Factors associated with early atherosclerosis and arterial calcifications in young subjects with a benign phenotype of obesity.

We assessed (i) the association between early arterial disease and factors linked to adiposity, dietary habits, and family in a young cohort of 151 obese children and adolescents with less than or equal to one cardiovascular (CV) risk factor, (ii) whether in subjects with carotid calcifications there was an imbalance of calcium-phosphorus homeostasis. Measurement included: carotid ultrasound, oral glucose tolerance test, anthropometry, body composition, dietary history, white blood cells count, lipids, uric acid, adiponectin, insulin, C-reactive protein, plasminogen activator inhibitor 1 (PAI-1), 25-hydroxyvitamin D, parathyroid hormone (PTH), calcium and phosphorus. Obese children with carotid artery intima media thickness (cIMT) values >75° percentile (0.55 mm), compared to those with lower cIMT, were more obese, more often pubertal and had higher prevalence of family history of CV disease (CVD) (P < 0.05), higher plasma PAI-1 and uric acid (P < 0.001) and lower adiponectin (P < 0.05) and high-density lipoprotein (HDL) cholesterol levels (P < 0.05). After adjustment for sex, age, puberty, obesity, and insulin levels, only PAI-I remained significantly different between the two groups (10.9 (7.2-29.8) vs. 6.2 (4.3-10.6) ng/ml, P < 0.001). Dietary intake did not affect cIMT values. Eight percent of subjects showed nonatherosclerotic carotid calcifications with patchy pattern. These children had a worse lipid profile (P < 0.05) and higher plasma PTH levels (48.6 ± 21.5 vs 38.5 ± 16.9 pg/ml, P < 0.05) that were inversely associated with 25-hydroxyvitamin D levels (r = 0.245, P < 0.01). Present results suggest that (i) several adiposity-related factors may play a role in promoting the development of early arterial diseases in young subjects with a benign phenotype of obesity, (ii) a PTH rise resulting from a subclinical imbalance in calcium-phosphorus homeostasis may affect the biological process of vascular calcifications.

Acute effects of 17beta-estradiol on left internal mammary graft after coronary artery bypass grafting.

BACKGROUND: Vasospasm of arterial conduits used for coronary surgical procedures is an important cause of postoperative graft failure. Mounting experimental evidence suggests that estrogen reverses acetylcholine-induced vasospasm of the coronary arteries in animals and humans. Estrogen also affects endothelium-derived constrictor factors. We therefore investigated the in vivo vasomotor responses to transdermal 17beta-estradiol of the left internal mammary artery (LIMA) grafted on the anterior descending coronary artery. METHODS: We studied 20 women, mean age of 62 +/- 7.2 years (range, 48 to 73 years), who had undergone cardiopulmonary bypass for coronary artery bypass grafting. They received transdermal 17beta-estradiol on the fifth day after operation. The diameter, cross-sectional area, and blood flow of the LIMA graft were measured by transthoracic color Doppler echography before (basal values) and after the transdermal administration of 50 microg of 17beta-estradiol (control). RESULTS: LIMA graft vasodilation after the administration of 17beta-estradiol was observed. A significant increase in diameter (2.06 +/- 0.4 mm versus 2.37 +/- 0.28 mm; p = 0.035) and cross-sectional area (3.45 +/- 1. 2 mm2 versus 4.24 +/- 1 mm2; p = 0.039) was registered. The LIMA graft mean flow increased by 49% (44.76 +/- 27.19 mL/min versus 56.62 +/- 27.69 mL/min), but this increase was not statistically significant (p = 0.06). CONCLUSIONS: The acute postoperative transdermal administration of 17beta-estradiol induced a significant increase of LIMA graft diameter and cross-sectional area in postmenopausal women who underwent coronary artery bypass grafting. The LIMA graft vasodilation was also associated with an improvement in LIMA blood flow.