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Backgrounds: Coronary computed tomography angiography (CTA) allows for the assessment of atherosclerotic plaque burden across the entire coronary vasculature. No studies have examined the relationship between the underlying pathology of the culprit lesion and total plaque burden in patients with acute coronary syndromes. The aim of this study was to compare the total plaque burden between patients with plaque rupture versus plaque erosion., Methods: A total of 232 patients who presented with their first non-ST-segment elevation acute coronary syndrome and underwent both CTA and optical coherence tomography imaging before intervention were selected. Quantitative analysis was performed using semi-automated software (Autoplaque version 3.0, Cedars-Sinai Medical Center). An attenuation of <30 Hounsfield units defined low-density non-calcified plaque (LDNCP). All 3 vessels were assessed using the modified 17-segment American Heart Association model for coronary segment classification., Results: Among 232 patients, 125 (53.9%) had plaque rupture and 107 (46.1%) had plaque erosion. Total plaque burden (48.2 [39.8-54.9] % vs. 44.1 [38.6-50.0] %, P ​= ​0.006), total non-calcified plaque (NCP) burden (46.6 [39.1-53.3] % vs. 43.0 [37.6-49.2] %, P ​= ​0.013), total LDNCP burden (2.3 [1.4-3.0] % vs. 1.7 [1.2-2.6] %, P ​= ​0.016), and total calcified plaque (CP) burden (0.8 [0.1-1.6] % vs. 0.4 [0.0-1.4] %, P ​= ​0.047) were significantly greater in patients with culprit plaque rupture than in those with culprit plaque erosion., Conclusion: Patients with plaque rupture, compared with those with plaque erosion, had a greater total plaque burden, NCP burden, LDNCP burden, and CP burden., Clinical Trial Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT04523194., Competing Interests: Declaration of competing interest Disclosures: Dr. Niida received a grant from the Japan Heart Foundation/Bayer Yakuhin Research Grant Abroad. Outside the present study, Dr. Dey has received software royalties from Cedars-Sinai Medical Center and has a patent. Dr. Ferencik has received consulting fees from Siemens Healthineers, HeartFlow, and Elucid and stock options from Elucid. Dr. Jang has received educational grants from Abbott Vascular and a consulting fee from Svelte Medical Systems. The remaining authors have nothing to disclose., (Copyright © 2024 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

Background: The relationship between plaque burden and microscopic characterization of plaque features as it pertains to clinical presentation has not been fully investigated. The aim of this study was to compare the relationship between plaque burden and plaque vulnerability in patients with acute coronary syndromes (ACS) versus chronic coronary syndrome (CCS)., Methods: Patients who underwent both coronary computed tomography angiography (CTA) and optical coherence tomography (OCT) before coronary intervention were enrolled. All plaques were detected in culprit vessels using CTA, and total plaque volume (TPV) and OCT features were assessed at the corresponding sites. All plaques were divided into three groups according to the tertile levels of TPV (low TPV: <96.5 ​mm 3 , moderate TPV: 96.5-164.7 ​mm 3 , high TPV: ≥164.8 ​mm 3 )., Results: A total of 990 plaques were imaged by OCT in 419 patients: 445 plaques in 190 (45.3%) patients with ACS and 545 in 229 (54.7%) with CCS. Macrophage was more prevalent in plaques with greater TPV in patients who presented with ACS but not in those who presented with CCS (low vs. moderate vs. high TPV group: macrophage 57.4% vs. 71.8% vs. 82.4% in ACS; 63.4% vs. 67.8% vs. 66.7% in CCS; interaction P ​= ​0.004). Lipid arc increased as TPV increased, especially in patients who presented with ACS. Conversely, the layer index increased as TPV increased in patients with CCS., Conclusion: Greater plaque burden was closely related to higher levels of plaque vulnerability in ACS and greater volume of layered plaque in CCS., Trial Registration: clinicaltrials.gov Identifier: NCT04523194., Competing Interests: Declaration of competing interest Dr. Jang reports receiving educational grants from Abbott Vascular. Dr. Ferencik has received consulting fees from Siemens Healthineers, HeartFlow, Elucid, and Biomarin, stock options from Elucid, and is on the advisory board of Cleerly. All other authors have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

Background: Protruding aortic plaque is known to be associated with an increased risk for future cardiac and cerebrovascular events. However, the relationship between protruding aortic plaque and coronary plaque characteristics has not been systematically investigated., Methods and Results: A total of 615 patients who underwent computed tomography angiography, and preintervention optical coherence tomography imaging were included. Coronary plaque characteristics were compared to evaluate coronary plaque vulnerability in patients with protruding aortic plaque on computed tomography angiography. 615 patients, the 186 (30.2%) patients with protruding aortic plaque were older and had more comorbidities such as hypertension, chronic kidney disease, and a prior myocardial infarction than those without. They also had a higher prevalence of coronary plaques with vulnerable features such as thin-cap fibroatheroma (85 [45.7%] versus 120 [28.0%], P <0.001), lipid-rich plaque (165 [88.7%] versus 346 [80.7%], P =0.014), macrophages (147 [79.0%] versus 294 [68.5%], P =0.008), layered plaque (117 [62.9%] versus 213 [49.7%], P =0.002), and plaque rupture (96 [51.6%] versus 111 [25.9%], P <0.001). Patients with protruding aortic plaque experienced more major adverse cardiac and cerebrovascular events, including all-cause mortality, nonfatal acute coronary syndromes, and stroke (27 [14.7%] versus 21 [4.9%], P <0.001; 8 [4.3%] versus 1 [0.2%], P <0.001; 5 [2.7%] versus 3 [0.7%], P =0.030; and 5 [2.7%] versus 2 [0.5%], P =0.013, respectively)., Conclusions: The current study demonstrates that patients with protruding aortic plaque have more features of coronary plaque vulnerability and are at increased risk of future adverse events.

Background: High cardiovascular mortality has been reported in young patients with diabetes. However, the underlying pathology in different age groups of patients with diabetes has not been studied., Methods and Results: The aim of this study was to investigate the plaque characteristics and underlying pathology of acute coronary syndrome in different age groups of patients with or without diabetes in a large cohort. Patients who presented with acute coronary syndrome and underwent preintervention optical coherence tomography imaging were included. Culprit plaque was classified as plaque rupture, plaque erosion, or calcified plaque and stratified into 5 age groups. Plaque characteristics including features of vulnerability were examined by optical coherence tomography. Among 1394 patients, 482 (34.6%) had diabetes. Patients with diabetes, compared with patients without diabetes, had a higher prevalence of lipid-rich plaque (71.2% versus 64.8%, P =0.016), macrophage (72.0% versus 62.6%, P <0.001), and cholesterol crystal (27.6% versus 19.7%, P <0.001). Both diabetes and nondiabetes groups showed a decreasing trend in plaque erosion with age (patients with diabetes, P =0.020; patients without diabetes, P <0.001). Patients without diabetes showed an increasing trend with age in plaque rupture ( P =0.004) and lipid-rich plaque ( P =0.018), whereas patients with diabetes had a high prevalence of these vulnerable features at an early age that remained high across age groups., Conclusions: Patients without diabetes showed an increasing trend with age in plaque rupture and lipid-rich plaque, whereas patients with diabetes had a high prevalence of these vulnerable features at an early age. These results suggest that atherosclerotic vascular changes with increased vulnerability start at a younger age in patients with diabetes., Registration: URL: https://www.clinicaltrials.gov; Unique identifiers: NCT04523194, NCT03479723. URL: https://www.umin.ac.jp/ctr/. Unique identifier: UMIN000041692.

Outcomes after myocardial infarction in women remain poor. The number of cardiovascular risk factors in women increase with age, however the relation between risk factors and culprit plaque characteristics in this population is poorly understood. The aim of the study was to investigate the relation between risk factors and culprit plaque characteristics in women with acute coronary syndrome (ACS). A total of 382 women who presented with ACS and underwent pre-intervention optical coherence tomography imaging of the culprit lesion were included in this analysis. The culprit plaques were categorized as plaque rupture, plaque erosion or calcified plaque, and then stratified by age and risk factors. The predominant pathology of ACS was plaque erosion in young patients (<60 years), which decreased with age (p <0.001). Current smokers had a high prevalence of plaque rupture (60%) and lipid plaque (79%). Women with diabetes tended to have more lipid plaque (70%) even at a young age. In women with hyperlipidemia, the prevalence of lipid plaques was modest in younger ages, but rose gradually with age (p <0.001). An increasing age trend for lipid plaque was also observed in women with hypertension (p = 0.03) and current smokers (p = 0.01). In conclusion, early treatment of risk factors such as diabetes in young women might be important before accelerated progression of atherosclerosis begins as age advances. Clinical trial registration: http://www.clinicaltrials.gov, NCT01110538, NCT03479723 and NCT02041650., Competing Interests: Declaration of Competing Interest Dr. Jang received educational grants from Abbott Vascular and consulting fees from Svelte Medical Systems, Inc. The authors have no competing interests to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Compared with plaque rupture, plaque erosion has distinct features, which can be diagnosed only by intravascular optical coherence tomography. Computed tomography angiography (CTA) features of plaque erosion have not been reported. The aim of the present study was to identify the CTA features specific for plaque erosion in patients with non-ST-segment elevation acute coronary syndromes to enable a diagnosis of erosion without invasive procedures. Patients with non-ST-segment elevation acute coronary syndromes who underwent preintervention CTA and optical coherence tomography imaging of culprit lesions were enrolled. Plaque volume and high-risk plaque (HRP) features were assessed by CTA. Among 191 patients, plaque erosion was the underlying mechanism in 89 patients (46.6%) and plaque rupture in 102 patients (53.4%). The total plaque volume (TPV) was lower in plaque erosion than in plaque rupture (133.6 vs 168.8 mm 3 , p = 0.001). Plaque erosion had a lower prevalence of positive remodeling than plaque rupture (75.3% vs 87.3%, p = 0.033). As the number of HRP features decreased, plaque erosion became more prevalent (p = 0.014). In the multivariable logistic regression analysis, lower TPV and less prevalent HRP features were associated with a higher prevalence of plaque erosion. The addition of TPV ≤116 mm 3 and HRP features ≤1 to the known predictors significantly increased the area under the curve of the plaque erosion prediction receiver operator characteristics. Plaque erosion, compared with plaque rupture, had a lower plaque volume and less prevalent HRP features. CTA may be helpful for identifying the underlying pathology of acute coronary syndromes., Competing Interests: Disclosures Dr. Jang has received educational grant support from Abbott Vascular and a consulting fee from Svelte Medical Systems. Outside the present study, Dr. Dey has received software royalties from Cedars-Sinai Medical Center and has a patent. Dr. Ferencik has received consulting fees from Siemens Healthineers, HeartFlow, and Elucid. The remaining authors have no conflicts of interest to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)

Background: Layered plaque is a signature of previous subclinical plaque destabilization and healing. Following plaque disruption, thrombus becomes organized, resulting in creation of a new layer, which might contribute to rapid step-wise progression of the plaque. However, the relationship between layered plaque and plaque volume has not been fully elucidated., Methods: Patients who presented with acute coronary syndromes (ACS) and underwent pre-intervention optical coherence tomography (OCT) and intravascular ultrasound (IVUS) imaging of the culprit lesion were included. Layered plaque was identified by OCT, and plaque volume around the culprit lesion was measured by IVUS., Results: Among 150 patients (52 with layered plaque; 98 non-layered plaque), total atheroma volume (183.3 mm 3 [114.2 mm 3 to 275.0 mm 3 ] vs. 119.3 mm 3 [68.9 mm 3 to 185.5 mm 3 ], p = 0.004), percent atheroma volume (PAV) (60.1%[54.7-60.1%] vs. 53.7%[46.8-60.6%], p = 0.001), and plaque burden (86.5%[81.7-85.7%] vs. 82.6%[77.9-85.4%], p = 0.001) were significantly greater in patients with layered plaques than in those with non-layered plaques. When layered plaques were divided into multi-layered or single-layered plaques, PAV was significantly greater in patients with multi-layered plaques than in those with single-layered plaques (62.1%[56.8-67.8%] vs. 57.5%[48.9-60.1%], p = 0.017). Layered plaques, compared to those with non-layered pattern, had larger lipid index (1958.0[420.9 to 2502.9] vs. 597.2[169.1 to 1624.7], p = 0.014)., Conclusion: Layered plaques, compared to non-layered plaques, had significantly greater plaque volume and lipid index. These results indicate that plaque disruption and the subsequent healing process significantly contribute to plaque progression at the culprit lesion in patients with ACS., Clinical Trial Registration: http://www., Clinicaltrials: gov , NCT01110538, NCT03479723, UMIN000041692., (© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Background: Vascular inflammation plays a key role in atherogenesis and in the development of acute coronary syndromes. Coronary inflammation can be measured by peri-coronary adipose tissue (PCAT) attenuation on computed tomography angiography. We examined the relationships between the level of coronary artery inflammation assessed by PCAT attenuation and coronary plaque characteristics by optical coherence tomography., Methods: A total of 474 patients (198 acute coronary syndromes and 276 stable angina pectoris) who underwent preintervention coronary computed tomography angiography and optical coherence tomography were included. To compare the relationships between the level of coronary artery inflammation and detailed plaque characteristics, we divided the subjects into high (n=244) and low (n=230) PCAT attenuation groups using a threshold value of -70.1 Hounsfield units., Results: The high PCAT attenuation group, compared with the low PCAT attenuation group, had more males (90.6% versus 69.6%; P <0.001), more non-ST-segment elevation myocardial infarction (38.5% versus 25.7%; P =0.003), and less stable angina pectoris (51.6% versus 65.2%; P =0.003). Aspirin, dual antiplatelet, and statins were less frequently used in the high PCAT attenuation group compared to the low PCAT attenuation group. Patients with high PCAT attenuation, compared with those with low PCAT attenuation, had lower ejection fraction (median 64% versus 65%; P =0.014) and lower levels of high-density lipoprotein cholesterol (median 45 versus 48 mg/dL; P =0.027). Optical coherence tomography features of plaque vulnerability were significantly more common in patients with high PCAT attenuation, compared to those with low PCAT attenuation, including lipid-rich plaque (87.3% versus 77.8%; P =0.006), macrophage (76.2% versus 67.8%; P =0.041), microchannels (61.9% versus 48.3%; P =0.003), plaque rupture (38.1% versus 23.9%; P <0.001), and layered plaque (60.2% versus 50.0%; P =0.025)., Conclusions: Optical coherence tomography features of plaque vulnerability were significantly more common in patients with high PCAT attenuation, compared with those with low PCAT attenuation. Vascular inflammation and plaque vulnerability are intimately related in patients with coronary artery disease., Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT04523194.

Background: Vascular inflammation has been recognized as one of the key factors in the pathogenesis of acute coronary syndromes (ACS). Pericoronary adipose tissue (PCAT) attenuation by computed tomography angiography has emerged as a marker specific for coronary artery inflammation. We examined the relationship between clinical presentation and coronary artery inflammation assessed by PCAT attenuation and coronary plaque characteristics., Methods: Patients with ACS or stable angina pectoris (SAP) who underwent preintervention coronary computed tomography angiography and optical coherence tomography were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries. PCAT attenuation and optical coherence tomography findings were compared between patients with ACS versus SAP., Results: Among 471 patients (ACS: 198, SAP: 273), PCAT attenuation was higher in ACS patients than in SAP patients both at the culprit plaque level (-67.5±9.6 Hounsfield unit [HU] versus -71.5±11.0 HU, P< 0.001) and at the culprit vessel level (-68.3±7.7 HU versus -71.1±7.9 HU, P< 0.001). The mean PCAT attenuation of all 3 coronary arteries was also significantly higher in ACS patients than in SAP patients (-68.8±6.3 HU versus -70.5±7.1 HU, P =0.007). After adjusting patient characteristics, not only thin-cap fibroatheroma (OR: 3.41; 95% CI: 1.89-6.17) and macrophages (OR: 3.32; 95% CI: 1.76-6.26) but also PCAT attenuation around the culprit plaque (OR: 1.03; 95% CI: 1.00-1.05) was associated with the clinical presentation of ACS., Conclusions: PCAT attenuation at culprit plaque, culprit vessel, and pan-coronary levels was higher in ACS patients than in SAP patients. Vascular inflammation appears to play a crucial role in the development of ACS., Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT04523194.

Background: Despite the significant decline in cardiovascular mortality in women over the past several decades, sex differences in the underlying pathology of acute coronary syndromes remain poorly understood. Previous postmortem studies have demonstrated sex differences in coronary plaque morphology with a higher prevalence of plaque erosion in young women and more plaque rupture in older women after menopause, whereas men showed no increase in prevalence of plaque rupture with age. However, in vivo data are limited., Methods: This study included patients who presented with acute coronary syndrome and underwent preintervention optical coherence tomography imaging of the culprit lesion. The culprit plaque was categorized as plaque rupture, plaque erosion or culprit plaque with calcification, and stratified by age. Features of plaque vulnerability at culprit lesion were also analyzed., Results: In 1368 patients (women=286), women and men had a similar distribution of culprit plaque morphology (plaque rupture versus plaque erosion). However, significant sex differences were found in the underlying mechanisms of acute coronary syndrome among different age groups: women showed a significant ascending trend with age in plaque rupture ( P <0.001) and the features of plaque vulnerability such as lipid plaque ( P <0.001), thin-cap fibroatheroma ( P =0.005), and microstructures including macrophages, cholesterol crystals, and calcification ( P =0.026). No trend was observed in men., Conclusions: Age related sex differences in culprit plaque morphology and vulnerability were identified in patients with acute coronary syndrome: prevalence of plaque rupture and vulnerability increased with age in women but not in men., Registration: URL: https://www., Clinicaltrials: gov; Unique identifier: NCT01110538 and NCT03479723.

Objectives: The aim of this study was to compare the level of coronary inflammation between plaque rupture and plaque erosion using pericoronary adipose tissue (PCAT) attenuation., Background: Vascular inflammation plays a key role in plaque rupture, while the role of inflammation in plaque erosion remains less well defined. PCAT attenuation determined using computed tomography has emerged as a marker specific for coronary artery inflammation., Methods: Patients with non-ST-segment elevation acute coronary syndromes who underwent preintervention coronary computed tomographic angiography and optical coherence tomographic culprit lesion imaging were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries., Results: Among 198 patients, plaque rupture was the underlying mechanism in 107 (54.0%) and plaque erosion in 91 (46.0%). Plaque rupture had higher PCAT attenuation than plaque erosion both at the culprit plaque level (-65.8 ± 7.5 HU vs -69.5 ± 11.4 HU; P = 0.010) and at the culprit vessel level (-67.1 ± 7.1 HU vs -69.6 ± 8.2 HU; P = 0.024). The mean PCAT attenuation of all 3 coronary arteries was also significantly higher in patients with plaque rupture than in plaque erosion, indicating a higher level of inflammation (-67.9 ± 5.7 HU vs -69.9 ± 6.8 HU; P = 0.030). In multivariable analysis, plaque rupture was significantly associated with high PCAT attenuation., Conclusions: PCAT attenuation in culprit plaque, culprit vessel, and all 3 coronary arteries was higher in plaque rupture than in plaque erosion. The results suggest that pancoronary inflammation plays a more significant role in plaque rupture than in plaque erosion. (Massachusetts General Hospital and Tsuchiura Kyodo General Hospital Coronary Imaging Collaboration; NCT04523194)., Competing Interests: Funding Support and Author Disclosures Dr Jang’s research was supported by Mr and Mrs Allan and Gill Gray and by Mr and Mrs Michael and Kathryn Park. Dr Dey is supported by National Heart, Lung, and Blood Institute grants (1R01HL148787-01A1 and 1R01HL151266). The funders had no role in the design or conduct of this research. Dr Jang has received educational grant support from Abbott Vascular; and consulting fees from Svelte Medical Systems and Mitobridge. Outside the present study, Dr Dey has received software royalties from Cedars-Sinai Medical Center; and has a patent. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2022 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Recently, layered plaque, an optical coherence tomography equivalent of healed plaque, has been gaining attention. However, detailed layered plaque characteristics including the burden of plaque layer have not been investigated. Patients with acute coronary syndromes who underwent preintervention optical coherence tomography imaging of culprit lesion were included. Layer index, a product of the mean layer arc and layer length, was correlated with the pattern of layer and culprit pathology. In addition, layer index was compared between culprit and nonculprit plaques. Finally, predictors for greater layer index were identified using general linear modeling. In 349 patients, 99 culprit plaques had layered phenotype (28.4%), whereas among 465 nonculprit plaques, 165 had layered pattern (35.5%). Layer index was greater in multilayer pattern versus single-layer pattern (1,688.5 vs 996.6, p <0.001), interrupted layer phenotype versus intact layer phenotype (1,276.5 vs 646.8, p <0.001), rupture versus erosion at culprit lesion (1,191.0 vs 861.8, p <0.001), and culprit versus nonculprit plaque (1,475.6 vs 983.4, p <0.001). The general linear modeling revealed that multilayer pattern (regression coefficient b [B] 7.332, p <0.001), interrupted layer phenotype (B 4.624, p <0.001), culprit lesion (B 2.792, p = 0.001), lipid-rich plaque (B 1.953, p = 0.032), and culprit plaque rupture (B: 1.943, p = 0.008) were the significant predictors for greater layer index. In conclusion, layer index (burden of layered plaque) was greater in multilayer pattern, interrupted layer phenotype, at culprit plaque, lipid-rich plaque, and in cases with culprit plaque rupture., Competing Interests: Disclosures The authors have no conflicts of interest to declare., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Background: South Asians, and Indians in particular, are known to have a higher incidence of premature atherosclerosis and acute coronary syndromes (ACS) with worse clinical outcomes, compared to populations with different ethnic backgrounds. However, the underlying pathobiology accounting for these differences has not been fully elucidated., Methods: ACS patients who had culprit lesion optical coherence tomography (OCT) imaging were enrolled. Culprit plaque characteristics were evaluated using OCT., Results: Among 1315 patients, 100 were South Asian, 1009 were East Asian, and 206 were White. South Asian patients were younger (South Asians vs. East Asians vs. Whites: 51.6 ± 13.4 vs. 65.4 ± 11.9 vs. 62.7 ± 11.7; p < 0.001) and more frequently presented with ST-segment elevation myocardial infarction (STEMI) (77.0% vs. 56.4% vs. 35.4%; p < 0.001). On OCT analysis after propensity group matching, plaque erosion was more frequent (57.0% vs. 38.0% vs. 50.0%; p = 0.003), the lipid index was significantly greater (2281.6 [1570.8-3160.6] vs. 1624.3 [940.9-2352.4] vs. 1303.8 [1090.0-1757.7]; p < 0.001), and the prevalence of layered plaque was significantly higher in the South Asian group than in the other two groups (52.0% vs. 30.0% vs. 34.0%; p = 0.003)., Conclusions: Compared to East Asians and Whites, South Asians with ACS were younger and more frequently presented with STEMI. Plaque erosion was the predominant pathology for ACS in South Asians and their culprit lesions had more features of plaque vulnerability., Clinical Trial Registration: http://www.clinicaltrials.gov, NCT03479723., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Background A recent study reported that the outcome of patients with plaque erosion treated with stenting is poor when the underlying plaque is lipid rich. However, the detailed phenotype of patients with plaque erosion, particularly as related to different age groups, has not been systematically studied. Methods and Results Patients with acute coronary syndromes caused by plaque erosion were selected from 2 data sets. Demographic, clinical, angiographic, and optical coherence tomography findings of the culprit lesion were compared between 5 age groups. Among 579 erosion patients, male sex and current smoking were less frequent, and hypertension, diabetes, and chronic kidney disease were more frequent in older patients. ST-segment-elevation myocardial infarction was more frequent in younger patients. Percentage of diameter stenosis on angiogram was greater in older patients. The prevalence of lipid-rich plaque (27.3% in age <45 years and 49.4% in age ≥75 years, P <0.001), cholesterol crystal (3.9% in age <45 years and 21.8% in age ≥75 years, P =0.027), and calcification (5.5% in age <45 years and 54.0% in age ≥75 years, P <0.001) increased with age. After adjusting risk factors, younger patients were associated with the presence of thrombus, and older patients were associated with greater percentage of diameter stenosis and the presence of lipid-rich plaque and calcification. Conclusions The demographic, clinical, angiographic, and plaque phenotypes of patients with plaque erosion distinctly vary depending on age. This may affect the clinical outcome in these patients. Registration URL: https://www.clinicaltrials.gov. Unique identifiers: NCT03479723, NCT02041650.

Objectives: This study sought to identify morphological predictors of rapid plaque progression., Background: Two patterns of plaque progression have been described: slow linear progression and rapid step-wise progression. The former pattern will cause stable angina when the narrowing reaches a critical threshold, whereas the latter pattern may lead to acute coronary syndromes or sudden cardiac death., Methods: Patients who underwent optical coherence tomography (OCT) imaging during the index procedure and follow-up angiography with a minimum interval of 6 months were selected. Nonculprit lesions with a diameter stenosis of ≥30% on index angiography were assessed. Lesion progression was defined as a decrease of angiographic minimum lumen diameter ≥0.4 mm at follow-up (mean, 7.1 months). Baseline morphological characteristics of plaques with rapid progression were evaluated by OCT. In a subgroup with follow-up OCT imaging for plaques with rapid progression, morphological changes from baseline to follow-up were assessed., Results: Among 517 lesions in 248 patients, 50 lesions showed rapid progression. These lesions had a significantly higher prevalence of lipid-rich plaque (76.0% vs. 50.5%, respectively), thin-cap fibroatheroma (TCFA) (20.0% vs. 5.8%, respectively), layered plaque (60.0% vs. 34.0%, respectively), macrophage accumulation (62.0% vs. 42.4%, respectively), microvessel (46.0% vs. 29.1%, respectively), plaque rupture (12.0% vs. 4.7%, respectively), and thrombus (6.0% vs. 1.1%, respectively) at baseline compared with those without rapid progression. Multivariate analysis identified lipid-rich plaque (odds ratio [OR]: 2.17; 95% confidence interval [CI]: 1.02 to 4.62; p = 0.045]), TCFA (OR: 5.85; 95% CI: 2.01 to 17.03; p = 0.001), and layered plaque (OR: 2.19; 95% CI: 1.03 to 4.17; p = 0.040) as predictors of subsequent rapid lesion progression. In a subgroup analysis for plaques with rapid progression, a new layer was detected in 25 of 41 plaques (61.0%) at follow-up., Conclusions: Lipid-rich plaques, TCFA, and layered plaques were predictors of subsequent rapid plaque progression. A new layer, a signature of previous plaque disruption and healing, was detected in more than half of the lesions with rapid progression at follow-up. (Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538)., Competing Interests: Funding Support and Author Disclosures Dr. Jang has received educational grants from Abbott Vascular; and research was supported by Mr. and Mrs. Michael and Kathryn Park and by Mrs. and Mr. Gill and Allan Gray, who had no role in the design or conduct of this research. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2021 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Antiplatelet agents and statin therapies are widely used in patients with known cardiovascular disease. Plaque rupture (PR) and plaque erosion (PE) are the most frequent underlying mechanisms of acute coronary syndromes (ACS). The conditions and medications that are associated with ST-segment elevation myocardial infarction (STEMI) following PR or PE have not been systematically studied. A total of 838 ACS patients (494 with STEMI, 344 with NSTE-ACS) who were diagnosed with PR or PE by optical coherence tomography were included. The patients were categorized into two groups based on underlying pathology, and the baseline characteristics and culprit plaque morphology associated with STEMI were investigated within each group. Among 838 patients, 467 (55.7%) had PR, and 371 (44.3%) were diagnosed with PE. Among patients with PR, older age, hyperlipidemia, no antiplatelet therapy, higher level of low-density lipoprotein cholesterol, and greater lipid burden and macrophage infiltration were associated with increased probability of STEMI. Among patients with PE, no dual antiplatelet therapy and no statin therapy were associated with increased probability of STEMI. The incidence of STEMI caused by PR was significantly lower on antiplatelet therapy (P < 0.001), and the incidence of STEMI caused by PE was significantly lower on antiplatelet therapy (P < 0.001) or on statin therapy (P < 0.001). Antiplatelet therapy is associated with lower probability of STEMI, regardless of underlying pathology, and statin therapy is associated with lower probability of STEMI in PE as clinical presentation of ACS. Statin therapy prior to the onset of acute coronary syndromes (ACS) may reduce the probability of plaque rupture. Antiplatelet therapy prior to the onset of ACS is associated with reduced probability of ST-segment elevation myocardial infarction (STEMI) following both plaque rupture and plaque erosion, and dual antiplatelet therapy offers additional protection compared to a single antiplatelet agent in plaque erosion. The combination of statin and antiplatelet therapy may have an additive effect on reducing the probability of STEMI caused by plaque erosion. Yellow: lipid pool(necrotic core); red: fibrin-rich thrombus; gray; platelet-rich thrombus.

Background: Despite the exposure of the entire vasculature to the atherogenic effects of systemic risk factors, atherosclerotic plaques preferentially develop at sites with disturbed flow. This study aimed at exploring in vivo the relationship between local endothelial shear stress (ESS) and coronary plaque characteristics in humans using computational fluid dynamics and frequency-domain optical coherence tomography., Methods and Results: Three-dimensional coronary artery reconstruction was performed in 21 patients (24 arteries) presenting with acute coronary syndrome using frequency-domain optical coherence tomography and coronary angiography. Each coronary artery was divided into sequential 3-mm segments and analyzed for the assessment of local ESS and plaque characteristics. A total of 146 nonculprit segments were evaluated. Compared with segments with higher ESS [≥1 Pascal (Pa)], those with low ESS (<1 Pa) showed higher prevalence of lipid-rich plaques (37.5% versus 20.0%; P=0.019) and thin-cap fibroatheroma (12.5% versus 2.0%; P=0.037). Overall, lipid plaques in segments with low ESS had thinner fibrous cap (115 μm [63-166] versus 170 μm [107-219]; P=0.004) and higher macrophage density (normalized standard deviation: 8.4% [4.8-12.6] versus 6.2% [4.2-8.8]; P=0.017). Segments with low ESS showed more superficial calcifications (minimum calcification depth: 93 μm [50-140] versus 152 μm [105-258]; P=0.049) and tended to have higher prevalence of spotty calcifications (26.0% versus 12.0%; P=0.076)., Conclusions: Coronary regions exposed to low ESS are associated with larger lipid burden, thinner fibrous cap, and higher prevalence of thin-cap fibroatheroma in humans. Frequency-domain optical coherence tomography-based assessment of ESS and wall characteristics may be useful in identifying vulnerable coronary regions., Clinical Trial Registration Url: http://www.clinicaltrials.gov. Unique identifier: NCT01110538., (© 2014 American Heart Association, Inc.)

Objectives: The study sought to identify specific morphological characteristics of ruptured culprit plaques (RCP) responsible for acute events, and compare them with ruptured nonculprit plaques (RNCP) and nonruptured thin-cap fibroatheroma (TCFA) in patients presenting with acute coronary syndromes (ACS)., Background: Nonruptured TCFA and multiple ruptured plaques are detected in the same patients with ACS. It remains unknown whether certain morphological characteristics determine rupture of TCFA and subsequently result in ACS., Methods: We analyzed 126 plaques (RCP = 49, RNCP = 19, TCFA = 58) from 82 ACS patients using optical coherence tomography (OCT) and intravascular ultrasound (IVUS). Fibrous cap thickness was determined by OCT. Plaque burden and lumen area were measured with IVUS., Results: Fibrous cap was thinner in RCP (43 ± 11 μm) and RNCP (41 ± 10 μm) than in TCFA (56 ± 9 μm, p < 0.001 and p < 0.001, respectively). Plaque burden was greater in RCP (82 ± 7.2%), compared with RNCP (64 ± 7.2%, p < 0.001) and TCFA (62 ± 12.5%, p < 0.001). Lumen area was smaller in RCP (2.1 ± 0.9 mm(2)), compared with RNCP (4.6 ± 2.3 mm(2), p = 0.001) and TCFA (5.1 ± 2.7 mm(2), p < 0.001). The fibrous cap thickness <52 μm had good performance in discriminating ruptured plaque from TCFA (area under the curve [AUC] = 0.857, p < 0.001), and plaque burden >76% and lumen area <2.6 mm(2) had good performance in discriminating RCP from RNCP and TCFA (AUC = 0.923, p < 0.001 and AUC = 0.881, p < 0.001, respectively)., Conclusions: Fibrous cap thickness is a critical morphological discriminator between ruptured plaques and nonruptured TCFA, while plaque burden and lumen area appear to be important morphological features of RCP. These findings suggest that plaque rupture is determined by fibrous cap thickness, and a combination of large plaque burden and luminal narrowing result in ACS., (Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: Recent studies described different clinical and underlying plaque characteristics between patients with and without plaque rupture presenting with acute coronary syndrome (ACS). In light of the systemic nature of atherosclerosis, we hypothesized that nonculprit plaques might also express different morphological features in these 2 groups of patients., Methods: Thirty-eight patients with ACS who underwent 3-vessel optical coherence tomography imaging were identified from the Massachusetts General Hospital Optical Coherence Tomography Registry. Based on culprit plaque morphology, the study population was divided into 2 groups: patients with plaque rupture at the culprit lesion (group 1) and patients with nonruptured plaque at the culprit lesion (group 2). Prevalence and features of nonculprit plaques were compared between the 2 groups., Results: A total of 118 nonculprit plaques were analyzed. Patients in group 1 (n = 17) had nonculprit plaques with higher prevalence of thin-cap fibroatheroma (52.9% vs 19.0%, P = .029) and disruption (35.3% vs 4.8%, P = .016) compared with patients in group 2 (n = 21). Nonculprit plaques in group 1 showed wider maximum lipid arc (198.9° ± 41.7° vs 170.2° ± 41.9°, P = .003), greater lipid length (7.8 ± 4.4 mm vs 5.1 ± 2.4 mm, P = .003), higher lipid index (1196.9 ± 700.5 vs 747.7 ± 377.3, P = .001), and thinner fibrous cap (107.0 ± 56.5 μm vs 137.3 ± 69.8 μm, P = .035) compared with those in group 2., Conclusions: The present study showed distinctive features of nonculprit plaques between patients with ACS caused by plaque rupture and patients with ACS caused by nonruptured plaques. Patients with plaque rupture had increased pancoronary vulnerability in nonculprit plaques, suggesting that a more aggressive treatment paradigm aiming at the stabilization of vulnerable plaques may offer additional benefit to these patients., (© 2014.)

Objectives: The aim of this study was to characterize the morphological features of plaque erosion and calcified nodule in patients with acute coronary syndrome (ACS) by optical coherence tomography (OCT)., Background: Plaque erosion and calcified nodule have not been systematically investigated in vivo., Methods: A total of 126 patients with ACS who had undergone pre-intervention OCT imaging were included. The culprit lesions were classified as plaque rupture (PR), erosion (OCT-erosion), calcified nodule (OCT-CN), or with a new set of diagnostic criteria for OCT., Results: The incidences of PR, OCT-erosion, and OCT-CN were 43.7%, 31.0%, and 7.9%, respectively. Patients with OCT-erosion were the youngest, compared with those with PR and OCT-CN (53.8 ± 13.1 years vs. 60.6 ± 11.5 years, 65.1 ± 5.0 years, p = 0.005). Compared with patients with PR, presentation with non-ST-segment elevation ACS was more common in patients with OCT-erosion (61.5% vs. 29.1%, p = 0.008) and OCT-CN (100% vs. 29.1%, p < 0.001). The OCT-erosion had a lower frequency of lipid plaque (43.6% vs. 100%, p < 0.001), thicker fibrous cap (169.3 ± 99.1 μm vs. 60.4 ± 16.6 μm, p < 0.001), and smaller lipid arc (202.8 ± 73.6° vs. 275.8 ± 60.4°, p < 0.001) than PR. The diameter stenosis was least severe in OCT-erosion, followed by OCT-CN and PR (55.4 ± 14.7% vs. 66.1 ± 13.5% vs. 68.8 ± 12.9%, p < 0.001)., Conclusions: Optical coherence tomography is a promising modality for identifying OCT-erosion and OCT-CN in vivo. The OCT-erosion is a frequent finding in patients with ACS, especially in those with non-ST-segment elevation ACS and younger patients. The OCT-CN is the least common etiology for ACS and is more common in older patients. (The Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538)., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Recent studies have reported the development of neoatherosclerosis inside stents and subsequent acute coronary syndrome secondary to disruption of neointimal hyperplasia. The aim of the study was to compare the characteristics of neointimal hyperplasia and its time course between bare metal stents (BMSs) and drug-eluting stents (DESs) using optical coherence tomography. A total of 138 stents were divided into 3 groups according to the follow-up period: early phase, <9 months (25 BMSs and 27 DESs); intermediate phase, ≥9 and <48 months (18 BMSs and 43 DESs); and delayed phase, ≥48 months (13 BMSs and 12 DESs). Optical coherence tomographic analysis included the presence of lipid-laden intima, percentage of lipid-rich plaque, and signal attenuation. The optical coherence tomographic findings were compared between the BMSs and DESs in each period, and the difference between the periods was also determined. In the early phase, a greater incidence of lipid-laden plaque (37% vs 8%, p = 0.02) and a greater percentage of lipid-rich plaque (12.9 ± 25.1% vs 1.2 ± 4.3%, p = 0.01) were found in the DESs than in the BMSs. In the intermediate phase, the DES group continuously showed a significantly greater incidence of lipid-laden plaque (63% vs 28%, p = 0.03) and greater percentage of lipid-rich plaque (24.8 ± 28.1% vs 4.1 ± 7.3%, p <0.01). In addition, signal attenuation was greater in the DES group, suggesting early changes in neointimal hyperplasia properties. In the delayed phase, lipid-laden plaque was the predominant type in both groups. In conclusion, lipid-rich neoatherosclerosis develops inside stents earlier in DESs than in BMSs. After 48 months, most restenotic stents will have developed lipid-laden neointima in both groups., (Copyright © 2012. Published by Elsevier Inc.)

Background: Patients with acute coronary syndrome (ACS) have a higher incidence of recurrent ischemic events. The aim of this study was to compare the plaque characteristics of nonculprit lesions between ACS and non-ACS patients using optical coherence tomography (OCT) imaging., Methods and Results: Patients who had 3-vessel OCT imaging were selected from the Massachusetts General Hospital (MGH) OCT Registry. MGH registry is a multicenter registry of patients undergoing OCT. The prevalence and characteristics of nonculprit plaques were compared between ACS and non-ACS patients. A total of 248 nonculprit plaques were found in 104 patients: 45 plaques in 17 ACS patients and 203 plaques in 87 non-ACS patients. Compared with plaques of non-ACS patients, plaques of ACS patients had a wider lipid arc (147.3 ± 29.5° versus 116.2 ± 33.7°, P<0.001), a longer lipid length (10.7 ± 5.9 mm versus 7.0 ± 3.7 mm, P=0.002), a larger lipid volume index [averaged lipid arc×lipid length] (1605.5 ± 1013.1 versus 853.4 ± 570.8, P<0.001), and a thinner fibrous cap (70.2 ± 20.2 µm versus 103.3 ± 46.8 µm, P<0.001). Moreover, thin-cap fibroatheroma (64.7% versus 14.9%, P<0.001), macrophage (82.4% versus 37.9%, P=0.001), and thrombus (29.4% versus 1.1%, P<0.001) were more frequent in ACS patients. Although the prevalence of microchannel did not differ between the groups, the closest distance from the lumen to microchannel was shorter in ACS subjects than in non-ACS (104.6 ± 67.0 µm versus 198.3 ± 133.0 µm, P=0.027)., Conclusions: Nonculprit lesions in patients with ACS have more vulnerable plaque characteristics compared with those with non-ACS. Neovascularization was more frequently located close to the lumen in patients with ACS.