Key result
Layered culprit plaques are linked to ~39% more multivessel disease and higher lipid plaque prevalence.
Why the study?
Healed plaques represent previous plaque destabilization and can be diagnosed in living patients, but their prevalence, angiographic, and optical coherence tomography features in stable angina pectoris required investigation.
Do patients with stable angina pectoris and layered culprit plaques have more vulnerable plaque features compared to those with nonlayered plaques?
Observational (n=163)
Do patients with stable angina pectoris and layered culprit plaques have more vulnerable plaque features compared to those with nonlayered plaques?
Absolute Event Rate: 62.1% vs 44.7%
p-value: p=0.027
In patients with stable angina pectoris, healed (layered) culprit plaques are common and associated with more vulnerable plaque features and advanced atherosclerosis.
Healed plaques associate with panvascular vulnerability in stable angina; leaves open whether OCT detection warrants intensified therapy or trials.
Objective: Healed plaques, signs of previous plaque destabilization, are frequently found in the coronary arteries. Healed plaques can now be diagnosed in living patients. We investigated the prevalence, angiographic, and optical coherence tomography features of healed plaques in patients with stable angina pectoris. Approach and Results: Patients with stable angina pectoris who had undergone optical coherence tomography imaging were included. Healed plaques were defined as plaques with one or more signal-rich layers of different optical density. Patients were divided into 2 groups based on layered or nonlayered phenotype at the culprit lesion. Among 163 patients, 87 (53.4%) had layered culprit plaque. Patients with layered culprit plaque had more multivessel disease (62.1% versus 44.7%, P =0.027) and more angiographically complex culprit lesions (64.4% versus 35.5%, P <0.001). Layered culprit plaques had higher prevalence of lipid plaque (83.9% versus 64.5%, P =0.004), macrophage infiltration (58.6% versus 35.5%, P =0.003), calcifications (78.2% versus 63.2%, P =0.035), and thrombus (28.7% versus 14.5%, P =0.029). Lipid index ( P =0.001) and percent area stenosis ( P =0.015) were greater in the layered group. The number of nonculprit plaques, evaluated using coronary angiograms, tended to be greater in patients with layered culprit plaque (4.2±2.5 versus 3.5±2.1, P =0.053). Nonculprit plaques in patients with layered culprit lesion had higher prevalence of layered pattern ( P =0.002) and lipid phenotype ( P =0.005). Lipid index ( P =0.013) and percent area stenosis ( P =0.002) were also greater in this group. Conclusions: In patients with stable angina pectoris, healed culprit plaques are common and have more features of vulnerability and advanced atherosclerosis both at culprit and nonculprit lesions.
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Russo et al. (2020) conducted an observational in Stable angina pectoris (n=163). Layered culprit plaque vs. Nonlayered culprit plaque was evaluated on Multivessel disease (p=0.027). In patients with stable angina pectoris, layered culprit plaques were associated with more multivessel disease (62.1% vs 44.7%, P=0.027) and higher prevalence of lipid plaque (83.9% vs 64.5%, P=0.004).
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