Systemic and local inflammation in patients with unstable atherosclerotic plaques.

The response to injury in the vasculature and the heart is inflammation. Atherosclerosis is often the result of injury followed by inflammation and atherosclerosis. Vascular and myocardial infections from various pathogens, including viruses, bacteria, chlamydia, and other infections result in vascular inflammation and almost certainly play a role in the development of atherosclerosis and acute coronary heart disease syndromes in at least some patients.

How to study the effects of platelet aggregation and thrombosis on coronary vasomotion and their clinical relevance.

Following arterial injury, platelets may activate and adhere to the damaged vessel wall, release vasoactive products, and produce vasoconstriction or even vasospasm. In the last few years the hypothesis of intracoronary thrombosis, triggered by plaque ulceration or fissuration, has gained wide acceptance as one of the key events in the pathophysiology of acute coronary syndromes. Following arterial injury, platelets readily adhere to the subendothelium and release a variety of chemical mediators which, apart from recruiting additional platelets from the circulation, are also powerful vasoactive substances.

Near-infrared spectroscopic characterization of human advanced atherosclerotic plaques.

Unlabelled: OBJECTIVES; Living human carotid atherosclerotic plaques were examined in vitro by near-infrared (NIR) spectroscopy to determine the spectral features of plaque vulnerability.

Background: Plaque disruption, a major cause of heart attacks and strokes, cannot generally be predicted, but is thought to depend mainly on plaque composition. Near-infrared spectroscopy has been used to detect components in tissues noninvasively.

Design of a trial evaluating myocardial cell protection with cariporide, an inhibitor of the transmembrane sodium-hydrogen exchanger: the Guard During Ischemia Against Necrosis (GUARDIAN) trial.

Inhibition of the sodium-hydrogen exchanger (NHE) is a powerful experimental tool to inhibit sodium and calcium accumulation within the ischemic myocyte and halt progression of cell ischemia to cell necrosis. This paper describes the protocol and rationale of a first large-scale clinical trial designed to evaluate the safety and efficacy of cariporide, a novel specific and potent inhibitor of the exchanger.