Journal of Investigative Medicine

The aim of this study was to determine if differences in coronary endothelial function are observed between asymptomatic women with type 2 diabetes mellitus (DM) and control subjects using coronary phase contrast flow velocity magnetic resonance imaging in response to cold pressor stress, an established endothelium-dependent vasodilatory stress.

Phase contrast flow velocity imaging of the right coronary artery was performed in 7 asymptomatic premenopausal women with DM and 8 healthy female participants in response to the cold pressor test at 3 T.

There was no significant difference in percent increase in coronary flow velocity from rest to peak flow velocity between DM and control subjects (32% ± 22% vs 46% ± 17%; P = 0.11). However, percent increase in coronary flow velocity was lower in DM than in control subjects (−3% ± 14% vs 31% ± 30%; P = 0.01) during the second minute of cold pressor stress, when endothelial-mediated vasodilation should occur.

Asymptomatic women with DM demonstrate reduced coronary flow velocity during the second minute of cold pressor stress, indicating coronary endothelial dysfunction.

A single-nucleotide polymorphism in the aldosterone synthase gene (CYP11B2) promoter [−344C/T, rs1799998] has been reported to associate with cardiovascular phenotypes.

The Dallas Heart Study is a large, multiethnic cohort with a high prevalence of hypertension. We genotyped 3452 Dallas Heart Study participants for −344C/T. Generalized linear models were used to assess whether variation at −344C/T associated with plasma aldosterone concentration (PAC), systolic and diastolic blood pressure (SBP and DBP), plasma glucose (in persons with no diabetes), HOMA IR (Homeostasis Model Assessment as an Index of Insulin Resistance), and left ventricular (LV) mass indexed to height. Systolic blood pressure and DBP were significantly higher in blacks compared with whites (P < 0.001 for SBP and for DBP) and Hispanics (P < 0.001 for SBP and for DBP). Log-transformed body mass index was also significantly higher in blacks compared with whites (P < 0.001), but not Hispanics (P = 0.10). Log-transformed PAC was higher in whites compared with blacks (P < 0.001), but did not differ significantly in whites compared with Hispanics (P = 0.73). In univariate and multivariable analysis, −344C/T was not significantly associated with PAC within any ethnicity. In univariate and multivariable analysis, −344C/T was not associated with SBP or DBP within any ethnicity. After adjustment for multiple testing, univariate and multivariable analyses revealed no association between −344C/T and plasma glucose in patients with no diabetes, HOMA IR, or LV mass indexed to height.

We were unable to reproduce previously reported associations between −344C/T and PAC, blood pressure, plasma glucose, or LV mass. Methodological differences might explain the differences between our findings and those previously reported.

Endothelial dysfunction plays an important role in the pathophysiology of coronary artery disease (CAD). Previous studies suggested that human endothelial cell-specific molecule-1 (endocan) may be a novel endothelial dysfunction marker. This study aims to investigate the relationship between serum endocan level and the presence and severity of CAD in patients with hypertension.

A total of 190 eligible hypertension patients were enrolled in this study. Serum endocan level was measured by enzyme-linked immunosorbent assay. The presence and severity of CAD were evaluated by coronary angiography.

Hypertensive patients with CAD had significantly higher serum endocan level than those without CAD (1.63 ± 0.51 ng/mL vs 1.31 ± 0.65 ng/mL, P < 0.05). Multivariate logistic regression revealed that serum endocan level was independently associated with the presence of CAD (odds ratio, 2.662; 95% confidence interval, 1.560–4.544; P < 0.001). Spearman rank correlation analysis demonstrated that serum endocan level was associated with SYNergy between PCI with TAXUS and Cardiac Surgery score (r = 0.349, P = 0.001).

Serum endocan level is independently correlated with the presence and severity of CAD in hypertension patients, and those with high endocan level may have an increased risk of developing atherosclerosis.

Cardiovascular disease (CVD) is the most frequent cause of death in nonalcoholic fatty liver disease (NAFLD). Insulin resistance, hepatic dysfunction, and chronic inflammation are factors interacting in explaining the increased CVD incidence in NAFLD. We aimed to evaluate the effects of insulin resistance and inflammatory biomarkers on asymmetric dimethylarginine (ADMA) levels, a predictor of CVD. We also investigated relationship between these markers and histological findings in patients with NAFLD.

Plasma ADMA, high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and homeostasis model assessment of insulin resistance (HOMA-IR) were measured in 70 patients with histologically verified NAFLD (53 with nonalcoholic steatohepatitis [NASH], 17 with non-NASH) and 12 controls.

The HOMA-IR (5.3 [3.9] vs 1.9 [1], P < 0.001), hs-CRP (5.6 [4.2] vs 2.2 [2.3] mg/L, P < 0.001), ADMA (0.81 [0.25] vs 0.48 [0.24] μmol/L, P = 0.005), and IL-6 (4.1 [1.2] vs 1.0 [0.4] pg/mL, P < 0.001) levels were all found higher in the NAFLD group than the control group. The ADMA levels were significantly higher in patients with NAFLD independent from HOMA-IR and body composition (P = 0.02). The IL-6 and HOMA-IR levels of the NASH group were found significantly higher than those of the non-NASH group. The only determinant significantly correlated to ADMA was HOMA-IR.

Our data suggested that although ADMA levels are independently higher in NAFLD, the only determinant correlated to ADMA is HOMA-IR and not inflammatory biomarkers (hs-CRP, IL-6) or presence/absence of NASH.

Sclerostin inhibits osteoblast functions, differentiations, and survival rates. The aim of this study was to investigate the association between circulating sclerostin (an emerging biomarker and important regulator of bone formation) and neonatal parameters in mothers with vitamin D deficiency.

Forty-five mothers and their newborns were recruited in the study. The mothers were divided into 2 groups as vitamin D–deficient group 25(OH)D (25-hydroxyvitamin D3 < 20 ng/mL) and vitamin D–sufficient group 25(OH)D (>20 ng/mL). Their newborns had measurements of weight, height, calcium, phosphate, alkaline phosphatase, sclerostin, and 25(OH)D at birth.

The mothers with vitamin D deficiency had significantly lower vitamin D levels than the mothers with vitamin D sufficiency (8.7 [3.4] ng/mL vs 26.7 [4.0] ng/mL, P < 0.001). There were no significant differences between women with vitamin D deficiency and women with vitamin D sufficiency for sclerostin concentrations (205.4 [64.8] pg/mL vs 291.6 [122.9] pg/mL). However, 25(OH)D (10.1 [8.1] ng/mL vs 33.4 [11.6] ng/mL, P < 0.001) and sclerostin concentrations (182.9 [15.3] pg/mL vs 288.8 [32.3] pg/mL, P = 0.01) were lower in newborns born by mothers with vitamin D deficiency compared and with newborns of mothers with vitamin D sufficiency. Circulating sclerostin measurements were not associated with 25(OH)D levels of both mothers and their newborns.

We found significantly lower sclerostin levels in newborns born by women with vitamin D deficiency compared with newborns of nondeficient mothers.