Plaque disruption promoted by local inflammation and oxidative stress seem to be the triggering mechanisms of acute coronary syndromes. Oxidized low-density lipoproteins (LDL) play a key role in this inflammatory process. Within the inflammatory region, angiotensin-converting enzyme (ACE) accumulation has been described, leading to enhanced production of local angiotensin II which stimulates adhesion molecule expression and increases oxidative stress (leading to excessive degradation of EDNO). 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 may be the use of antithrombotic therapy.