3-vessel Optical Coherence Tomography Research Articles

Pancoronary plaque characteristics in STEMI patients with rapid plaque progression: An optical coherence tomography study

BackgroundNon-culprit plaque progression is associated with recurrent cardiac ischemic events and worse clinical outcomes. Given that atherosclerosis is a systemic disease, the pancoronary characteristics of patients with rapid plaque progression are unknown. This study aims to identify pancoronary plaque features in patients with ST-segment elevation myocardial infarction (STEMI) with and without rapid plaque progression, focused on the patient level. Methods and resultsFrom January 2017 to July 2019, 291 patients underwent 3-vessel optical coherence tomography imaging at the time of the primary procedure and a follow-up angiography interval of 12 months. The final analysis included 237 patients. Overall, 308 non-culprit lesions were found in 78 STEMI patients with rapid plaque progression, and 465 non-culprit plaques were found in 159 STEMI patients without rapid plaque progression. These patients had a higher pancoronary vulnerability (CLIMA-defined high-risk plaque: 47.4% vs. 33.3%; non-culprit plaque rupture: 25.6% vs. 14.5%) and a significantly higher prevalence of other vulnerable plaque characteristics (i.e., lipid-rich plaque, cholesterol crystal, microchannels, calcification, spotty calcification, and thrombus) at baseline versus those without rapid plaque progression. Lesions with rapid progression were highly distributed at the LAD, tending to be near the bifurcation. In multivariate analysis, age ≥ 65 years was an independent predictor of subsequent rapid lesion progression at the patient level, whereas microchannel, spotty calcification, and cholesterol crystal were independent predictors for STEMI patients ≥65 years old. ConclusionsSTEMI patients with subsequent rapid plaque progression had higher pancoronary vulnerability and commonly presented vulnerable plaque morphology. Aging was the only predictor of subsequent rapid plaque progression.

Pancoronary plaque characteristics and clinical outcomes in acute coronary syndrome patients with cancer history

Background and aimsThe prevalence of acute coronary syndrome (ACS) patients with cancer history is increasing and it is associated with higher mortality. However, there is limited evidence on the characteristics of coronary plaque in ACS patients with cancer history. This study explored the pancoronary plaque characteristics in ACS patients with cancer history by optical coherence tomography (OCT). MethodsA total of 306 ACS patients treated by 3-vessel OCT at the time of percutaneous coronary intervention (PCI) were included, retrospectively. Patients were divided into two groups according to the presence or absence of cancer history: one group with cancer history (n = 98) and a matched group without cancer history (n = 208). ResultsA total of 314 culprit lesions and 514 nonculprit lesions were identified by OCT in this study. In culprit lesions, ACS patients with cancer history had higher incidence of thin cap fibroatheroma (TCFA) (p = 0.016), cholesterol crystals (p = 0.028), calcification (p = 0.001) and thrombus (p = 0.001), and had thinner fibrous cap thickness (FCT) (p = 0.011), greater maximum lipid arc (p = 0.042) and lipid index (p < 0.001), compared to matched ACS patients without cancer history. In nonculprit lesions, ACS patients with cancer history had higher prevalence of high-risk plaque (14.7% vs. 7.7%, p = 0.017), nonculprit rupture (14.7% vs. 6.3%, p = 0.003), and TCFA (52.2% vs. 28.3%, p < 0.001), and had higher incidence of calcification (p = 0.003), thrombus (p = 0.029), cholesterol crystals (p = 0.002) and microchannels (p = 0.029). These non-culprit lesions had longer lesion length (p = 0.001), thinner FCT (p < 0.001), greater maximum lipid arc (p = 0.016) and lipid index (p < 0.001). ConclusionsACS patients with cancer history showed more high-risk plaque features in culprit and nonculprit lesions, compared with ACS patients without cancer history. Therefore, ACS patients with cancer history may have greater pancoronary vulnerability. This may predict a poorer prognosis for ACS patients with cancer history.

Identification of High-Risk Coronary Lesions by 3-Vessel Optical Coherence Tomography

BackgroundOptical coherence tomography (OCT) may provide a method for detecting histologically defined high-risk plaques in vivo. ObjectivesThe authors aimed to investigate the prognostic value of OCT for identifying patients and lesions that are at risk for adverse cardiac events. MethodsBetween January 2017 and May 2019, OCT of all the 3 main epicardial arteries was performed in 883 patients with acute myocardial infarction (MI) who were referred for primary percutaneous coronary intervention. The primary endpoint was the composite of cardiac death, nonculprit lesion–related nonfatal MI, and unplanned coronary revascularization. Patients were followed for up to 4 years (median 3.3 years). ResultsThe 4-year cumulative rate of the primary endpoint was 7.2%. In patient-level analysis, thin-cap fibroatheroma (TCFA) (adjusted HR: 3.05; 95% CI: 1.67-5.57) and minimal lumen area (MLA) <3.5 mm2 (adjusted HR: 3.71; 95% CI: 1.22-11.34) were independent predictors of the primary endpoint. In lesion-level analysis, nonculprit lesions responsible for subsequent events were not angiographically severe at baseline (mean diameter stenosis 43.8% ± 13.4%). TCFA (adjusted HR: 8.15; 95% CI: 3.67-18.07) and MLA <3.5 mm2 (adjusted HR: 4.33; 95% CI: 1.81-10.38) were predictive of events arising from each specific lesion. TCFAs with an MLA <3.5 mm2 carried a higher risk and were sufficient for identifying patients at risk for the composite of cardiac death and nonculprit lesion–related nonfatal MI. ConclusionsOCT imaging of angiographically nonobstructive territories in patients with acute MI can aid in identifying patients and lesions at increased risk for adverse cardiac events.

Cholesterol crystals in non-culprit plaques of STEMI patients: A 3-vessel OCT study

BackgroundCholesterol crystals (CCs) are regular microstructures found within the necrotic core of atherosclerotic plaques and have been hypothesized to be related to plaque destabilization. We attempted to investigate the potential association between CCs and non-culprit plaque vulnerability in patients with ST-segment elevated myocardial infarction (STEMI) and study morphological features of CCs in ruptured non-culprit plaques. MethodsA total of 261 patients with ST-segment elevation myocardial infarction who underwent 3-vessel optical coherence tomography (OCT) imaging were included. Non-culprit plaques were divided into two groups according to the presence or absence of CCs in the plaque to compare the morphological characteristics of the plaques. The differences in parameters of the non-culprit plaque CCs were explored between ruptured plaques and unruptured plaques. ResultsTotally, 530 non-culprit plaques (29 ruptured plaques and 501 unruptured plaques) were identified by OCT. The incidence of CCs was 21.1%. Compared with non-culprit plaques without CCs, those with CCs had a larger lipid burden. Macrophages (p < 0.001) and spotty calcification (p = 0.002) were more frequently observed in non-culprit plaques with CCs. The frequency of CCs was significantly higher (p = 0.001) and the CCs were larger (p = 0.046) and more superficial (p = 0.005) in ruptured non-culprit plaques than in unruptured non-culprit plaques. The maximum lipid arc and fibrous cap thickness were independent predictors of plaque rupture, but the presence of CCs was not. ConclusionsNon-culprit plaques with CCs have more vulnerable features. CCs are more frequently found in ruptured non-culprit plaques and larger and more superficial CCs are associated with plaque rupture.

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.

Plaque erosion can occur quietly without causing clinical symptoms, followed by a healing process resulting in healed plaque. This study aimed to assess culprit and non-culprit plaque characteristics of patients with acute myocardial infarction (AMI) caused by plaque erosion with vs. without healed phenotype at the culprit plaque using optical coherence tomography (OCT).Methods and Results: A total of 117 AMI patients caused by plaque erosion who underwent OCT imaging of 3 coronary arteries were included. Patients were divided into 2 groups based on presence or absence of a healed phenotype at the culprit site. Culprit and non-culprit plaque characteristics were compared between the 2 groups. A healed phenotype at the culprit lesion was identified in 47.9% of AMI patients caused by plaque erosion. Patients with a healed phenotype at the culprit site were more frequently with hyperlipidemia, and had a higher prevalence of macrophage infiltration, microchannels, cholesterol crystals, and calcification at the culprit lesion. Moreover, patients with a healed phenotype at the culprit site had more non-culprit plaques and more characteristics of plaque vulnerability at the non-culprit lesion. In addition, patients with a healed phenotype at the culprit site presented with more severe luminal stenosis at both the culprit and non-culprit lesion. A healed phenotype was identified in 47.9% of AMI patients caused by plaque erosion at the culprit site. A healed phenotype within eroded culprit plaque was associated with signs of pancoronary vulnerability and advanced atherosclerosis.

Increased Vulnerability and Distinct Layered Phenotype at Culprit and Nonculprit Lesions in STEMI Versus NSTEMI

ObjectivesThis study aimed to investigate the pancoronary plaque vulnerability (including culprit and nonculprit lesions) and layered phenotype in patients with ST-segment elevation myocardial infarction (STEMI) vs non-STEMI (NSTEMI). BackgroundPancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis. MethodsA total of 464 patients with AMI who underwent 3-vessel optical coherence tomography imaging were consecutively studied and divided into a STEMI group (318 patients; 318 culprit and 1,187 nonculprit plaques) and a NSTEMI group (146 patients; 146 culprit and 560 nonculprit plaques). Patients were followed up for a median period of 2 years. ResultsCompared with NSTEMI, culprit lesions in STEMI had more plaque rupture, thrombus, thin-cap fibroatheroma (TCFA), calcification, macrophage accumulation, and microvessels. The prevalence of plaque rupture (8.2% vs 4.8%; P = 0.018), microvessels (57.5% vs 45.2%; P < 0.001), and calcification (40.7% vs 30.2%; P = 0.003) at nonculprit lesions was higher in STEMI than NSTEMI. The layer area and thickness at the culprit and nonculprit lesions were significantly larger in STEMI than in NSTEMI. Multivariate analyses showed that culprit layer area (odds ratio: 1.443; 95% CI: 1.138-1.830; P = 0.002) was predictive of STEMI (vs NSTEMI), in addition to culprit TCFA, culprit thrombus, and non–left circumflex artery location of the culprit lesion. Although the type of AMI was not related to clinical outcomes, high-sensitivity C-reactive protein, culprit calcified nodule, and nonculprit TCFA predicted the 2-year major adverse cardiovascular events in patients with AMI. ConclusionsPatients with STEMI had increased plaque vulnerability (ie, more plaque rupture and microvessels) and distinct layered phenotype at the culprit and nonculprit lesions compared with patients with NSTEMI. Culprit lesion features of large layer area, TCFA, thrombus, and non–left circumflex artery location predicted the clinical presentation of STEMI.

Association of the age shock index with coronary plaque characteristics in ST-segment elevation myocardial infarction: A 3-vessel optical coherence tomography study.

We investigated whether the age shock index (SI) was associated with coronary plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI) using optical coherence tomography (OCT). The age SI is a simple clinical parameter that effectively predicts poor clinical outcomes among patients with STEMI. This retrospective study evaluated 408 STEMI patients who underwent 3-vessel OCT during emergency percutaneous coronary interventions at a single center between January 2017 and October 2018. Patients were divided into groups with low or high age SI values (<41 vs. ≥41). Plaque characteristics were compared between the two groups for both culprit lesions (n = 408) and non-culprit lesions (n = 1,077). In culprit lesions, patients with a high age SI (≥41) were more likely to have plaque rupture (61.0% vs. 56.8%, p = .002) and thinner fibrous caps (fibrous cap thickness [FCT]: 40.0 [33.0-53.0] μm vs. 46.0 [36.0-63.8] μm, p = .021). In non-culprit lesions, patients with a high age SI were more likely to have high-risk plaques (29.9% vs. 17.8%, p = .018; simultaneous presence of a minimal lumen area of <3.5 mm2 , maximum lipid arc of >180°, FCT of <75 μm, and macrophage accumulation). Plaque-based analyses revealed that patients with a high age SI had larger lipid cores and lesser FCT. Patients with STEMI and a high age SI had increased risks of culprit plaque rupture and high-risk non-culprit plaques, and vulnerable plaque features at the culprit and non-culprit lesions. Therefore, a high age SI in patients with STEMI may indicate greater pancoronary vulnerability.

Pancoronary Plaque Characteristics in STEMI Caused by Culprit Plaque Erosion Versus Rupture: 3-Vessel OCT Study

ObjectivesThis study sought to investigate nonculprit plaque characteristics in patients with ST-segment elevation myocardial infarction (STEMI) presenting with plaque erosion (PE) and plaque rupture (PR). Pancoronary vulnerability was considered at nonculprit sites: 1) the CLIMA (Relationship Between OCT Coronary Plaque Morphology and Clinical Outcome) study (NCT02883088) defined high-risk plaques with simultaneous presence of 4 optical coherence tomography (OCT) features (minimum lumen area <3.5 mm2; fibrous cap thickness [FCT] <75 μm; maximum lipid arc >180º; and macrophage accumulation); and 2) the presence of plaque ruptures or thin-cap fibroatheromas (TCFA). BackgroundPE is a unique clinical entity associated with better outcomes than PR. There is limited evidence regarding pancoronary plaque characteristics of patients with culprit PE versus culprit PR. MethodsBetween October 2016 and September 2018, 523 patients treated by 3-vessel OCT at the time of primary percutaneous intervention were included with 152 patients excluded from final analysis. ResultsOverall, 458 nonculprit plaques were identified in 202 STEMI patients with culprit PE; and 1,027 nonculprit plaques were identified in 321 STEMI patients with culprit PR. At least 1 CLIMA-defined OCT nonculprit high-risk plaque was seen in 11.4% of patients with culprit PE, but twice as many patients were seen with culprit PR (25.2%; p < 0.001). This proportion was also seen when individual high-risk features were analyzed separately. When patients with PE were divided by a heterogeneous substrate (fibrous or lipid-rich plaque) underlying the culprit site, the prevalence of nonculprits with FCT <75 μm, macrophages, and TCFA showed a significant gradient from PE(Fibrous) to PElipid-rich plaque (LRP) to PR. Interestingly, nonculprit rupture was rarely found in patients with culprit PE(Fibrous) (1.9%), although it was exhibited with comparable prevalence in patients with culprit PE(LRP) (16.3%) versus PR (17.8%). Culprit PE predicted decreased pancoronary vulnerability independent of conventional risk factors. ConclusionsSTEMI patients with culprit PE have a limited pancoronary vulnerability that may explain better outcomes in these patients than in STEMI patients with culprit PR.

Frequency, Predictors, Distribution, and Morphological Characteristics of Layered Culprit and Nonculprit Plaques of Patients With Acute Myocardial Infarction: In Vivo 3-Vessel Optical Coherence Tomography Study.

Subclinical atherothrombosis and plaque healing may lead to rapid plaque progression. The histopathologic healed plaque has a layered appearance when imaged using optical coherence tomography. We assessed the frequency, predictors, distribution, and morphological characteristics of optical coherence tomography layered culprit and nonculprit plaques in patients with acute myocardial infarction. A prospective series of 325 patients with acute myocardial infarction underwent optical coherence tomography imaging of all 3 native coronary arteries. Layered plaque phenotype had heterogeneous signal-rich layered tissue located close to the luminal surface that was clearly demarcated from the underlying plaque. Layered plaques were detected in 74.5% of patients with acute myocardial infarction. Patients with layered culprit plaques had more layered nonculprit plaques; and they more often had preinfarction angina, ST-segment-elevation myocardial infarction, higher low-density lipoprotein cholesterol, and absence of antiplatelet therapy. Layered plaques tended to cluster in the proximal segment of the left anterior descending artery and left circumflex artery but were more uniformly distributed in the right coronary artery. As compared with nonlayered plaques, layered plaques had greater optical coherence tomography lumen area stenosis at both culprit and nonculprit sites. The frequency of layered plaque phenotype (P=0.038) and maximum area of layered tissue (P<0.001) increased from nonculprit thin-cap fibroatheromas to nonculprit ruptures to culprit ruptures. Layered plaques were identified in 3-quarters of patients with acute myocardial infarction, especially in the culprit plaques of patients with ST-segment-elevation myocardial infarction. Layered plaques had a limited, focal distribution in the left anterior descending artery, and left circumflex artery but were more evenly distributed in the right coronary artery and were characterized by greater lumen narrowing at both culprit and nonculprit sites. Graphic Abstract: A graphic abstract is available for this article.

Spatial Distribution of Vulnerable Plaques: Comprehensive In Vivo Coronary Plaque Mapping

ObjectivesThe authors performed a comprehensive analysis on the distribution of coronary plaques with different phenotypes from our 3-vessel optical coherence tomography (OCT) database. BackgroundPrevious pathology studies demonstrated that thin-cap fibroatheroma (TCFA) is localized in specific segments of the epicardial coronary arteries. A detailed description of in vivo coronary plaques of various phenotypes has not been reported. MethodsOCT images of all 3 coronary arteries in 131 patients were analyzed every 1 mm to assess plaque phenotype and features of vulnerability. In addition, plaques were divided into tertiles according to percent area stenosis (%AS). ResultsAmong 534 plaques identified in 393 coronary arteries, 27.0% were fibrous plaques, 13.3% were fibrocalcific plaques, 40.8% were thick-cap fibroatheromas, and 18.9% were TCFAs. TCFAs showed clustering in the proximal segment, particularly in the left anterior descending artery. On the other hand, fibrous plaques were relatively evenly distributed throughout the entire length of the coronary arteries. In patients with acute coronary syndromes (ACS), TCFAs showed stronger proximal clustering in the left anterior descending, 2 clustering peaks in the right coronary artery, and 1 clustering peak in the circumflex artery. The pattern of TCFA distribution was less obvious in patients without ACS. The prevalence of TCFA was higher in the highest %AS tertile, compared with the lowest %AS tertile (30% vs. 9%; p < 0.001). ConclusionsThe present 3-vessel OCT study showed that TCFAs cluster at specific locations in the epicardial coronary arteries, especially in patients with ACS. TCFA was more prevalent in segments with tight stenosis. (The Massachusetts General Hospital Optical Coherence Tomography Registry; NCT01110538)

Nonculprit Plaque Characteristics in Patients With Acute Coronary Syndrome Caused by Plaque Erosion vs Plaque Rupture

Patients with culprit plaque rupture are known to have pancoronary plaque vulnerability. However, the characteristics of nonculprit plaques in patients with acute coronary syndromes caused by plaque erosion are unknown. To investigate the nonculprit plaque phenotype in patients with acute coronary syndrome according to culprit plaque pathology (erosion vs rupture) by 3-vessel optical coherence tomography imaging. In this observational cohort study, between August 2010 and May 2014, 82 patients with acute coronary syndrome who underwent preintervention optical coherence tomography imaging of all 3 major epicardial coronary arteries were enrolled at the Massachusetts General Hospital Optical Coherence Tomography Registry database. Analysis of the data was conducted between November 2016 and July 2017. Patients were classified into 2 groups based on the culprit lesion pathology: 17 patients with culprit plaque erosion and 34 patients with culprit plaque rupture. Thirty-one patients with the absence of culprit rupture or erosion were excluded from further analysis. Preintervention 3-vessel optical coherence tomography imaging. Plaque characteristics at the culprit and nonculprit lesions evaluated by optical coherence tomography. In 51 patients (37 men; mean age, 58.7 years), the characteristics of 51 culprit plaques and 216 nonculprit plaques were analyzed. In patients with culprit erosion, the mean (SD) number of nonculprit plaques per patient was smaller (3.4 [1.9] in erosion vs 4.7 [2.1] in rupture, P = .05). Patient-based analysis showed that none of 17 patients with culprit plaque erosion had nonculprit plaque rupture, whereas 26% of the patients (9 of 34) with culprit plaque rupture had nonculprit plaque rupture (P = .02). Plaque-based analysis showed that, compared with the culprit rupture group (n = 158), the culprit erosion group (n = 58) had lower prevalence of plaque rupture (0% vs 8%; P < .001), macrophage accumulation (29% vs 53%; P = .01), microvessels (21% vs 42%; P = .003), and spotty calcium (5% vs 22%; P = .006) in the nonculprit lesions. The prevalence of lipid-rich plaque, thin-cap fibroatheroma, and thrombus did not differ between the groups. Compared with those with culprit plaque rupture, patients with acute coronary syndrome caused by culprit plaque erosion had a smaller number of nonculprit plaques and the lower levels of panvascular instability, affirming that distinct pathophysiologic mechanisms operate in plaque erosion and plaque rupture.

Correlation of Serum Uric Acid Levels with Nonculprit Plaque Instability in Patients with Acute Coronary Syndromes: A 3-Vessel Optical Coherence Tomography Study.

Elevated serum uric acid (SUA) level is known to be a prognostic factor in patients with acute coronary syndrome (ACS). However, the correlation between SUA level and coronary plaque instability has not been fully evaluated. The aim of this study was to investigate the association between SUA level and plaque instability of nonculprit lesions in patients with ACS using optical coherence tomography. A total of 150 patients with ACS who underwent 3-vessel optical coherence tomography were selected. Patients were classified into 3 groups according to tertiles of SUA level. There was a trend towards a thinner fibrous cap (0.15 ± 0.06 versus 0.07 ± 0.01 versus 0.04 ± 0.01 mm2, p < 0.001) and a wider mean lipid arc (169.41 ± 33.16 versus 177.22 ± 37.76 versus 222.43 ± 47.65°, p < 0.001) with increasing SUA tertile. The plaques of the high and intermediate tertile groups had a smaller minimum lumen area than the low tertile group (6.02 ± 1.11 versus 5.38 ± 1.28 mm2, p < 0.001). In addition, thin-cap fibroatheromas, microvessels, macrophages, and cholesterol crystals were more frequent in the high tertile group than the low and intermediate groups. Multivariate analysis showed SUA level to be a predictor of plaque instability.

Prevalence and Predictors of Multiple Coronary Plaque Ruptures

Objective— Plaque rupture may be the local expression of a widespread coronary instability. This study aimed to investigate: (1) the prevalence and characteristics of nonculprit plaque rupture; (2) the pancoronary atherosclerotic phenotype in patients with and without nonculprit plaque rupture; and (3) the prevalence and predictors of multiple plaque ruptures. Approach and Results— Six hundred and seventy-five nonculprit plaques from 261 patients (34 acute myocardial infarction, 73 unstable angina pectoris, and 154 stable angina pectoris) were analyzed by 3-vessel optical coherence tomography. Nonculprit plaque ruptures were identified in 51 patients (20%). Patients with nonculprit plaque ruptures had higher prevalence of thin-cap fibroatheroma (51% versus 13%; P &lt;0.001) in the 3 major epicardial coronary vessels. Multiple plaque ruptures were observed in 20% of patients (38% acute myocardial infarction versus 10% unstable angina pectoris versus 19% stable angina pectoris; P =0.042). Thin-cap fibroatheroma, intimal vasculature, and macrophages were independent morphological predictors of multiple plaque ruptures, whereas acute myocardial infarction and chronic kidney disease were independent clinical predictors. Patients with nonculprit plaque ruptures showed higher 1-year rates of nontarget lesion revascularization (11.8% versus 4.4%; P =0.039). Conclusions— Nonculprit plaque ruptures were observed in 20% of patients with coronary artery disease and were associated with pancoronary vulnerability and higher 1-year revascularization rate.

INCIDENCE AND PREDICTORS OF MULTIPLE CORONARY PLAQUE RUPTURES: A 3-VESSEL OPTICAL COHERENCE TOMOGRAPHY STUDY

Plaque instability may be a widespread process throughout the coronary vasculature. We sought to investigate in vivo the incidence and predictors of multiple plaque ruptures (PRs) using 3-vessel optical coherence tomography (OCT) imaging. We analyzed 783 coronary arteries in 261 patients [34 acute

Abstract 17709: Framingham Risk Score and Coronary Plaque Characteristics as Assessed by Three-Vessel Optical Coherence Tomography Imaging

Introduction: Clinical prediction models, such as the Framingham Risk Score (FRS), are useful to identify patients at high risk for future events. However, their association with coronary plaque features is largely unknown. Aim: This study aimed at evaluating the relationship between FRS and coronary plaque features by optical coherence tomography (OCT). Methods: FRS was assessed in 176 patients with coronary artery disease [72 with acute coronary syndrome (ACS), and 104 with stable angina] who underwent 3-vessel OCT imaging. Based on the FRS values, patients were divided into 3 groups: lower FRS (FRS&lt;5%, n=26), intermediate FRS (5%≤FRS&lt;10%, n=105), and higher FRS (FRS≥10%, n=45). Nonculprit coronary plaque features were compared among the 3 groups. Results: A total of 448 nonculprit plaques were identified (lower FRS, n=61; intermediate FRS, n=267; higher FRS, n=120). Compared to the patients with lower and intermediated FRS, those with higher FRS were older (p&lt;0.001), and more likely to have male gender (p&lt;0.001), diabetes (p=0.023), lower HDL-cholesterol (p&lt;0.001) and higher creatinine levels (p=0.023). Compared to the patients with lower FRS, those with higher FRS had greater lipid index (mean lipid arc x lipid length), and tended to have higher prevalence of thin-cap fibroatheroma (TCFA). Patients with higher FRS showed greater prevalence of calcifications compared to those with lower and intermediate FRS. Prevalence of cholesterol crystals was progressively higher across the 3 groups. At multivariate analysis, presentation with ACS (OR, 2.37; 95% CI, 1.27–4.39; p=0.006), and FRS (OR, 1.57 per 5% risk increase; 95% CI, 1.01–2.42, p=0.043) were independent predictors of TCFA. Conclusions: Nonculprit plaques of patients with higher FRS showed greater lipid content, and higher prevalence of calcifications and cholesterol crystals compared to those of patients with lower and intermediate FRS. ACS presentation and FRS were independent predictors of TCFA.

Pancoronary plaque vulnerability in patients with acute coronary syndrome and ruptured culprit plaque: A 3-vessel optical coherence tomography study

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. 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. 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. 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.

Features of Coronary Plaque in Patients With Metabolic Syndrome and Diabetes Mellitus Assessed by 3-Vessel Optical Coherence Tomography

The pathophysiological basis for the association between metabolic syndrome (MetS) and coronary artery disease is not well understood. We sought to characterize coronary plaques in patients with MetS by using optical coherence tomography. We identified 451 coronary plaques from 171 subjects who underwent optical coherence tomographic imaging in 3 coronary arteries. Subjects were divided into 3 groups: diabetes mellitus (DM, n=77), MetS (n=35), and a control group (C group, n=59) without DM or MetS. Optical coherence tomographic analysis included the presence of lipid-rich plaque, maximum lipid arc, lipid-core length, lipid index (LI), fibrous cap thickness, and thin-cap fibroatheroma. We defined LI as mean lipid arc multiplied by lipid-core length. Lipid-core length and LI were significantly greater in DM and MetS than in C group (lipid-core length: 7.7 ± 4.0 and 7.0 ± 3.8 versus 5.5 ± 2.4 mm; P<0.001 and P=0.012, and LI: 1164 ± 716 and 1086 ± 693 versus 796 ± 417 mm; P<0.001 and P=0.008). Maximum lipid arc was significantly greater in DM than in C group, whereas no significant difference was observed between MetS and C group (196 ± 45°, 187 ± 42° versus 176 ± 52°; P=0.002 and P=0.182). Fibrous cap thickness and thin-cap fibroatheroma showed no significant difference among the 3 groups. In multivariate analysis, DM and MetS were independently associated with LI, whereas only acute coronary syndrome was the independent predictor for thin-cap fibroatheroma. Compared with control subjects, coronary plaques in MetS contain larger lipid. However, the MetS criteria used in this study could not distinguish the vulnerable features such as thin-cap fibroatheroma, suggesting the necessity of complementary information to identify patients at high risk for cardiovascular events.

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Comparison of Nonculprit Coronary Plaque Characteristics Between Patients With and Without Diabetes: A 3-Vessel Optical Coherence Tomography Study

The aim of the present study was to compare the characteristics of nonculprit coronary plaques between diabetes mellitus (DM) and non-DM patients using 3-vessel optical coherence tomography (OCT) imaging. DM patients have a higher recurrent cardiovascular event rate. Patients who had undergone 3-vessel OCT imaging were identified from the Massachusetts General Hospital OCT Registry. Characteristics of nonculprit plaques were compared between DM and non-DM patients. A total of 230 nonculprit plaques were identified in 98 patients. Compared with non-DM patients, DM patients had a larger lipid index (LI) (averaged lipid arc × lipid length; 778.6 ± 596.1 vs. 1358.3 ± 939.2, p < 0.001) and higher prevalence of calcification (48.4% vs. 72.2%, p = 0.034) and thrombus (0% vs. 8.3%, p = 0.047). DM patients were divided into 2 groups based on glycated hemoglobin (A(1C)) levels of ≤7.9% and ≥8.0%. LI was significantly correlated with diabetic status (778.6 ± 596.1 [non-DM] vs. 1,171.5 ± 708.1 [A(1C) ≤7.9%] vs. 1,638.5 ± 1,173.8 [A(1C) ≥8%], p value for linear trend = 0.005), and fibrous cap thickness was inversely correlated with the A(1C) level (99.4 ± 46.7 μm [non-DM] vs. 91.7 ± 29.6 μm [A(1C) ≤7.9%] vs. 72.9 ± 22.7 μm [A(1C) ≥8%], p value for linear trend = 0.014). Patients with A(1C) ≥8% also had the highest prevalence of thin-cap fibroatheroma (TCFA) and macrophage infiltration. Compared with non-DM patients, DM patients have a larger LI and a higher prevalence of calcification and thrombus. The LI was larger and TCFA and macrophage infiltration were frequent in patients with A(1C) ≥8%.

Nonculprit Plaques in Patients With Acute Coronary Syndromes Have More Vulnerable Features Compared With Those With Non–Acute Coronary Syndromes

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 &lt;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 &lt;0.001), and a thinner fibrous cap (70.2 ± 20.2 µm versus 103.3 ± 46.8 µm, P &lt;0.001). Moreover, thin-cap fibroatheroma (64.7% versus 14.9%, P &lt;0.001), macrophage (82.4% versus 37.9%, P =0.001), and thrombus (29.4% versus 1.1%, P &lt;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.