Objective-The purpose of this study was to investigate the relationship of plasma homocysteine (tHcy) levels with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) in high-risk patients undergoing coronary angiography for suspected CAD. Methods and Results-In 936 consecutive patients, we measured LVEF, tHcy, folate levels, and quantified CAD with a modified Duke Index score. We also genotyped patients at the methylen-tetrahydrofolate-reductase 677C3 T polymorphism. Hyperhomocysteinemia (HHcy) was defined as tHcy levels Ն15.46 mol/L; total and cardiovascular mortality was assessed at follow-up that lasted 43 months (median). CAD was confirmed in 75% of patients and ruled out in the rest (non-CAD group). No relationship of HHcy with either arterial hypertension or the CAD score was found. In contrast, there was a significant inverse relationship of tHcy with LVEF in arterial hypertensive but not in normotensive patients, regardless of previous myocardial infarction. At logistic regression, HHcy was the strongest predictor (Pϭ0.001) of a low (Ͻ40%) LVEF, followed by type 2 diabetes mellitus and cigarette smoking. At follow-up, HHcy significantly predicted cardiovascular mortality but only in the arterial hypertension subgroup. Key Words: homocysteine Ⅲ arterial hypertension Ⅲ coronary artery disease Ⅲ survival Ⅲ MTHFR 677C3 T polymorphism Ⅲ left ventricular ejection fraction H yperhomocysteinemia (HHcy) might play a causative role in the development of coronary artery disease (CAD) and cardiovascular (CV) disease 1 and originates from an interplay of environmental factors, such as folate and B 12 vitamin deficiency, and genetic factors, including the thermolabile variant (677C3 T) of methylen-tetrahydrofolatereductase (MTHFR) gene. 2,3 On the basis of plasma homocysteine (tHcy) concentrations, HHcy has been classified as mild/moderate (15 to 30 mol/L), intermediate (30 to 100 mol/L), and severe (Ͼ100 mol/L). 4 Mild/moderate HHcy is common (5% to 7%) in the population and might increase the risk of CV disease, 3,5,6 but its association with such phenotype is weaker than that of severe HHcy. Prospective studies in high-risk subjects suggested that HHcy can be a risk factor for overall mortality, 7 recurrent CV events, and hospitalization, 8 but studies of healthy subjects did not confirm this contention. 8 -10 Thus, it would appear that mild/ moderate HHcy plays a minor role for CV disease and might attain a greater importance only in high-risk patients. Conclusions-InTheoretically, HHcy could increase blood pressure by decreasing the endothelial production of NO, inducing accumulation of the endogenous NO synthase inhibitor asymmetrical dimethylarginine, 11 or lowering NO bioactivity through induction of oxidative stress. 12,13 Nonetheless, only a weak association between HHcy and arterial hypertension was found, 14 -18 and there are no data in high-risk patients.HHcy can exert nefarious effects on the heart by inducing coronary arteriolar remodeling, left ventricular (LV) hypertrophy,...

In high-risk CAD patients, plasma adiponectin above the median (6.38 microg/ml) implies a paradoxical higher risk of CV death. However, when relevant covariates that differ between high- and low-plasma adiponectin groups are considered, this association wanes, indicating that the clustering of plasma adiponectin with other covariates can abolish its impact on CV prognosis.

Abstract.Adiponectin is an adipocyte-derived circulating peptide that plays an important role in adipose tissue metabolism, insulin sensitivity and cardiovascular disease. The adrenal gland, by secreting glucorticoid and mineralocorticoid hormones, intervenes in cardiovascular and glucose metabolism regulation and is surrounded by adipose tissue. Hence, we investigated the hypothesis that adiponectin receptor types 1 and 2 (adipo-R1 and adipo-R2) are expressed in the human adrenal gland and in adrenocortical zona glomerulosa cell-derived aldosterone-producing adenoma (APA) tissue. We used real-time reverse transcription-polymerase chain reaction to demonstrate the mRNA of adipo-R1 and adipo-R2 in 10 histologically normal human adrenal cortexes that were obtained from patients with renal cancer undergoing nephrectomy with ipsilateral adrenalectomy and in 10 APAs. Melting curve analysis and sequencing were used to confirm the specificity of the amplicons obtained. Results consistently showed the expression of specific mRNAs of adiponectin receptors in all histologically normal human adrenal cortexes and APAs. This novel finding suggests that adiponectin could play a regulatory role in adrenocortical function and growth in humans.

The GTE prevented hypertension and target organ damage induced by a high Ang II dose, likely by prevention or scavenging of superoxide anion generation.

The T(-786)C SNP in the promoter of eNOS bears independent prognostic information and is associated with changes in markers of oxidant stress in high-risk white patients referred for coronary angiography.