Clinical Phenotype and Microvascular Dynamics of Subjects with Endothelial Dysfunction as Assessed by Peripheral Tonometry.

Objective: To evaluate the characteristics and the determinants of ED, as measured by PAT.

Methods: We measured basal and post-ischemic digital pulse amplitude (EndoPAT(®)) in a mixed outpatient population of 206 diabetic and 101 non-diabetic subjects, of whom 50% with clinically manifest CVD, undergoing to an extensive clinical, biochemical, and vascular phenotype characterization.

Results: The major characteristics of ED (tertile 1 vs 3), in addition to lower post-ischemic vasodilatory reserve (34 vs 203%), were a 3-fold higher baseline pulse amplitude and a delayed (60 second) peak response.

Effect of mild hyperisulinemia on conduit vessel endothelial function: role of noradrenergic activation.

Objective: The evidence that an exogenously induced modest hyperinsulinemia deteriorates conductance artery endothelial function - flow-mediated dilatation (FMD) - in healthy individuals is in contrast with in-vitro and in-vivo studies that consistently found that insulin facilitates both nitric oxide release and the endothelium-dependent dilatation. The aim of this study was to verify whether this effect is caused by the enhancement of insulin-induced adrenergic tone.

Method: In 10 healthy male volunteers, endothelium-dependent (FMD) and endothelium-independent (glyceryl trinitrate, GTN) dilatation were evaluated by high-resolution ultrasound of the brachial artery, combined with a computerized edge detection system, at baseline (-60 and 0 min) and after 120 and 240 min during insulin infusion (INS study).

Anti-inflammatory and antioxidant properties of HDLs are impaired in type 2 diabetes.

Objective: In mice, 4F, an apolipoprotein A-I mimetic peptide that restores HDL function, prevents diabetes-induced atherosclerosis. We sought to determine whether HDL function is impaired in type 2 diabetic (T2D) patients and whether 4F treatment improves HDL function in T2D patient plasma in vitro.

Research Design And Methods: HDL anti-inflammatory function was determined in 93 T2D patients and 31 control subjects as the ability of test HDLs to inhibit LDL-induced monocyte chemotactic activity in human aortic endothelial cell monolayers.

Effects of GIK (glucose-insulin-potassium) on stress-induced myocardial ischaemia.

Despite the evidence in experimental animal models that insulin, or GIK (glucose-insulin-potassium), improves left ventricular function and perfusion during both acute and chronic ischaemia, clinical studies have generated conflicting results. We tested the hypothesis that pretreatment with GIK attenuates the vascular and functional effects of stress-induced myocardial ischaemia in humans. Twenty-two patients with evidence of inducible myocardial ischaemia were enrolled; 11 patients with normal ventricular function underwent two dipyridamole echocardiography tests, and 11 with regional contractility defects from previous myocardial infarction were submitted to two ECG exercise tests combined with 201Tl myocardial perfusion scintigraphy; the tests were preceded by 60 min of either normal saline or an isoglycaemic GIK infusion.

Metabolic syndrome: at the crossroads of cardiorenal risk.

The metabolic syndrome (MS), a cluster of cardiovascular risk factors closely linked to insulin resistance whose prevalence is high and rapidly rising in the Western population, has been recognized as a predictor of diabetes and future cardiovascular disease in the general population, as well as in various clinical settings. There is evidence that the MS increases cardiovascular risk, independently from the concomitant effect of several traditional cardiovascular risk factors. Emerging data suggest that MS might also be a risk factor for chronic kidney disease, although its effects on the emergence of chronic kidney disease or its progression beyond the contribution of dys-glycemia and high blood pressure are far from being established with certainty.