Healed Plaques in Patients With Stable Angina Pectoris

Abstract

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.

Prevalence of Healed Plaque and Factors Influencing Its Characteristics Under Optical Coherence Tomography in Patients With Coronary Artery Disease: A Systematic Review, Meta-Analysis, and Meta-Regression

“…Additionally, our results indicated that the prevalence of healed plaques was higher in culprit plaques (48%) than in non-culprit plaques (24%). As previously described, although non-culprit lesions associated with culprit events are more likely to approach 70% or more of plaque burden, and patients with non-culprit plaque rupture have a high-risk atherosclerosis phenotype of the whole coronary artery ( 31 , 32 ), healed culprit plaque in patients has a more layered and a more lipid plaque phenotype with more characteristics of plaque vulnerability ( 24 , 25 , 28 ). However, based on the previous studies mentioned above, more OCT-based studies are needed to clarify the characteristics of healed plaques combined with non-culprit plaques with or without the pursuant culprit lesions.…”

OCT Findings in MINOCA

“…The process of lesion progression to a layered plaque phenotype may take from weeks to months. Moreover, a recent OCT study reported that a layered plaque phenotype may be found in more than 50% of patients with stable angina [51]. To our knowledge, there was only one case report for the OCT finding of intraplaque hemorrhage.…”

Culprit and Non-Culprit Plaque Characteristics With vs. Without a Healed Phenotype in Patients With Acute Myocardial Infarction Caused by Plaque Erosion ― A 3-Vessel OCT Study ―

“…7 Russo et al had reported that plaques with healed phenotype at the culprit site showed more signs of vulnerability (more lipid plaque, greater lipid burden, and more macrophage infiltration) than non-healed ones. 18 Shimokado et al also found that microvessels and macrophages were more frequently identified in OCT-derived healed plaque. 5 Macrophages indicating higher local inflammation are the sign of plaque activity and play an important role in extracellular matrix degradation and fibrous cap disruption, as well as plaque progress.…”

“…23 In addition, patients with healed phenotype at the culprit site had a higher incidence of calcification than those without. Russo et al 18 For patient-based analysis of non-culprit lesions (Table 4, Figure 4), patients with healed plaque at the culprit site had higher incidence of lipid plaque (91.1% vs. 75.4%, P=0.025), microchannels (78.6% vs. 59.0%, P=0.023), cholesterol crystals (25.0% vs. 4.9%, P=0.003), calcification (58.9% vs. 39.3%, P=0.034) and healed plaque (69.6% vs. 42.6%, P=0.003) than those without healed plaque at the culprit site.…”