- According to diagnostic criteria developed for use with optical coherence tomography, the prevalence of plaque erosion in patients with acute coronary syndromes (ACS) is 25%–44%
- A study of 1,241 patients with ACS (477 with plaque erosion and 607 with plaque rupture) identified five risk factors for plaque erosion: age <68, anterior ischemia, absence of diabetes, normal kidney function and hemoglobin >15 g/dL
- In the same study, patients with ACS caused by plaque erosion had lower levels of inflammatory markers (high-sensitivity C-reactive protein and white blood cell count) and a more favorable lipid profile than those with plaque rupture
- Angiography of patients with erosion-induced ACS reveals less extent and severity of atherosclerosis and less complex lesions than in plaque rupture; in addition, plaque erosion is most likely to affect the left anterior descending coronary artery
- A proof-of-concept study found that in patients whose ACS was due to plaque erosion, antithrombotic therapy alone without stenting was safe and effective
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Superficial plaque erosion is one of the two major mechanisms of acute coronary syndromes (ACS). The other, plaque rupture, gets more attention, but with the advent of optical coherence tomography (OCT), the prevalence of plaque erosion in patients with ACS has been reported to be 25%–44%.
In JAMA, Dhaval Kolte, MBBS, PhD, interventional cardiologist at the Corrigan Minehan Heart Center at Massachusetts General Hospital, and Ik-Kyung Jang, MD, PhD, director of the Cardiology Laboratory for Integrative Physiology and Imaging, and a colleague discuss the mechanisms and clinical features of erosion-induced ACS and explain that antithrombotic therapy without stenting may be a management option.
Mechanisms and Diagnosis
Plaque erosion is thought to involve two steps:
- Local blood flow perturbation around a plaque in the coronary artery activates the innate immune toll-like receptor 2 and leads to the death of endothelial cells on the plaque surface
- Neutrophil extracellular traps form on the denuded plaque surface, prompting thrombus formation
OCT diagnosis of plaque erosion requires the presence of a thrombus overlying a plaque that has an intact fibrous cap. Other key morphologic characteristics that distinguish plaque erosion from plaque rupture are preserved vascular structure and a larger lumen.
Clinical and Laboratory Findings
A study of 1,241 patients with ACS, reported in the Journal of the American Heart Association, compared 477 individuals with plaque erosion and 607 with plaque rupture. Five risk factors were independently associated with plaque erosion: age <68, anterior ischemia, absence of diabetes, normal kidney function and hemoglobin >15 g/dL. A potential explanation for the high hemoglobin is that hemoconcentration can increase blood viscosity, resulting in high endothelial shear stress that activates platelets and the coagulation system.
In the same study, patients with ACS caused by plaque erosion had lower levels of inflammatory markers (high-sensitivity C-reactive protein and white blood cell count) and a more favorable lipid profile than those with plaque rupture.
Compared with patients with ACS due to plaque rupture, those with plaque erosion have less extent and severity of atherosclerosis and less complex lesions. In addition, plaque erosion is more likely to affect the left anterior descending coronary artery than the right or circumflex coronary arteries.
The single-center, prospective, proof-of-concept EROSION trial demonstrated the feasibility and safety of antithrombotic therapy without stenting in patients with erosion-induced ACS. As reported in the European Heart Journal, of 405 patients with ACS, 103 (25%) had plaque erosion. All patients received aspirin, ticagrelor and unfractionated heparin before catheterization.
For 60 patients with plaque erosion who had residual stenosis <70% and TIMI flow grade 3, no stent was implanted and antithrombotic therapy was continued. 47 of those patients (78%) met the primary endpoint of >50% reduction of thrombus volume at 1 month. No patient died or developed secondary ACS. This preliminary evidence will need to be confirmed in future randomized controlled trials.
More research is needed to develop risk scores that can predict the likelihood of plaque erosion in patients with ACS. For example, in the study of 1,241 patients with ACS, the likelihood of plaque erosion was 73% when all five risk factors (age <68, anterior ischemia, absence of diabetes, normal kidney function and hemoglobin >15 g/dL) were present.
Also needed are point-of-care assays and noninvasive imaging modalities to detect plaque erosion and, most important, novel therapies targeted toward the molecular pathways involved in its development.
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