One of the most prominent pathogenic mechanisms producing acute coronary syndrome (ACS) is plaque erosion (PE). Because of the widespread use of intracavitary imaging, the prevalence of PE is becoming more widely recognised. Eroding plaques, unlike traditionally vulnerable plaques, exhibit distinct pathological characteristics.
In addition, recent studies revealed differences in the pathophysiological mechanisms and clinical outcomes between PE and plaque rupture (PR).
Researchers conducted a review of the literature to evaluate the pathological features of eroded plaques. Their studies revealed that PE has different pathological features than PR, according to autopsy and imaging investigations. A thin fibrous cap and a discontinuous intimal layer have been described as characteristics of PR. In ruptured plaque, local endothelial cells exist but are dysfunctional, whereas PE has an intact and dense fibrous covering with no local endothelial cells. Patients with PR have a lipid metabolic disorder as their primary symptom. In PR, a more significant necrotic core with accumulated lipids and inflammatory cells is common.
PE on the other hand, is defined as fibrous plaques with a high concentration of smooth muscle cells and extracellular matrix, such as hyaluronic acid (HA) and proteoglycan, but few macrophages and T cells. In addition, the lipid core is tiny or not apparent. Compared to ruptured plaques, eroded plaques have a larger lumen area, and it was discovered that more than half of the eroded plaques have stenosis of 75% or more.
For certain individuals with eroding plaques, antithrombotic medication alone may be safe and helpful, although more clinical trials are needed to be done to prove this theory. Patients with eroding plaques may have a better long-term prognosis than those with ruptured plaques.
The authors of the study concluded that PE is a prevalent and significant ACS pathogenic mechanism with pathological symptoms and mechanisms that are distinct from PR. The mechanism of degraded plaque is yet unknown and has to be investigated further. PE in STEMI patients is a predictable clinical phenomenon that differs from PR.