Imaging
Healed Coronary Plaque Assessed by Light-Based Intracoronary Imaging Techniques ― The Good, the Bad, and the Ugly? ―
2022 Volume 86 Issue 5 Pages 855-856
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2022 Volume 86 Issue 5 Pages 855-856
Healed coronary plaque (HCP) has been recognized as a potential substrate of plaque progression or acute coronary syndrome (ACS).1,2 Pathological studies have demonstrated that atherosclerotic plaques often destabilize without resulting in ACS.1,2 Burke et al reported that HCPs were identified in 53% of subjects who had no evidence of prior myocardial infarction but experienced sudden coronary death.2 Therefore, the onset of ACS likely depends on a balance between activation (instability) and passivation (healing) of atherosclerotic plaques. When atherosclerotic plaque rupture/disruption or superficial erosion occur in human coronary arteries, the exposure of necrotic core or other tissue factors stimulates local fibrin deposition and subsequent thrombus formation.3 The plaque healing process usually stems from the synthesis of a provisional extracellular matrix (e.g., proteoglycans and type III collagen) promoted by proliferating smooth muscle cells. Type III collagen is steadily replaced by type I collagen, and the plaque surface is re-endothelialized with neointimal tissue. Once the plaque healing process has been completed, the atherosclerotic plaque may undergo further cycles of destabilization and repeat healing, with accumulation of granulation tissue. It should thus be noted that plaque healing may differ from plaque stabilization, which is a progressive transformation of a lipid-rich plaque into a more fibrotic or calcific plaque (Figure).
A representative case presenting with plaque progression and healed coronary plaque. A 56-year-old man presented with progressive chest pain suggestive of acute coronary syndrome. He underwent percutaneous coronary intervention (PCI) and a drug-eluting stent was implanted in the proximal right coronary artery. (A) A post-procedural coronary angiogram showed mild stenosis at the distal right coronary artery (white arrow), whereas optical frequency domain imaging (OFDI) showed a thin-cap fibroatheroma (yellow arrows) and the surrounding lipid-rich plaque (white asterisks). (B) A repeat coronary angiogram 4 months after the PCI revealed apparent progression of the stenosis (white arrow), and OFDI investigation revealed a healed coronary plaque at the culprit site (yellow asterisks).
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HCP has recently gained academic and clinical interest in light of the development of light-based intracoronary imaging techniques such as optical coherence tomography (OCT) or optical frequency domain imaging (OFDI) that allow in vivo assessment of atherosclerotic plaque morphology and composition. Thanks to these imaging techniques, a HCP can be recognized as heterogeneous layers with a different optical signal intensity from that of underlying plaque. Shimokado et al validated the OCT-derived HCP in comparison with histopathological specimens,4 reporting an excellent agreement with sensitivity, specificity, positive predictive value, and negative predictive value of 81%, 98%, 93%, and 93%, respectively. Moreover, Shimokado et al. demonstrated that HCPs were observed in 77% (46/60) of lesions or subjects presenting with chronic coronary syndrome (CCS).4 However, it is sometimes challenging to differentiate intraplaque hemorrhage, which is another substrate of plaque progression, from HCP only on OCT or OFDI images.5 Intravascular ultrasound in conjunction with OCT could be useful in such ambiguous cases.
HCPs are more frequently identified in patients with CCS than those with ACS.6 In CCS, a serial OCT study demonstrated that 29% of non-culprit lesions showed HCP progression over time.7 Conversely in ACS, Fracassi et al investigated preprocedural OCT of the culprit vessel and identified HCPs in 29% (108/376) of patients.8 Dyslipidemia, diabetes, and a history of myocardial infarction were more common in patients with HCP than those without. OCT revealed that plaque rupture, thin-cap fibroatheroma, and macrophage accumulation were more common in patients with HCP. In addition, high-sensitivity C-reactive protein was significantly higher in patients with HCP. Interestingly, patients with HCP presented more frequently with non-ST-segment elevation ACS, and those without HCP presented more frequently with ST-segment elevation myocardial infarction than their counterparts.8 Recently Kurihara et al reported that patients with HCP had a greater risk of major adverse cardiac events (i.e., cardiac death, ACS, or revascularization) within 2 years after the index percutaneous coronary intervention, and the presence of HCP appeared to be an independent predictor of revascularizations.6
In this issue of Journal, Yin et al assessed plaque characteristics in patients with acute myocardial infarction due to plaque erosion in their 3-vessel OCT investigations.9 Their tremendous efforts and considerable experience with OCT investigations in ACS patients should be commended. As in the landmark EROSION study,10 the work of Yin et al addressed the clinical, angiographic, and OCT characteristics of patients with or without HCPs only in the phenotype of plaque erosion, which generally accounts for 20–40% of myocardial infarction. The authors demonstrated that patients presenting with HCP at the culprit site had dyslipidemia more frequently and had more diseased angiographic/OCT findings at both culprit and non-culprit lesions than patients without HCP.9 During the clinical follow-up of 25 months, the incidence rate of major adverse cardiac events (i.e., cardiac death, reinfarction, ischemia-driven revascularization, or rehospitalization due to unstable or progressive angina) in patients with HCP was nearly twice that in patients without HCP (22.2% vs. 11.5%), although the difference did not reach statistical significance.9 Obviously the sample size was too small or the follow-up period was too short to demonstrate definitive conclusions. In this regard it will be interesting to see studies with larger sample sizes and longer follow-up periods.
In conclusion, the plaque healing process is associated with plaque progression due to coronary atherosclerosis. From the perspective of intracoronary imaging, the OCT-derived HCP is considered as a footprint and a nidus of local thrombotic formation and inflammatory responses in the coronary vasculature. Such a thrombotic milieu may result in different clinical manifestations, namely silence (the “good”), unstable angina (the “bad”), or myocardial infarction (the “ugly”), depending on thrombogenicity and severity of the plaque burden or luminal narrowing. More intensive anti-inflammatory, antithrombotic therapies, as well as lipid-lowering therapy, should be considered not only to prevent future cardiovascular events, but also to minimize the risk of plaque progression over time whenever a HCP is identified at culprit or non-culprit lesions.
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