Characteristics of coronary artery ectasia and accompanying plaques: an optical coherence tomography study.

Coronary artery ectasia (CAE) in adults is often caused by atherosclerotic plaques. CAE can affect atherosclerotic plaques through hemodynamic changes. However, no study has evaluated the characteristics of CAE with atherosclerotic plaques. Therefore, we aimed to disclose the characteristics of atherosclerotic plaques in patients with CAE using optical coherence tomography (OCT). We evaluated patients with CAE, confirmed by coronary angiography, who underwent pre-intervention OCT between April 2015 and April 2021. Each millimeter of the OCT images was analyzed to assess the characteristics of CAEs, plaque phenotypes, and plaque vulnerability. A total of 286 patients (344 coronary vessels) met our criteria, 82.87% of whom were men. Right coronary artery lesions were the most common, comprising 44.48% (n = 153) of the total. We found 329 CAE vessels with plaques, accounting for 95.64% of the coronary vessels. After grouping CAEs and plaques by their relative positions, we found that the length of plaques within CAE lesions was longer than that of plaques in other sites (P < 0.001). Plaques within CAE lesions had greater maximum lipid angles and lipid indexes (P = 0.007, P = 0.004, respectively) than those on other sites. This study revealed the most common vascular and morphological characteristics of CAE. While the accompanying plaques were not affected by the location or morphology of the CAE vessels, they were affected by their position relative to the CAE lesion.

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

BACKGROUND: Optical coherence tomography (OCT) may provide a method for detecting histologically defined high-risk plaques in vivo. OBJECTIVES: The authors aimed to investigate the prognostic value of OCT for identifying patients and lesions that are at risk for adverse cardiac events. METHODS: Between 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). RESULTS: The 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. CONCLUSIONS: OCT imaging of angiographically nonobstructive territories in patients with acute MI can aid in identifying patients and lesions at increased risk for adverse cardiac events.

Predictors of Adverse Prognosis in Patients With Acute Coronary Syndrome Caused by Plaque Erosion With a Nonstent Strategy.

Background The EROSION (Effective Anti-Thrombotic Therapy Without Stenting: Intravascular Optical Coherence Tomography-Based Management in Plaque Erosion) study demonstrated that antithrombotic therapy without stenting was safe and feasible in selected patients with acute coronary syndrome caused by plaque erosion. However, the factors related to the prognosis of these patients are not clear. This study aimed to explore the predictors of an adverse prognosis of a nonstent strategy in a larger sample size. Methods and Results A total of 252 (55 patients were from the EROSION study) patients with acute coronary syndrome with plaque erosion who met the inclusion criteria of the EROSION study and completed clinical follow-up were enrolled. Patients were divided into 2 groups according to the occurrence of major adverse cardiovascular events (MACE), which were defined as the composite of cardiac death, recurrent myocardial infarction, ischemia-driven target lesion revascularization, rehospitalization because of unstable or progressive angina, major bleeding, and stroke. Among 232 patients with acute coronary syndrome included in the final analysis, 50 patients (21.6%) developed MACE at a median follow-up of 2.9 years. Compared with patients without MACE, patients with MACE were older and had a higher degree of percentage of area stenosis (72.2%±9.4% versus 64.2%±15.7%, P<0.001) and thrombus burden (24.4%±10.4% versus 20.4%±10.9%, P=0.010) at baseline. Multivariate Cox regression analysis confirmed that age, percentage of area stenosis, and thrombus burden were predictors of MACE. The best cutoff values of predictors were age ≥60 years, percentage of area stenosis ≥63.5%, and thrombus burden ≥18.5%, respectively, and when they were all present, the rate of MACE rose to 57.7%. Conclusions The nonstent treatment strategy of patients with acute coronary syndrome caused by plaque erosion was heterogeneous, and patients aged ≥60 years, percentage of area stenosis ≥63.5%, and thrombus burden ≥18.5% may predict a worse clinical outcome.

Prevalence, Morphology, and Predictors of Intra-Stent Plaque Rupture in Patients with Acute Coronary Syndrome: An Optical Coherence Tomography Study.

Previous studies have shown that plaque rupture (PR) is the most important cause of acute coronary syndrome (ACS). However, the potential impact of intra-stent PR on stent failure manifesting as ACS and the optical coherence tomography (OCT) features of these lesions was still less clear. Therefore, we aimed to investigate the characteristics of OCT-defined in-stent PR and identify the potential risk factors for PR in ACS patients. All 213 ACS patients were stratified into two groups according to the occurrence of in-stent PR. The baseline characteristics of all patients were investigated. A multivariable logistic regression was performed to identify factors associated with the formation of PR. OCT findings showed that 80 patients had in-stent PR, and 133 patients were without PR. Patients who suffered in-stent PR had higher blood lipid levels (P < .050) and longer duration of stent failure (P = .001). Moreover, thrombolysis in myocardial infarction (TIMI) 0/1 flow was more prone to the formation of PR (P = .010), and lesions in the PR group harbored more macrophages and cholesterol crystals (P < .001 and P = .024). On multivariate analysis, presentation of myocardial infarction (MI) and OCT findings of lipidic neointima length showed a 3.6-fold (P = .004) and 1.3-fold (P < .001) higher risk for occurrence of in-stent PR. ACS patients who suffered in-stent PR had a longer duration of stent failure and more ISR occurring in non-culprit vessels. Given the distinguishing features between ACS patients with in-stent PR and non-PR, potential targeted therapy was warranted to improve the prognosis of patients with in-stent PR.

Clinical Outcomes of Different Calcified Culprit Plaques in Patients with Acute Coronary Syndrome.

Background: Previous studies have found that coronary artery calcification is closely associated with the occurrence of major adverse cardiac events (MACE). This study aimed to investigate the characteristics and clinical outcomes of different calcified plaques in patients with acute coronary syndrome (ACS) by using optical coherence tomography (OCT). Methods: 258 ACS patients with calcified culprit plaques who underwent OCT-guided stent implantation were enrolled. They were divided into three subtypes based on the calcified plaque morphology, including eruptive calcified nodules, calcified protrusion, and superficial calcific sheet. Results: Compared with superficial calcific sheet and calcified protrusion, eruptive calcified nodules had the greatest calcium burden and a higher rate of stent edge dissection (p < 0.001) and incomplete stent apposition (p < 0.001). In a median follow-up period of 2 years, 39 (15.1%) patients experienced MACE (a composite event of cardiac death, target-vessel myocardial infarction, ischemia-driven revascularization), with a significantly higher incidence in the eruptive calcified nodules group (32.1% vs. 10.1% vs. 13.0%, p = 0.001). A multivariate Cox analysis demonstrated that the eruptive calcified nodules (hazard ratio 3.14; 95% confidence interval, 1.64−6.02; p = 0.001) were an independent predictor of MACE. Conclusions: MACE occurred more frequently in ACS patients with eruptive calcified nodules, and the eruptive calcified nodules were an independent predictor of MACE.

Optical Coherence Tomographic Features of Pancoronary Plaques in Patients With Acute Myocardial Infarction Caused by Layered Plaque Rupture Versus Layered Plaque Erosion.

Atherosclerotic plaque instability could occur on the basis of healed plaque which has a layered appearance on optical coherence tomography. This study aimed to investigate pancoronary plaque features of layered plaque rupture (LPR) and layered plaque erosion (LPE) in patients with acute myocardial infarction. Among 388 patients with acute myocardial infarction who underwent preintervention optical coherence tomography imaging of three coronary arteries, 190 patients with layered culprit plaque (49.0%) were identified and further divided into 2 groups: LPR group and LPE group. Clinical characteristics, pancoronary plaque features and clinical outcomes were compared between the 2 groups. Patients with LPR were older, less often male and current smoker, and had a lower coronary flow grade than those with LPE. At the culprit lesion, LPR group had a higher prevalence of lipid plaque, thin-cap fibroatheroma (TCFA), macrophage, and microchannel, and presented with more severe lumen area stenosis than LPE group. At nonculprit lesions, LPR group had a higher prevalence of TCFA and had greater layered tissue thickness and area than LPE group. The ischemia-driven revascularization rate was higher in LPR group. Moreover, we found that TCFA, diameter stenosis >56.5%, and mean lipid arc >179.1° were predictors for layered culprit plaque. In conclusion, patients with LPR had more vulnerable plaque features at culprit and nonculprit lesions and had higher incidence of ischemia-driven revascularization than those with LPE. TCFA, diameter stenosis >56.5%, and mean lipid arc >179.1° were predictors of layered culprit plaque.

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.

BACKGROUND: 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. CONCLUSIONS: 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.

Morphological Characteristics of Eroded Plaques with Noncritical Coronary Stenosis: An Optical Coherence Tomography Study.

AIMS: Recent studies suggested plaque erosion with noncritical stenosis could be treated distinctly from that with critical stenosis, but their morphological features remained largely unknown. The present study aimed to investigate morphological features of eroded plaques with different lumen stenosis using optical coherence tomography (OCT). METHODS: A total of 348 ST-segment elevated myocardial infarction patients with culprit OCT-defined plaque erosion (OCT-erosion) were analyzed. Based on the severity of lumen area stenosis, all patients with OCT-erosions were divided into the following three groups: Group A (area stenosis ＜50%, n=50); Group B (50% ≤ area stenosis ＜75%, n=146); Group C (area stenosis ≥ 75%, n=152). RESULTS: Compared with patients in Groups A and B, patients in Group C were older (p=0.008) and had higher prevalence of hypertension (p=0.029). Angiographic analysis showed that 72.0% of the eroded plaques in Group A were located in the left anterior descending artery, followed by 67.8% in Group B, and 53.9% in Group C (p=0.039). OCT analysis showed that Group A had the highest prevalence of fibrous plaques (p＜0.001) and nearby bifurcation (p=0.036), but the lowest prevalence of lipid-rich plaques (p＜0.001), macrophage accumulation (p＜0.001), microvessels (p=0.009), cholesterol crystals (p＜0.001), and calcification (p=0.023). Multivariable regression analysis showed fibrous plaque (odds ratio [OR]: 3.014, 95% confidence interval [CI]: 1.932-4.702, p＜0.001) and nearby bifurcation (OR: 1.750, 95% CI: 1.109-2.761, p=0.016) were independently associated with OCT-erosion with an area stenosis of ＜75%. CONCLUSIONS: More than half of OCT-erosions presented with ＜75% area stenosis, having distinct morphological features from those of OCT-erosions with critical stenosis. Fibrous plaque and nearby bifurcation were independently associated with noncritically stenotic OCT-erosion, suggesting that eroded plaques might need individualized treatment.

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

OBJECTIVES: This 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). BACKGROUND: Pancoronary vulnerability should account for distinct clinical manifestations of acute myocardial infarction (AMI). Layered plaque is indicative of previous coronary destabilization and thrombosis. METHODS: A 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. RESULTS: Compared 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. CONCLUSIONS: Patients 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.

In vivo evidence of atherosclerotic plaque erosion and healing in patients with acute coronary syndrome using serial optical coherence tomography imaging.

BACKGROUND: The EROSION study (Effective Anti-Thrombotic Therapy Without Stenting: Intravascular Optical Coherence Tomography-Based Management in Plaque Erosion) allowed us to observe the healing process of coronary plaque erosion in vivo. The present study aimed to investigate the incidence of newly formed healed plaque and different baseline characteristics of acute coronary syndrome (ACS) patients caused by plaque erosion with or without newly formed healed plaque using optical coherence tomography (OCT). METHODS: A total of 137 ACS patients with culprit plaque erosion who underwent pre-intervention OCT imaging and received no stent implantation were enrolled. Patients were stratified according to the presence or absence of newly formed healed phenotype at 1-month (137 patients) or 1-year OCT follow-up (52 patients). Patient's baseline clinical, angiographic, OCT characteristics and outcomes were compared. RESULTS: There were 55.5% (76/137) of patients developed healed plaque at 1 month, and 69.2% (36/52) of patients developed healed plaque at 1 year. Patients with newly formed healed plaque had larger thrombus burden, and lower degree of area stenosis (AS%) at baseline than those without, and thrombus burden and AS% were predictors of plaque healing. The healing process was accompanied by the significant increase of AS% and incidence of microchannels, and greater inflammatory response. The outcomes appeared to be similar between the two groups. CONCLUSIONS: Newly formed healed plaque was found in more than half of ACS patients with plaque erosion without stenting. Patients with newly formed healed plaque had lower luminal stenosis and larger thrombus burden. During healing process, luminal stenosis increased gradually.

Predictors of Coronary Plaque Erosion in Current and Non-Current Smokers With ST-Segment Elevation Myocardial Infarction　- An Optical Coherence Tomography Study.

BACKGROUND: Smoking is an important risk factor of plaque erosion. This study aimed to investigate the predictors of plaque erosion in current and non-current smokers presenting with ST-segment elevation myocardial infarction (STEMI).Methods and Results:A total of 1,320 STEMI patients with culprit plaque rupture or plaque erosion detected by pre-intervention optical coherence tomography were divided into a current smoking group (n=715) and non-current smoking group (n=605). Plaque erosion accounted for 30.8% (220/715) of culprit lesions in the current smokers and 21.2% (128/605) in the non-current smokers. Multivariable analysis showed age <50 years, single-vessel disease and the absence of dyslipidemia were independently associated with plaque erosion rather than plaque rupture, regardless of smoking status. In current smokers, diabetes mellitus (odds ratio [OR]: 0.29; 95% confidence interval [CI]: 0.10-0.83; P=0.021) was negatively associated with plaque erosion as compared with plaque rupture. In non-current smokers, minimal lumen area (MLA, OR: 1.37; 95% CI: 1.16-1.62; P<0.001) and nearby bifurcation (OR: 3.20; 95% CI: 1.98-5.16; P<0.001) were positively related to plaque erosion, but not plaque rupture. CONCLUSIONS: In patients with STEMI, the presence of diabetes mellitus significantly increased the risk of rupture-based STEMI but may not have reduced the risk of plaque erosion-based STEMI in current smokers. Nearby bifurcation and larger MLA were associated with plaque erosion in non-current smokers.

Systemic and local factors associated with reduced thrombolysis in myocardial infarction flow in ST-segment elevation myocardial infarction patients with plaque erosion detected by intravascular optical coherence tomography.

Local factors of plaque rupture (e.g. lipid burden) are related to preprocedural thrombolysis in myocardial infarction (TIMI) flow grade during primary percutaneous coronary intervention (PCI). However, the pathological mechanism differs between plaque erosion and rupture. We aimed to identify the factors associated with reduced TIMI flow in plaque erosion. A total of 329 ST-segment elevation myocardial infarction (STEMI) patients with optical coherence tomography (OCT) identified plaque erosion were divided into 2 groups by preprocedural TIMI flow grade [TIMI 0-1 group (n = 219) and TIMI 2-3 group (n = 110)]. Patients in TIMI 0-1 group were older (age > 50 years, 68.5% vs. 51.8%, P = 0.003), and had more diabetes mellitus (18.3% vs. 8.2%, P = 0.015). Plaque erosion with TIMI flow 0-1 was less frequently located in the left anterior descending artery (LAD, 58.4% vs. 72.7%, P = 0.011), but more frequently located in the right coronary artery (RCA, 34.2% vs. 7.3%, P = 0.001) than those with TIMI flow 2-3. TIMI 0-1 group had more lipid plaques (53.9% vs. 41.8%, P = 0.039), macrophage accumulation (59.8% vs. 41.8%, P = 0.002), and calcification (34.2% vs. 21.8%, P = 0.020). In the multivariable analysis, age > 50 years, diabetes mellitus, RCA location, and macrophage accumulation were the independent predictors of reduced TIMI flow grade in STEMI patients with plaque erosion. Systemic factors (older age and diabetes mellitus) and local factors (RCA location and macrophage accumulation) were independently associated with reduced coronary flow in STEMI patients with plaque erosion. CLINICAL TRIAL REGISTRATION : ClinicalTrials.gov NCT03084991 May 17, 2017 (retrospectively registered).

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.

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.