Myocardial infarction (MI) is the number one cause of death worldwide, despite numerous improvements in treatment strategy.

Atherothrombosis underlies most MIs and results from atherosclerotic plaque rupture or erosion in the coronary artery. A plaque prone to rupture is called a vulnerable plaque and has a thin fibrotic cap, large necrotic core and few fibrotic tissue to stabilize the plaque. When the fibrotic cap ruptures the lipid-rich, procoagulant and proinflammatory content from inside the plaque gets into contact with blood and creates an immediate occlusive thrombus and a subsequent MI. Traditionally the view was that most MI arose from plaque rupture. However, recently it has been shown that plaque rupture accounts for a relatively small number of MI’s nowadays, possibly due to successful antithrombotic treatment.

Plaque erosion almost accounts for 40% of MI’s, but relatively little is known about the pathology. Compared to a vulnerable plaque, eroded plaques are characterized by an absent or disturbed endothelial layer that lines the blood vessel, less infiltrating inflammatory cells and more migrating, proliferating and differentiating vascular smooth muscle cells. Although the lesions on itself usually do not form a critical occlusion, it is the dysregulated/absent endothelial layer that promotes thrombus formation on top of the intima.

The mechanisms that trigger a plaque to become an eroded instead of a vulnerable plaque or vice versa are not known. Additionally, data suggests that a plaque is rather plastic and can switch from a vulnerable plaque towards an eroded phenotype over time. The currently known differences between eroded and vulnerable plaques, such as different fibrotic and inflammatory characterizations which brings in the need for tailored treatment. However, the complexity of interactions between systems like the coagulation cascade and the inflammatory pathway that orchestrate phenotypes of eroded and vulnerable plaques have to be elucidated first.