L-arginine ameliorates the abnormal sympathetic response of the dysfunctional human coronary microvasculature.

A nitric oxide (NO)-related defect may contribute to abnormal coronary sympathetic responses that can cause ischemia in patients with endothelial dysfunction. Because L-arginine, the NO synthase (NOS) precursor, augments NO bioactivity, we hypothesized that L-arginine would improve dysfunctional coronary sympathetic responses. Eleven patients with atherosclerosis or its risk factors were challenged with the cold pressor test, a specific provocative test of cardiac sympathetic activity, after 3 separate and sequential intracoronary infusions, as follows: 1) Normal saline; 2) L-NMMA, a competitive inhibitor of NOS; and 3) L-arginine.

Inflammatory markers increase following exposure to radiographic contrast media.

Purpose: Increased levels of markers of systemic inflammation have been noted in patients following coronary angiographic procedures. The purpose of the present study was to examine the influence of the type of the angiographic procedure as well as the type of radiographic contrast media (RCM) on markers of inflammation.

Material And Methods: Thirty-seven patients undergoing diagnostic or interventional coronary angiographic procedures were randomly assigned to receive one of three RCM - an ionic low osmolar agent; a non-ionic, iso-osmotic agent; or a non-ionic, low osmolar agent.

Assessment of contemporary stent deployment using intravascular ultrasound.

Four second- and third-generation coronary stents were evaluated using QCA and intravascular ultrasound for adequacy of stent expansion, the influence of disease burden on adequacy of deployment, and postdeployment structural effects on the artery. Despite satisfactory stent deployment rates on angiography of 92 %, adequate stent deployment by IVUS ranged from 38% to 55%. There was no significant difference in deployment success across the four stent types.

Cholesterol, cholesterol lowering, and endothelial function.

A strong relationship between hypercholesterolemia and atherosclerosis has been established through epidemiological, experimental, and clinical trial data. Traditional theories on the pathophysiology of this relationship involve the deposition, modification, and cellular uptake of cholesterol, and the release of inflammatory and growth factors resulting in smooth muscle cell proliferation and collagen matrix production. The vasculature has recently been found to be an active and complex organ, with the endothelium playing a controlling role in vascular tone, lipid breakdown, thrombogenesis, inflammation, and vessel growth.