Summary
Myocardial infarction is a prevalent, life-threatening consequence of athero-thrombosis.
Post-mortem histology and intravascular imaging in live patients have shown that approximately
one third of myocardial infarctions are caused by a thrombus overlying an intact,
non-ruptured atherosclerotic plaque. Histology identifies erosion of luminal endothelial
cells from smooth muscle and proteoglycan-rich, thick fibrous cap atheromas as the
underlying pathology. Unlike plaque ruptures, endothelial erosions tend to occur on
thick-capped atherosclerotic plaques and may or may not be associated with inflammation.
Smoking and female gender are strong risk factors for erosion. Multiple mechanisms
may contribute to endothelial erosion, including endothelial dysfunction, TLR signalling,
leukocyte activation and modification of sub-endothelial matrix by endothelial or
smooth muscle cells, which may trigger loss of adhesion to the extracellular matrix
or endothelial apoptosis. Diagnosis of endothelial erosion by intravascular imaging,
especially high resolution optical coherence tomography, may influence treatment strategies,
offering prognostic value and utility as an endpoint in trials of agents designed
to preserve an intact coronary endothelium.
Keywords
Atherothrombosis - endothelial cells - imaging - shear stress