Plaque erosion: an underestimated mechanism of vulnerable plaque.
Dr. A LafontParis, FranceVice-Chairman of the ESC working group on Interventional Cardiology and Coronary Pathophysiology
Vulnerable plaque has been classically related to plaque rupture, yet autopsy studies have detected that plaque erosion (i.e., endothelial abrasion) was detected in 25-40% of patients with sudden coronary death in the absence of plaque rupture. This finding is worrisome since there are neither diagnostic nor therapeutic strategies targeted against plaque erosion. Moreover, it appears that plaque erosion represents an entity which is distinct from plaque rupture.
Major improvements have been made to try to understand the mechanism(s) which may lead to acute coronary occlusion (1-4). Initially, plaque rupture was defined as the mechanism responsible for the evolution from vulnerable plaque to acute occlusion. Although plaque rupture remains a major cause of plaque complications, other mechanisms have emerged, i.e., plaque erosion, and much less frequently, calcified nodules protruding in the artery lumen (5-7). The fact that coronary thrombosis may occur without plaque rupture is a revolution that needs to be taken into account in the definition of vulnerability.
Recently, the Becker group studied the histology of 11 patients less than 35 years of age who presented sudden cardiac death (
This shows that thrombus formation occurred at least several weeks prior to death in the case of plaque erosion (89%) whereas the thrombus was fresh in the two cases of plaque rupture at the culprit plaque level. This study is particularly interesting because of the profile of the population at risk which is characterized by its very young age (30.9+/-4): indeed, this population had distinct features which are in contrast with the population at risk of plaque rupture. These very young patients with plaque erosion were most frequently smokers (44%) and female (44%), high cholesterol being present in only 11% of the patients. Moreover, this study confirms the work of the Virmani group: in a young population, plaque erosion is the principal lesion responsible for sudden coronary death. This clearly defines plaque erosion as an entity which may be independent of plaque rupture. There is a need to define new strategies for the detection and treatment of plaque erosion. Indeed, there is a lack of experimental models, as well as human biological markers, or even in vivo imaging techniques able to detect it. Eventually, more care should be paid to this population at risk whose clinical symptoms may not receive sufficient attention in emergency units.
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