Prognostic value of systemic endothelial dysfunction in patients with acute coronary syndromes: further evidence for the existence of the "vulnerable" patient.

Background: Endothelial vasodilator dysfunction may serve as a marker integrating the vascular risk of an individual; however, whether systemic vasodilator function predicts disease progression and cardiovascular event rates in patients with manifest acute coronary syndromes (ACS) is unknown.

Methods And Results: In 198 patients with angiographically documented ACS, forearm blood flow (FBF) responses to acetylcholine (ACH; 10 to 50 microg/min) and sodium nitroprusside (SNP; 2 to 8 microg/min) were measured by venous occlusion plethysmography before hospital discharge within 5 days of an episode of an ACS. Cardiovascular events (cardiovascular death, myocardial infarction, and ischemic stroke) served as outcome variables over a mean follow-up period of 47.

C-reactive protein levels determine systemic nitric oxide bioavailability in patients with coronary artery disease.

Aim: Elevated C-reactive protein (CRP) levels are associated with impaired endothelial vasoreactivity in patients with coronary artery disease (CAD). Because inflammatory cytokines experimentally reduce basal and stimulated endothelial nitric oxide (NO) release, we hypothesised that patients with elevated CRP-levels are characterised by a systemic impairment in NO bioavailability.

Methods And Results: Forearm blood flow (FBF) responses were measured by venous occlusion plethysmography in 75 male patients with documented CAD.

Interleukin-10 serum levels and systemic endothelial vasoreactivity in patients with coronary artery disease.

Objectives: Because the endothelium is a major target for inflammatory cytokines, we investigated whether elevated interleukin (IL)-10 serum levels are associated with improved endothelial vasoreactivity in patients with coronary artery disease (CAD).

Background: Chronic inflammation plays a pivotal role in the progression of atherosclerosis. Interleukin-10 is an anti-inflammatory cytokine that exerts important protective effects on atherosclerotic lesion development in experimental animals.

Elevated secretory non-pancreatic type II phospholipase A2 serum activity is associated with impaired endothelial vasodilator function in patients with coronary artery disease.

Low-grade inflammatory activity is associated with an increased risk for ischaemic coronary events. sPLA(2) (secretory non-pancreatic type II phospholipase A(2)) serum activity is increased in chronic inflammatory diseases and may also contribute to atherogenesis. Since the endothelium is a major target for inflammatory cytokines, we hypothesized that elevated serum activity of sPLA(2) is associated with an impaired vasodilator function in patients with documented CAD (coronary artery disease).

Inhibition of cytochrome P450 2C9 improves endothelium-dependent, nitric oxide-mediated vasodilatation in patients with coronary artery disease.

Background: Nitric oxide (NO)- and prostacyclin-independent vasodilatation in several vascular beds has been linked to the activation of cytochrome P450 (CYP) epoxygenases expressed in endothelial cells. However, these enzymes, which generate vasodilator epoxyeicosatrienoic acids, may also produce oxygen-derived free radicals, which attenuate the bioavailability of NO. Here, we studied the involvement of CYP 2C9 in modulating endothelium-dependent and -independent changes in forearm blood flow (FBF) in healthy volunteers and in patients with manifest coronary artery disease.