Coronary endothelial dysfunction and impaired microcirculation response to atrial natriuretic peptide in hyperinsulinemia.

Endothelial dysfunction occurs in hyperinsulinemia (HI). Coronary microcirculation responses to vasoactive agents are examined in 57 patients with angiographically normal coronary arteries. Patients were divided into 2 groups, 37 with normoinsulinemia (NI) and 20 with HI based on results of a 75-g oral glucose tolerance test.

Examination of the microcirculation damage in smokers versus nonsmokers with vasospastic angina pectoris.

Endothelial dysfunction is considered one of the mechanisms underlying vasospastic angina pectoris (VSA). It is also known that smokers have abnormalities in endothelial dysfunction. Although smoking is a major risk factor for coronary artery disease, microvascular abnormalities have not been well shown.

P-selectin expression, but not GPIIb/IIIa activation, is enhanced in the inflammatory stage of Takayasu's arteritis.

Background: Inflammation and thrombosis are closely related processes, but the association between disease activity and thrombogenicity in Takayasu's arteritis (TA) is poorly understood. To investigate the link between platelet activation and disease activity, flow cytometric analyses of platelet P-selectin and activated GPIIb/IIIa expression were performed in patients with TA.

Methods And Results: Twenty-two patients with TA, classified into active (Group A, n = 9) and inactive (Group I, n = 13) according to blood-derived inflammatory markers, and 14 healthy age- and gender-matched controls (Group C) were studied.

Perindopril augments ecto-ATP diphosphohydrolase activity and enhances endothelial anti-platelet function in human umbilical vein endothelial cells.

Objectives: Recent clinical trials have demonstrated that angiotensin-converting enzyme inhibitors (ACEIs) reduce thrombotic events by unknown mechanisms in patients with atherosclerotic cardiovascular diseases.

Design: We studied the in-vitro effects of perindopril, an ACEI, on the ability of human umbilical vein endothelial cells (HUVEC) to inhibit platelet aggregation.

Methods: Platelet aggregation in the presence of HUVEC and endothelial surface expression and activities of ecto-ATP diphosphohydrolase (ecto-ADPase), CD39, were determined.

Smokers lack morning increase in platelet sensitivity to nitric oxide.

This study investigated whether a circadian variation is present in the sensitivity of platelets to nitric oxide (NO) and, if so, if long-term smoking modifies it. Blood samples were taken at 0:00, 6:00, 9:00, 12:00, and 18:00 from 14 nonsmokers and 10 smokers. Dose-response curves for platelet aggregation by collagen were constructed in both the presence and absence of 1.

Opening of K(ATP) channel attenuates the increase in QT dispersion produced by the first balloon inflation during coronary angioplasty.

Increased QT dispersion predicts the occurrence of lethal ventricular arrhythmias complicating percutaneous transluminal coronary angioplasty (PTCA). Moreover, these arrhythmias occur more frequently at the first balloon inflation. Activation of the K(ATP) channel may influence QT dispersion and ventricular arrhythmias during coronary angioplasty, so 40 consecutive patients with stable angina were randomized to receive 3 mg/h of nicorandil infusion or placebo and QT dispersion and the incidence of ventricular ectopy were investigated before and throughout PTCA.

Acute vigorous exercise primes enhanced NO release in human platelets.

Activation of platelets by acute vigorous exercise has been demonstrated by various parameters, including an increase in agonist-induced platelet [Ca2+]i levels. However, direct evidence is lacking regarding how acute exercise affects platelet-derived NO. Twenty-three healthy male non-smokers (21-59 years) underwent a symptom-limited treadmill exercise test.