is based on the atherosclerosis of coronary artery and may manifest with myocardial infarction or angina pectoris. Although it is widely accepted that genetic factors are linked to CAD and several disease-related genes have been reported, only a few could be replicated suggesting that there might be some other CAD-related genes. To identify novel susceptibility loci for CAD, we used microsatellite markers in the screening and found six different candidate CAD loci. Subsequent single nucleotide polymorphism (SNP) association studies revealed an association between CAD and megakaryoblastic leukemia factor-1 gene (MKL1). The association with a promoter SNP of MKL1, -184C > T, was found in a Japanese population and the association was replicated in another Japanese population and a Korean population. Functional analysis of the MKL1 promoter SNP suggested that the higher MKL1 expression was associated with CAD. These findings suggest that MKL1 is involved in the pathogenesis of CAD.

Coronary artery disease (CAD) and stroke are the major health problems in many countries because of their increasing prevalence and high mortality. It is well known that CAD and stroke are based on atherosclerosis and shared environmental and genetic risk factors. Recently, an association of a functional sequence variation -154G>A in the angiotensin receptor-like 1 (AGTRL1) with a susceptibility to stroke was reported. In this study, we investigated a total of 1479 CAD cases and 2062 controls from the Japanese and Korean populations to validate the association of AGTRL1 with CAD. However, we obtained no evidence of the association in both the Japanese (odds ratio (OR)=0.95, 95% confidence interval (CI); 0.82-1.10, P=0.47, allele count model) and Korean (OR=0.90, 95% CI; 0.77-1.05, P=0.18, allele count model) populations. In addition, there was no trend of association between the risk allele and severity of coronary atherosclerosis. These data suggested that AGTRL1 did not contribute much to the atherosclerosis of the coronary artery.

Coronary artery disease (CAD) has become a major health problem in many countries because of its increasing prevalence and high mortality. Recently, an association of a functional sequence variation, -8C>G, in the human proteasome subunit alpha type 6 gene (PSMA6) with the susceptibility to CAD was reported. To validate the association, we investigated a total of 1330 cases and 2554 controls from Japanese and Korean populations for PSMA6 genotypes, and no evidence of the association was obtained in both Japanese (odds ratio (OR)=1.03, 95% confidence interval (CI); 0.90-1.19, P=0.66, allele count model) and Korean populations (OR=1.00, 95% CI; 0.86-1.17, P=0.95, allele count model). However, when a meta-analysis of data from this study and previously reported six replication studies was done, OR was 1.08 for the G allele (95% CI; 1.02-1.14, P=0.0057), suggesting that the contribution of PSMA6 to CAD was not large enough to be readily replicated. Further studies are required to establish the contribution of this variant in the susceptibility to CAD.

Coronary artery disease (CAD) has become a major health problem in many countries. Recent genome-wide association studies have identified the association between rs1333049 on chromosome 9p21 and susceptibility to CAD in Caucasoid populations. In this study, we evaluated the associations of rs1333049 with CAD in Japanese (604 patients and 1,151 controls) and Koreans (679 patients and 706 controls). We found a significant association in both Japanese [odds ratio (OR)=1.30, 95% confidence interval (CI); 1.13-1.49, p=0.00027, allele count model] and Koreans (OR=1.19, 95% CI; 1.02-1.38, p=0.025, allele count model). These observations demonstrated that chromosome 9p21 was the susceptibility locus for CAD also in East Asians.

Low-intensity resistance exercise can effectively induce muscle hypertrophy and increases in strength when combined with moderate blood flow restriction ( BFR). As this type of exercise does not require lifting heavy weights, it might be a feasible method of cardiac rehabilitation, in which resistance exercise has been recommended to be included. Although previous studies with healthy subjects showed relative safety of BFR exercise, we cannot exclude the possibility of unfavourable effects in patients with cardiovascular disease. We therefore aimed to investigate haemostatic and inflammatory responses to BFR exercise in patients with ischaemic heart disease ( IHD). Nine stable patients with IHD who were not taking anticoagulant drugs performed four sets of knee extension exercise at an intensity of 20% one-repetition maximum (1 RM) either with or without BFR. Blood samples were taken before, immediately after and 1 h after the exercise session and analysed for noradrenaline, D-dimer, fibrinogen/fibrin degradation products ( FDP) and high-sensitive C-reactive protein (hs CRP). Plasma noradrenaline concentration increased after the exercise, and the increase was significantly larger after the exercise with BFR than without BFR. On the other hand, increases in concentrations of plasma D-dimer and serum hs CRP were independent of the condition. However, increases in D-dimer and hs CRP were no longer observed after plasma volume correction, suggesting that hemoconcentration was responsible for these increases. Plasma FDP concentration did not change after the exercise. These results suggest that applying BFR during low-intensity resistance exercise does not affect exercise-induced haemostatic and inflammatory responses in stable IHD patients. [ABSTRACT FROM AUTHOR]