Healed Plaques Signal Vulnerability to Future Acute Coronary Syndrome
Key findings
- In 29% of 376 patients presenting with acute coronary syndrome (ACS), optical coherence tomographic (OCT) imaging detected a healed plaque at the site of the culprit lesion
- Healed plaques were frequently associated with plaque rupture, thin cap fibroatheromas and macrophage infiltration
- Multilayered healed plaques, which represent multiple previous thrombotic events, were associated with more severe stenosis than single-layered plaques
- Patients with ACS who have healed plaque may benefit from more aggressive secondary prevention aiming at suppression of inflammation and platelet activity
After a silent episode of atherosclerotic plaque rupture or erosion, the body's repair process results in healed plaque. On intravascular optical coherence tomography (OCT), such plaque is distinguishable as one or more layers of fibrous tissue, lipids and/or calcium.
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Multiple autopsy studies have found healed plaques in patients who experienced sudden cardiac death. Now, Ik-Kyung Jang, MD, PhD, director of the Cardiology Laboratory for Integrative Physiology and Imaging at Massachusetts General Hospital, and colleagues have conducted the first in vivo study of these plaques. They report in the Journal of the American College of Cardiology that healed plaques frequently show features of vulnerability to future major cardiac events and recommend that patients with such plaque at the time of acute coronary syndrome (ACS) should receive aggressive secondary prevention.
Study Subjects and Design
The study included 376 patients presenting with ACS who underwent OCT of the culprit lesion enrolled in either the Mass General OCT Registry or the EROSION trial between August 2010 and April 2016.
Clinical and Laboratory Data
Compared with patients who had nonlayered plaques, those with healed plaque:
- Had a higher prevalence of hyperlipidemia (44% vs. 33%; P = .04)
- Had a higher prevalence of diabetes (35% vs. 24%; P = .02)
- Were more likely to have a history of previous myocardial infarction (MI) (16% vs. 6%; P = .009)
- Were more likely to present with non–ST-elevation ACS (41% vs. 30%; P=0.04)
- Had a higher median level of high-sensitivity C-reactive protein (hsCRP) (4.98 vs. 3.00 mg/L; P = .03)
Angiographic Data
Healed plaques were more likely than nonlayered plaques to be complex (B2/C type) (72% vs. 59%; P = .02) and had a higher prevalence of multivessel disease (56% vs. 39%; P = .004). In addition, the average degree of stenosis was significantly higher (70% vs. 66%; P = .03).
OCT Data
Healed plaques were more likely than nonlayered plaques to exhibit:
- Plaque rupture (65% vs. 53%; P = .04)
- Lipid plaque (83% vs. 71%; P = .01)
- Thin cap fibroatheroma (TCFA), which is a precursor lesion that is prone to rupture (57% vs. 43%; P = .02)
- Accumulation of macrophages, which play a pivotal role in extracellular matrix degradation and fibrous cap disruption (80% vs. 56%; P = .001)
Subgroup Analysis
Healed plaques were further classified based on the number of detectable layers: single-layered (70%) or multilayered, indicative of multiple previous thrombotic events (30%).
On OCT analysis, the average area of stenosis significantly increased depending on the number of layers: 74% in nonlayered plaques, 78% in single-layered and 82% in multilayered (P = .002).
These data confirm a previous study that suggested repetitive episodes of subclinical thrombosis and subsequent healing are frequently the mechanism of plaque progression.
One-Year Clinical Outcomes
One-year follow-up data were available for 226 patients (60%). The incidence of death, acute MI and ischemia-driven revascularization were similar between patients with and without healed plaque. Only the rehospitalization rate was significantly higher in patients with healed plaque (33% vs. 17%; P = .01).
The Need for Aggressive Secondary Prevention
Patients with a healed plaque are predisposed to develop an acute coronary event, the researchers conclude. They call out TCFA, inflammation (higher hsCRP and macrophage infiltration) and greater plaque burden as features that may outweigh the protective mechanism of the body's repair phenomenon.
The researchers recommend that when a layered plaque is identified at the culprit lesion in an ACS patient, physicians should consider more intensive anti-inflammatory, antithrombotic and lipid-lowering therapy, not only to prevent future major cardiac events but also to minimize the chance of rapid plaque progression.
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