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Plaque erosion (PE) is a form of atherosclerotic plaque injury in which a blood clot (thrombus) forms on the surface of a plaque without rupture of the fibrous cap. It is one of the main mechanisms underlying acute coronary syndrome (ACS), being its second most common cause after plaque rupture (PR). Unlike PR, in which the fibrous cap covering the plaque breaks open and exposes a lipid-rich core, PE involves thrombus formation over a plaque with an intact fibrous cap. PE is often associated with different plaque characteristics and clinical presentations than PR. It is usually identified with intracoronary imaging, particularly optical coherence tomography (OCT). Management generally follows standard treatment for ACS, though selected cases have been treated without stent placement based on intracoronary imaging.

PE usually presents in the setting of ACS, most often as non-ST-segment elevation myocardial infarction (NSTEMI).^[1][2] It is identified less frequently in ST-segment elevation myocardial infarction (STEMI), which is more commonly associated with PR.^[3][4] This pattern has been linked to the more frequent presence of non-occlusive thrombus and a larger residual lumen in eroded plaques^[5][6]. Usually, NSTEMI reflects partial coronary obstruction, whereas STEMI indicates complete coronary occlusion.^[7] People with PE commonly present with angina, shortness of breath and other features of myocardial ischemia similar to those seen in other forms of coronary thrombosis.^[8][9] Symptoms and electrocardiographic findings do not reliably distinguish PE from PR.^[2][10]

No single cause of PE has been established, but it has been associated with a risk profile that differs in part from that of PR.^[4][11][12]

Patient-level associations

Compared with PR, PE is more often identified in younger individuals and in individuals who smoke. It has also been associated with fewer traditional cardiovascular risk factors and chronic comorbidities commonly reported in PR, including diabetes, hypertension, dyslipidemia and chronic kidney disease.^[13] This contributes to a younger and less comorbid clinical profile.

Lesion-level associations

At the lesion level, PE is commonly found near arterial bifurcations, particularly in the proximal segment of the left anterior descending artery (LAD) artery, where bifurcations were frequent. Compared with ruptured plaques, eroded plaques are usually associated with less severe stenosis and are often found distal to the stenotic segment.^[14][15][16]

The mechanisms of PE are not fully established.^[17] PE is characterised by thrombus formation over an atherosclerotic plaque whose fibrous cap remains intact, unlike PR, in which disruption of the fibrous cap exposes the necrotic core to circulating blood.^[18] Current models describe PE as a multistep process involving endothelial injury or loss, disturbed local flow, thrombo-inflammatory activation and platelet-rich thrombus formation on an intact plaque surface.^[3]

Plaque structure and endothelial loss

Eroded plaques are often described as having a thick fibrous cap, greater smooth muscle cell content and a proteoglycan-rich matrix, with less lipid accumulation and less inflammatory cell infiltration than ruptured plaques.

PE is also characterised by superficial endothelial denudation with loss of the endothelial cell lining at the plaque surface and exposure of the subendothelial matrix to blood, causing the luminal surface to appear irregular. When a thrombus is present, it overlies this denuded surface without the cavity formation typical of rupture.^[19]

Role of disturbed flow and thrombo-inflammatory activation

Erosion-prone lesions are often found near arterial bifurcations and other regions of disturbed flow, where altered shear stress may promote endothelial dysfunction.^[20][21] This local flow disturbance is thought to act together with inflammatory and innate immune pathways to promote endothelial injury and thrombosis.^[17][22]

Pro-inflammatory signalling may activate endothelial cells, promote release of matrix-degrading enzymes, and contribute to endothelial cell apoptosis and detachment from the basement membrane.^[22] Hyaluronan fragments and Toll-like receptor 2 signalling have been proposed as contributors to endothelial activation and weakening of intercellular junctions.

Neutrophils, a type of white blood cell involved in innate immunity, have also been linked to endothelial injury in PE, with higher myeloperoxidase levels and frequent Neutrophil extracellular traps (NETs) reported at the plaque-thrombus interface.^[20] NETs consist of extracellular DNA and prothrombotic proteins and may trap platelets, promoting thrombus formation at the plaque surface.^[23]

Thrombus formation

Once endothelial integrity is lost, the underlying proteoglycan-rich and smooth-muscle-cell-rich plaque matrix is exposed to circulating blood, promoting platelet adhesion and activation, particularly under high-shear arterial flow.^[24][25][26] The resulting thrombus is often described as platelet-rich, differing from the fibrin-rich thrombi associated with PR.^[27] This leads to coronary thrombosis over a plaque with an intact fibrous cap.

In living people, PE is identified mainly in those presenting with ACS during invasive coronary angiography, with intracoronary imaging, particularly OCT.^[28][29][19] OCT is used to assess the culprit lesion and can distinguish PE from PR by showing thrombus over an intact plaque surface without fibrous cap discontinuity.^[5][30] A definite OCT-based diagnosis can be made when an attached thrombus overlies an intact fibrous cap.^[19][31] A probable diagnosis is made when the luminal surface is irregular without visible thrombus, or when thrombus is present without imaging features of PR.^[5][32]

OCT cannot directly visualise the endothelial monolayer, so in vivo diagnosis relies on the absence of rupture rather than direct confirmation of endothelial loss.^[33][34] Diagnostic certainty may also be limited because the OCT criteria are indirect and only partly validated against histopathology.^[31][33] This can allow thrombus-obscured rupture or very small fibrous cap disruptions below OCT resolution to be misclassified as erosion.^[19][30]

Management of PE is usually framed within standard treatment for ACS, since the culprit lesion type is usually not known at first presentation.^[7][35] Conventional treatment includes antithrombotic therapy and revascularisation when indicated, most commonly by percutaneous coronary intervention (PCI) with stent implantation.^[8][36]

In selected cases of OCT-defined PE, particularly where coronary flow is preserved and residual stenosis or thrombus burden is limited, treatment without stenting has been explored using intensive antithrombotic therapy.^[1][31] Early studies suggest that this strategy may be feasible in carefully selected cases, but the evidence remains limited and stent-sparing management is not established as routine care.^[2]

In imaging-based studies of ACS, PE has been estimated to account for about 25% to 40% of culprit lesions.^[1] Estimates vary according to imaging modality, study population and the criteria used to distinguish erosion from PR.^[33]

PE is identified more commonly in younger age groups, whereas PR becomes more frequent in advanced age.^[2] Findings on sex distribution have been less consistent.^[3] Earlier autopsy studies found a higher proportion of ACS cases involving erosion in women, but later intravascular imaging studies have shown mixed results, with some reporting similar proportions in both men and women and others noting a higher frequency in younger women.^[4][11]

PE has often been associated with more favourable outcomes than PR in ACS. Reported findings include smaller infarct size, better-preserved left ventricular function after an acute event, and reduced rates of the no-reflow phenomenon following PCI.^[37][38] Lower rates of major adverse cardiovascular events (MACE) have also been reported in some studies.^[18] These differences may relate to the more preserved plaque structure and the thrombus characteristics seen in PE.^[6] Outcomes still vary according to thrombus burden, severity of the acute event, treatment received and residual stenosis.^[8]

PE came to be recognised as a distinct cause of coronary thrombosis in the late twentieth century, when autopsy studies showed that some thrombi formed on plaques with an intact fibrous cap rather than on ruptured plaques.^[4][39] This helped establish PE as a separate lesion type within ACS.

A later turning point was the introduction of OCT, which made it possible to study erosion-prone culprit lesions in living people.^[32] This allowed comparison of PE and PR in clinical populations and renewed interest in whether the two lesion types differ in presentation, management and prognosis.

Earlier autopsy studies generally reported lower frequencies of PE in ACS than later OCT-based studies. This discrepancy has been attributed partly to differences in case selection, since autopsy studies mainly examined fatal ACS, and also to the less consistent criteria used to distinguish PE from PR in earlier studies.^[3] Some reviews have also proposed that modern preventive therapy, including wider use of lipid-lowering therapy and improved control of hypertension and diabetes, may have reduced the formation of rupture-prone lesions more than erosion-prone lesions, though this remains uncertain.^[9][40]

Current research on PE focuses on improving diagnosis, clarifying its underlying mechanisms and determining whether some cases may be managed with more selective treatment.^[41][42] One unresolved issue is how closely OCT-defined PE corresponds to the histopathological lesion first described in autopsy studies.^[34] Studies are also examining whether circulating biomarkers or non-invasive imaging methods can help identify PE without routine intracoronary imaging.^[43] Mechanistic studies continue to examine endothelial injury, disturbed blood flow, innate immune signalling, neutrophil activity and thrombus formation to explain why some intact plaques become thrombogenic.^[17][20] Another area of study is whether selected individuals with OCT-defined PE can be treated safely without stent implantation.^[44]