Arterial structure and function and its short- and long-term changes after bariatric surgery.

Subclinical arterial damage connected with endothelial dysfunction is a common denominator of cardiovascular complications in a variety of metabolic diseases, including obesity. The aims of the study was to assess functional vascular changes measured by flow-mediated dilatation (FMD) and nitroglycerin-mediated dilation (NMD) of brachial artery, and to measure vascular structural alterations estimated by carotid intima-media complex thickness (IMT) in short- (10 days) and medium-term (6 months) time after bariatric surgery in patients with extreme obesity. Anthropometric, blood pressure (BP), FMD, NMD, IMT measurements, and laboratory assessment were performed on patients who met the eligibility criteria for bariatric surgery (age 18 - 60 years old, BMI ≥ 40.0 kg/m2 or with BMI 35.0 - 39.9 kg/m2 and co-morbidities), at baseline and during follow-up. The study population consisted of 71 patients: mean SD aged 45.6 (± 10.9) years; BMI = 47.7 (± 6.1) kg/m2; 45% of them were men). A significant reduction of systolic BP, glucose, HDL cholesterol, leptin, insulin and HOMA-IR were observed 10 days post intervention. A significant increase of FMD values was observed in the entire group 6 months after surgery (median (IQR) 6.2 (2.9 - 10.3) versus 8.5 (6.1 - 16.6), P < 0.05). Changes of NMD were insignificant. Carotid IMT diminished significantly after 6 months (median (IQR) 0.6 (0.5 - 0.7) versus 0.6 (0.5 - 0.6) mm, P < 0.05). A subgroup analysis revealed that FMD parameters had improved significantly after 6 months, mainly in men, hypertensives, and in the Roux-en Y bypass (RYGB) subgroup. In conclusion, endothelial function and subclinical atherosclerosis improved after bariatric surgery in patients with extreme obesity. A lack of changes of the dilatation independent of endothelial function may indicate the persistence of residual changes in the vascular bed.

Blood pressure and arterial stiffness in patients with high sodium intake in relation to sodium handling and left ventricular diastolic dysfunction status.

In a population with high sodium consumption, we assessed relation between brachial and central blood pressures, elastic properties of large arteries, echocardiographic left ventricular diastolic function and sodium reabsorption as fractional urinary lithium excretion in proximal (FELi) and fractional sodium reabsorption in distal tubules assessed using the endogenous lithium clearance. Mean±s.d. age of 131 treated hypertensive patients (66 men and 65 women) was 61.9±7.5 years. We found significant interaction between left ventricular diastolic function and FELi with respect to the values of brachial blood pressure: systolic (SBP), diastolic (DBP) and mean blood pressure (MBP) (all PINT<0.03). In patients with FELi below the median value and impaired left ventricular diastolic function, the values of SBP (149.3 vs 132.5 mm Hg; P=0.005), DBP (85.1 vs 76.1 mm Hg; P=0.001), MBP (106.5 vs 94.9 mm Hg; P=0.001), central SBP (SBPC) (137.4 vs 122.0 mm Hg; P=0.01), central DBP (DBPC) (84.8 vs 76.0 mm Hg; P=0.003), central MBP (MBPC) (106.9 vs 95.9 mm Hg; P=0.007), aortic pulse wave augmentation (18.0 vs 13.5 mm Hg; P=0.03), pulse wave velocity (14.6 vs 12.5 m s(-1); P=0.02) and central aortic pulse wave augmentation index (155.7% vs 140.9%; P=0.01) were significantly higher than in patients with normal left ventricular diastolic function. Such relationships were not observed in the entire group and patients with FELi above the median value. In the hypertensive population with high sodium intake, increased sodium reabsorption in proximal tubules may affect blood pressure parameters and arterial wall damage, thus contributing to the development of left ventricular diastolic function impairment.