[Unstable atheromatous plaque. Physiopathology and therapeutic approach to coronary insufficiency]

Plaque disruption promoted by local inflammation and oxidative stress seems to be the triggering mechanisms of acute coronary syndromes. Oxidized low-density lipoproteins (LDL) play a key role in the inflammatory process. Within the inflammatory region, angiotensin-converting enzyme (ACE) accumulation has been described, leading to enhanced production of angiotensin II which stimulates adhesion molecule formation and increases oxidative stress. According to recent clinical trials, drugs like statins or ACE inhibitors seem promising and could stabilize the plaque, probably by attenuation of the inflammatory process. Finally, as thrombus formation also plays a role in these acute coronary syndromes, another approach is the use of antithrombotic therapy.