Unstable atherosclerotic plaque - Pathophysiology and therapeutic guidelines

Plaque disruption promoted by local inflammation and oxidative stress seem to be the triggering mechanisms of acute coronary syndromes. Oxidized low-d ensity lipoproteins (LDL) play a Itey role in this inflammatory process. Wi thin the inflammatory region, angiotensin-converting enzyme (ACE) accumulat ion has been described, leading to enhanced production of local angiotensin II which stimulates adhesion molecule expression and increases oxidative s tress (leading to excessive degradation of EDNO). According to recent clinical trials, drugs like statins or ACE inhibitors s eem promising and could stabilize the plaque, probably by attenuation of th e inflammatory process. Finally, as thrombus formation also plays a role in these acute coronary syndromes, another approach may be the use of antithr ombotic therapy.