Characteristics Of Non-culprit Plaques Research Articles

Comparison of high-risk characteristics of non-culprit plaques in relation to plaque severity in acute coronary syndrome

IntroductionPatients with acute coronary syndrome (ACS) have high event rates related to non-culprit (NC) lesions, therefore plaque composition of these lesions is of great interest. Although marginal atherosclerotic lesions were studied extensively, more significant lesions might have more high-risk characteristics. AimTo compare differences in high-risk lesion characteristics between significant versus non-stenotic NC plaques in ACS and the discrepancies with chronic coronary syndrome (CCS) patients. MethodsNon-culprit vessels of 26 ACS patients with 26 angiographically significant lesions and 37 patients (17 ACS and 20 CCS) with 48 non-stenotic lesions were investigated with intravascular ultrasound (IVUS) and near-infrared spectroscopy (NIRS). Overall, 74 segments of 30 mm length were analyzed in 1 mm intervals. External elastic lamina (EEM), plaque burden (PB), minimal luminal area (MLA), percent atheroma volume (PAV) and lipid core burden index maximum 4 mm (maxLCBI4mm) were determined for each segment. ResultsCardiovascular risk factors were similar in all groups. PB was higher and MLA smaller in significant non-culprit ACS lesions vs non-stenotic lesions: PB 73.5 % (IQR 68.7–78.5) vs 59.2 (IQR 49.6–71.5), p = 0.003, MLA 3.0 mm2 (IQR 2.3–3.9) vs 4.0 mm2 (IQR 2.8–4.7). MaxLCBI4mm was similar 308.1 (±155.4) vs 287.8 (±165.7), p = 0.67.Among non-stenotic plaques, MaxLCBI4mm was comparable between ACS and CCS patients, 275.7 (±151.5) in CCS patients vs 287.8 (±165.7) in ACS patients, p = 0.79. ConclusionAlthough visually significant non-culprit lesions had a higher plaque burden compared to non-stenotic lesions, a significant relation between MaxLCBI4mm and hemodynamic significance of the plaques couldn't be established.

The association of cholesterol crystals and non-culprit plaque characteristics in AMI patients: an OCT study

Objective: To analyze plaque characteristics of non-culprit coronary lesions with cholesterol crystals in patients with acute myocardial infarction(AMI) by using optical coherence tomography(OCT). We also investigated the potential association between cholesterol crystals with plaque rupture and healed plaque at non-culprit segment. Methods: This study was a retrospective cohort study. Between January 2017 and December 2017, patients with AMI who underwent 3-vessel OCT imaging were included in this study. Patients were divided into two groups according to the presence or absence of cholesterol crystals at the non-culprit lesions. All patients underwent coronary angiography and OCT examination, and non-culprit plaque characteristics were compared between the two groups. The generalized estimating equation log-binomial multirariate regression model was used to assess the relationship between non-culprit lesions with cholesterol crystals and plaque rupture and plaque healing. The follow-up data collection ended in October 2023. Kaplan-Meier survival curves were plotted, and log-rank tests were used to compare the cumulative incidence of major adverse cardiovascular events between the two groups. Results: A total of 173 AMI patients were included (aged (56.8±11.6) years; 124 men (71.7%)). Among 710 non-culprit lesions identified by OCT, there were 102 (14.4%) in cholesterol crystals group and 608 (85.6%) in non-cholesterol crystals group. Compared with non-culprit lesions without cholesterol crystals, those with cholesterol crystals had smaller minimum lumen diameter, severer diameter stenosis, and longer lesion length (all P<0.01). The prevalence of plaque rupture (17.6% (18/102) vs. 4.9% (30/608), P=0.001) and thin-cap fibroatheroma (31.4% (32/102) vs. 11.5% (70/608), P<0.01) was higher in the cholesterol crystals groups than in the non-cholesterol crystals group. In addition, vulnerable plaque characteristics such as (44.1% (45/102) vs. 25.8% (157/608), P<0.01), macrophages were more frequently observed in non-culprit lesions with cholesterol crystals. The generalized estimating equation log-binomial multivariate regression analyses showed that non-culprit cholesterol crystals were positively correlated with healed plaque (OR=1.583, 95%CI: 1.004-2.495, P=0.048). Conversely, cholesterol crystals were not associated with plaque rupture (OR=1.632, 95%CI: 0.745-3.576, P=0.221). The follow-up time was 2 142 (1 880, 2 198) days. Non-culprit cholesterol crystals were not related to the major adverse cardiovascular events in patients with AMI (log-rank P=0.558). Conclusions: Among AMI patients, non-culprit lesions with cholesterol crystals presented with severer luminal stenosis and increased plaque vulnerability. The presence of non-culprit cholesterol crystals was associated with rather than plaque rupture.

Non-flow limiting non-culprit plaque characteristics in patients presenting with STEMI versus NSTEMI

Abstract Background Non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI) are often considered distinct clinical entities. Although differences in culprit plaque characteristics have been described extensively, less is known about differences in non-culprit (NC) plaque characteristics. Purpose To compare plaque characteristics of fractional flow reserve (FFR)-negative NC lesions as assessed by optical coherence tomography (OCT) in STEMI and NSTEMI patients. Methods PECTUS-obs is a prospective, observational study in which 438 patients presenting with STEMI or NSTEMI underwent OCT of any intermediate FFR-negative NC lesion (defined as a FFR &amp;gt;0.80) after treatment of the infarct related artery. Quantitative and qualitative OCT analyses were performed by an independent core laboratory. A high risk plaque (HRP) was defined as the presence of ≥2 of the following prespecified criteria: 1) a lipid arc ≥90°, 2) a minimal fibrous cap thickness &amp;lt;65 µm, or 3) either cap rupture or thrombus presence. In the present sub-analysis, lesion-level plaque characteristics were compared between patients presenting with STEMI versus NSTEMI while accounting for within-patient clustering and correcting for prespecified clinical variables (age, history of myocardial infarction, diabetes, and estimated glomerular filtration rate (eGFR)). Results Among 420 patients with at least one analyzable OCT, 217 (51.7%) presented with STEMI and 203 (48.3%) with NSTEMI. Patients with STEMI were younger (mean age 62±10 vs 65±11 years, p=0.004) and less frequently had diabetes (11.1% vs 18.2%, p=0.037) and hypercholesterolemia (31.8% vs 41.6%, p=0.038). Baseline mean eGFR (84±19 vs 75±19 ml/min, p&amp;lt;0.001) and low density lipoprotein-cholesterol levels (3.2±1.2 vs 2.9±1.2, p=0.010) were higher in STEMI patients with fewer of these patients using lipid lowering therapy (18.9% vs 33.0%, p&amp;lt;0.001) before enrollment. A total of 494 NC lesions were analyzed, which were equally distributed in number and location between groups. The mean fractional flow reserve was 0.89±0.05 and was comparable between groups (p=0.26). Patients with STEMI had a smaller minimal lumen area (2.56±1.48 vs 2.84±1.58 mm2, p=0.031) and minimal lumen diameter (1.47±0.44 vs 1.55±0.45 mm, p=0.026) with a subsequent larger percentage area stenosis (64±15 vs 61±17%, p=0.022). Lipid plaques were more common in STEMI patients (81.7% vs 70.7%, p=0.006) and the maximal lipid arc more frequently was ≥90º (79.0% vs 69.0%, p=0.018). There was no difference in the presence of plaque ruptures (8.3% vs 11.2%, p=0.31) or HRP (32.9% vs 29.3%, p=0.40), whereas macrophage accumulation was more prevalent in STEMI patients (27.8% vs 18.2%, p=0.040). Conclusions FFR-negative NC lesions in patients with STEMI have smaller luminal dimensions, and more frequently harbor lipid plaques and macrophage accumulation. No difference was observed in the prevalence of HRP or plaque rupture.

Abstract 16132: Cardiometabolic Risk Factors and Non-Culprit Plaque Characteristics in Patients With STEMI in REAL-TIMI 63B

Introduction: Greater non-calcified plaque volume (NCPV) measured by coronary CT angiography (CCTA) is associated with higher risk of future myocardial infarction in stable patients. However, NCPV and associations with clinical characteristics in patients presenting with a first acute STEMI are not well described. Methods: The REAL-TIMI 63B trial randomized 593 patients with no prior MI presenting with acute STEMI to intravenous recombinant human lecithin-cholesterol acyltransferase (MEDI6012) or placebo; a subset were to undergo CCTA 48-72h after STEMI. Global NCPV, low-attenuation PV (LAPV), and calcified PV (CPV) were measured by a centralized core laboratory blinded to treatment arm. Revascularized segments were excluded from coronary plaque quantification. Results: 188 patients had a CCTA performed at baseline. Of these, 80.3% had NCPV and 77.4% had LAPV outside of the revascularized segments. Median NCPV was 28.4mm 3 [IQR 1.4-92.1], LAPV 3.8mm 3 [0.1-14.9], and CPV 92.4mm 3 [22.6-201.8]. Among the characteristics examined, male vs. female sex (51.3 mm 3 [3.47-100.3] vs 5.6 mm 3 [0.0-17.3]; p=0.0003), BMI &gt;25 kg/m 2 (overweight or obese) (41.20 mm 3 [2.01-104.50] vs 10.98 mm 3 (0.0-61.5); p=0.01) and diabetes (82.6 mm 3 [59.0-123.4] vs 24.2 mm 3 [1.21-85.2]; p=0.038) were associated with greater NCPV (Figure). Conclusions: Among patients with no prior MI undergoing primary PCI for STEMI, we found that most patients had NCPV and LAPV outside the culprit lesion. Male sex and markers of cardiometabolic disease including higher BMI and diabetes were associated with a greater burden of NCPV. These observations underscore the need for intensive medical therapies that may stabilize vulnerable plaque in patients presenting with acute myocardial infarction.

Impact of the eicosapentaenoic acid to arachidonic acid ratio on plaque characteristics in statin-treated patients with coronary artery disease

BackgroundA low eicosapentaenoic acid (EPA)/arachidonic acid (AA) ratio is associated with an increased risk of cardiovascular events in patients with coronary artery disease (CAD). ObjectiveTo clarify the impact of the EPA/AA ratio on the characteristics of non-culprit coronary plaques in statin-treated patients with CAD. MethodsA total of 370 consecutive stable coronary disease patients treated with statins, who underwent percutaneous coronary intervention for the culprit lesion and optical coherence tomography (OCT) imaging of the non-culprit plaque in a culprit vessel were included. The characteristics of non-culprit plaques assessed using OCT were compared between the lower EPA/AA group (EPA/AA <0.4, n = 255) and the higher EPA/AA group (EPA/AA ≥0.4, n = 115). ResultsThe prevalence of lipid-rich plaque (58.8 vs. 41.7%, p = 0.003) and plaque with macrophages (56.5 vs. 31.3%, p <0.001) was significantly higher in the lower EPA/AA group than in the higher EPA/AA group. This association was observed even if the LDL-C level was <100 mg/dL. The prevalence of thin-cap fibroatheroma was significantly higher in patients with lower EPA/AA and higher LDL-C (≥100 mg/dL) than in those with higher EPA/AA and lower LDL-C (<100 mg/dL) (odds ratio: 2.750, 95% confidence interval: 1.182-6.988, p = 0.024). An EPA/AA <0.4 was independently associated with a higher prevalence of lipid-rich plaque, plaque with macrophages, and cholesterol crystals. ConclusionLower EPA/AA ratio was associated with higher prevalence of vulnerable characteristics in non-culprit plaques. The present results suggest the importance of EPA/AA ratio on the secondary prevention of CAD.

Triglyceride-glucose index and non-culprit coronary plaque characteristics assessed by optical coherence tomography in patients following acute coronary syndrome: A cross-sectional study.

BackgroundTriglyceride-glucose (TyG) index, a novel surrogate marker of insulin resistance, has been demonstrated to be significantly associated with cardiovascular disease. It remains indistinct regarding the association between TyG index and non-culprit coronary plaque characteristics in patients following acute coronary syndrome (ACS).MethodsThe present study retrospectively recruited patients who were diagnosed with ACS and underwent non-culprit optical coherence tomography (OCT) examination. The study population was divided into 2 groups based on the median of TyG index, which was calculated as Ln [fasting triglyceride (TG) (mg/dL) × fasting blood glucose (FBG) (mg/dL)/2]. The non-culprit plaque characteristics were determined by interpreting OCT images in accordance with the standard of previous consensus.Results110 patients (54.8 ± 12.1 years, 24.5% female) with 284 non-culprit plaques were included in the current analysis. TyG index was closely associated with high-risk plaque characteristics. Elevated TyG index was consistent to be an independent indicator for thin-cap fibroatheroma (TCFA) [odds ratio (OR) for per 1-unit increase 4.940, 95% confidence interval (CI) 1.652–14.767, P = 0.004; OR for taking lower median as reference 2.747, 95% CI 1.234–7.994, P = 0.011] and ruptured plaque (OR for per 1–unit increase 7.065, 95% CI 1.910–26.133, P = 0.003; OR for taking lower median as reference 4.407, 95% CI 1.208–16.047, P = 0.025) in fully adjusted model. The predictive value of TyG index for TCFA and ruptured plaque was moderate–to–high, with the area under the receiver operating characteristic curve (AUC) of 0.754 and 0.699 respectively. The addition of TyG index into a baseline model exhibited an incremental effect on the predictive value for TCFA, manifested as an increased AUC (0.681, 95% CI 0.570–0.793 vs. 0.782, 95% CI 0.688–0.877, P = 0.042), and significant continuous net reclassification improvement (0.346, 95% CI 0.235–0.458, P < 0.001) and integrated discrimination improvement (0.221, 95% CI 0.017–0.425, P = 0.034). TyG index failed to play an incremental effect on predicting ruptured plaque.ConclusionTyG index, which is simply calculated from fasting TG and FBG, can be served as an important and independent risk predictor for high-risk non-culprit coronary plaques in patients following ACS.

Lipoprotein (a) levels and vulnerable characteristics in nonculprit plaque in patients with acute coronary syndrome.

High plasma levels of Lp(a) are associated with a worse prognosis in patients with coronary artery disease. The aim of the present study is to clarify the association between high lipoprotein a [Lp(a)] levels and vulnerable characteristics of nonculprit plaques in patients with acute coronary syndrome (ACS). A total of 185 consecutive patients with ACS who underwent optical coherence tomography imaging of nonculprit plaques in the culprit vessels were enrolled. Patients were divided into the high Lp(a) group (≥30mg/dL; 50 nonculprit plaques in 49 patients) or the low Lp(a) group (<30mg/dL; 139 nonculprit plaques in 136 patients). The prevalence of thin-cap fibroatheroma (TCFA) was significantly higher in the high Lp(a) group than in the low Lp(a) group (38.0 vs. 21.6%, p=0.034). Multivariate logistic analysis demonstrated that a high Lp(a) level was independently associated with the prevalence of TCFA (odds ratio, 1.18; 95% confidence interval, 1.01-1.36; p=0.033). The prevalence of TCFA was significantly higher in the high Lp(a) group than in the low Lp(a) group among patients with plaque erosion (50.0 vs. 9.4%, respectively; p=0.027), although the difference was not statistically significant between the two groups in patients with plaque rupture. High Lp(a) levels were associated with a high prevalence of TCFA in nonculprit plaques among patients with ACS, particularly in patients with plaque erosion. The present results may partly explain the pathogenesis of worse clinical outcomes in patients with ACS and a high Lp(a) level as shown in clinical studies.

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). 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.

High sensitivity C-reactive protein is associated with vulnerable characteristics in non-culprit plaques in patients with ST-segment elevation myocardial infarction

Abstract Funding Acknowledgements Type of funding sources: None. Background Higher level of high sensitivity C-reactive protein (hsCRP) is associated with an increased risk of recurrent cardiovascular events in patients with ST-segment elevation myocardial infarction (STEMI). However, the association between hsCRP and the characteristics of non-culprit plaques in patients with STEMI remains to be elucidated. Purpose To clarify the morphological characteristics of non-culprit plaque in patients with STEMI according to the hsCRP levels using optical coherence tomography (OCT). Methods A total of 79 non-culprit plaques in 76 consecutive patients with STEMI, who underwent OCT imaging of the non-culprit plaques in a culprit vessel were included. The characteristics of non-culprit plaques assessed by OCT were compared between the higher hsCRP group (hsCRP ≥ 0.16 mg/dL, 38 plaques in 38 patients) and the lower hsCRP group (hsCRP &amp;lt; 0.16 mg/dL, 41 plaques in 38 patients). Results The prevalence of plaque with macrophage (63.2 vs. 31.7%, p = 0.006), plaque with large lipid (maximal lipid arc &amp;gt; 180 °) (57.9 vs. 31.7%, p = 0.018), healed plaque (50.0 vs. 26.8%, p = 0.045) and cholesterol crystal (18.4 vs. 2.4%, p = 0.045) was significantly higher in the higher hsCRP group than in the lower hsCRP group (Figure). In a multivariate analysis, the higher hsCRP was independently associated with the presence of plaque with macrophage (Odds ratio [OR], 3.031; 95% confidence interval [CI]: 1.112-8.264, p = 0.030), plaque with large lipid (OR, 2.897; 95% CI: 1.122-7.478, p = 0.026) and healed plaque (OR, 2.666; 95% CI: 1.030-6.896, p = 0.040). Conclusions Higher level of hsCRP is associated with a higher prevalence of vulnerable characteristics in non-culprit plaques in patients with STEMI. The present results may partly explain the pathogenesis of an increased incidence of recurrent cardiovascular events in patients with STEMI. Abstract Figure.

Greater plaque burden and cholesterol content may explain an increased incidence of non-culprit events in diabetic patients: a Lipid-Rich Plaque substudy.

Diabetes mellitus (DM) is associated with increased cardiovascular morbidity and mortality. The multicentre, prospective Lipid-Rich Plaque trial (LRP) examined non-culprit (NC) non-obstructive coronary segments with a combined near-infrared spectroscopy (NIRS)-intravascular ultrasound (IVUS) catheter. This study assessed the differences in NC plaque characteristics and their influence on major adverse cardiac events (MACE) in diabetic and non-diabetic patients. Patients with known DM status were divided into no diabetes, diabetes not treated with insulin (non-ITDM), and insulin-treated diabetes (ITDM). The association between presence and type of DM and NC-MACE was assessed at both the patient and coronary segment levels by Cox proportional regression modelling. Out of 1552 patients enrolled, 1266 who had their diabetes status recorded were followed through 24 months. Female sex, hypertension, chronic kidney disease, peripheral vascular disease, and high body mass index were significantly more frequent in diabetic patients. The ITDM group had more diseased vessels, at least one NC segment with a maxLCBI4 mm ≥400 in 46.2% of patients, and maxLCBI4 mm ≥400 in nearly one out of six Ware segments (15.2%, 125/824 segments). The average maxLCBI4 mm significantly increased from non-diabetic patients (NoDM) to non-insulin-treated diabetic patients (non-ITDM) to insulin-treated diabetic patients (ITDM; 137.7 ± 161.9, 154.8 ± 173.6, 182.9 ± 193.2, P < 0.001, respectively). In patients assigned to follow-up (692 ± 129 days), ITDM doubled the incidence of NC-MACE compared with the absence of diabetes (15.7% vs. 6.9%, P = 0.0008). The presence of maxLCBI4 mm>400 further increased the NC-MACE rate to 21.6% (Kaplan-Meier estimate). Cholesterol-rich NC plaques detected by NIRS-IVUS were significantly more frequent in diabetic patients, especially those who were insulin-treated, and were associated with an increased NC-MACE during follow-up.

Intracranial Atherosclerotic Plaque Characteristics and Burden Associated With Recurrent Acute Stroke: A 3D Quantitative Vessel Wall MRI Study.

Background: Intracranial atherosclerotic disease (ICAD) tends to affect multiple arterial segments, and previous studies rarely performed a comprehensive plaque analysis of the entire circle of Willis for the evaluation of recurrent stroke risk. We aimed to investigate the features of circle of Willis ICAD on 3D magnetic resonance vessel wall imaging (MR-VWI) and their relationships with recurrent acute stroke.Methods: Patients with either acute ischemic stroke (within 4 weeks after stroke) or chronic ischemic stroke (after 3 months of stroke) due to intracranial atherosclerotic plaque underwent 3D contrast-enhanced MR-VWI covering major cerebral arteries. Participants were divided into three groups: first-time acute stroke, recurrent acute stroke, and chronic stroke. Culprit plaque (defined as the only lesion or the most stenotic lesion when multiple plaques were present within the same vascular territory of the stroke) and non-culprit plaque characteristics, including total plaque number, plaque thickness, plaque area, plaque burden (calculated as plaque area divided by outer wall area), enhancement ratio (ER), eccentricity, and stenosis, were measured and compared across the three groups. Associations between plaque characteristics and recurrent acute stroke were investigated by multivariate analysis.Results: A total of 176 participants (aged 61 ± 10 years, 109 men) with 702 intracranial plaques were included in this study. There were 80 patients with first-time acute stroke, 42 patients with recurrent acute stroke, and 54 patients with chronic stroke. More intracranial plaques were found per patient in the recurrent acute stroke group than in the first-time acute stroke or chronic stroke group (5.19 ± 1.90 vs. 3.71 ± 1.96 and 3.46 ± 1.33, p < 0.001). Patients in the recurrent acute stroke group had greater culprit plaque burden (p < 0.001) and higher culprit ER (p < 0.001) than the other two groups. After adjustment of clinical demographic factors, in multivariate analysis, coronary artery disease (CAD) (odds ratio, OR = 4.61; p = 0.035), total plaque number (OR = 1.54; p = 0.003), culprit plaque ER (OR = 2.50; p = 0.036), and culprit plaque burden (OR per 10% increment = 2.44; p = 0.010) were all independently associated with recurrent acute stroke compared to the first-time acute stroke.Conclusion: Increased intracranial atherosclerotic plaque number, higher culprit plaque ER, greater culprit plaque burden, and CAD are independently associated with recurrent acute stroke.

Near infrared spectroscopy and optical coherence tomography derived plaque characteristics associated with increased plaque progression over 12-month follow up

Abstract Background Serial intravascular ultrasound (IVUS) studies demonstrated patterns of either plaque progression, regression or stabilization during pharmacotherapy including statin. At present little is known on specific plaque characteristics that are associated with excessive plaque growth. Purpose To evaluate the utility of near infrared spectroscopy (NIRS) and optical coherence tomography (OCT) to identify characteristics of non-culprit plaques associated with an increase in wall thickness (WT). Methods In this prospective, single-center study, patients with acute coronary syndrome (ACS) underwent, after successful treatment of the culprit lesions, both NIRS-IVUS and OCT assessment of a non-culprit artery at baseline and 12-month follow-up. For each vessel, 1.5-mm segments were identified, matched and divided into 45° sectors. A sector was considered as NIRS positive or labeled as OCT-detected fibrous cap atheroma (FCA), lipid rich or fibrous plaque when &amp;gt;75% of the sector area exhibited NIRS signal or specific OCT-detected feature. The relationship between change in IVUS-based WT, and the presence of NIRS positive signal or OCT-detected plaque components (FCA, lipid rich, fibrous) was evaluated using mixed ANCOVA, with NIRS status and OCT plaque components as fixed factors, and patient as random factor, adjusting for clustering effect of the data. All analyses of plaque WT change were adjusted for baseline WT. To examine the value of NIRS and OCT-detected plaque components in predicting plaque progression, a logistic mixed model was built with plaque progression defined as WT increase &amp;gt;0.2mm over the 12-month follow-up. Results A total of 38 patients (92% male, 21% diabetic) with 9167 matched sectors were analyzed at baseline and 12 months. Mean change in WT between baseline and 12 months was 0.014mm (95% confidence interval [CI] 0.011–0.018, p&amp;lt;0.001). Positive NIRS sectors showed more pronounced plaque progression than NIRS negative sectors (0.057mm, 95% CI 0.032–0.084 vs 0.014mm 95% CI 0.010–0.017, p=0.001) (Figure 1). FCA showed significant progression of WT over the 12-month follow-up (0.104mm, 95% CI 0.007–0.201), whereas a decrease in WT was observed in sectors with fibrous tissue (−0.031mm, 95% CI 0.048–0.014) (p=0.022). Baseline NIRS positive (OR 1.88, 95% CI 1.34–2.64) and OCT-detected lipid rich plaque (OR 1.47, 95% CI 1.20–1.81) were associated with 12-month plaque progression (&amp;gt;0.2mm) by logistic regression. Conclusions Positive NIRS signal and OCT-detected lipid plaque components imaged at baseline in non-culprit coronary arteries of patients presenting with ACS could identify vessel wall regions prone to plaque progression over a 12-month period. Figure 1. Plaque progression and NIRS Funding Acknowledgement Type of funding source: Other. Main funding source(s): M. Tomaniak acknowledges funding received as a Laureate of the European Society of Cardiology Research and Training Programme in the form of the ESC 2018 Grant.

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.

Association of ABO blood groups and non-culprit plaque characteristics in acute coronary syndrome: an optical coherence tomography study.

BackgroundCardiovascular disease (CVD) poses a serious threat to human health. Research shows that ABO blood groups, especially non-O blood types, are closely related to the incidence of cardiovascular diseases (CVDs). This study aimed to determine the associations of blood types with non-culprit coronary plaque characteristics using optical coherence tomography (OCT).MethodsA total of 257 acute coronary syndrome (ACS) patients (average age, 59.39±10.08 years, 80% male) who underwent OCT of 3 vessels were identified. Subjects were divided into 2 groups: the O blood group (71 patients with 121 plaques) and the non-O group (186 patients with 329 plaques). The non-culprit coronary plaque features of the two groups were compared using OCT.ResultsThe non-type O group had larger lipid arcs, thinner fibrous caps, and a greater number of thin-cap fibro atheromas (TCFAs). The type A, B, and AB blood groups had larger lipid arcs than the type O blood group, as well as thinner fibrous caps and more TCFAs. The type A blood group had thinner fibrous caps and a greater number of TCFAs than the type B and AB blood groups.ConclusionsACS patients with type non-O blood had more non-culprit plaques. Patients with type A blood, in particular, had more vulnerable characteristics than those with type O blood.

Characteristics of non-culprit plaques in acute coronary syndrome patients with calcified plaque at the culprit lesion.

To investigate the non-culprit plaques (NCPs) characteristics in acute coronary syndrome (ACS) patients with calcified plaques (CP). Recently, a new in vivo classification of calcified culprit plaques in patients with ACS was proposed. Characteristics of NCPs in this group of patients are unknown. A total of 692 NCPs from 492 ACS patients were retrospectively compared based on the culprit plaque phenotype: 71 from CP patients, 383 from plaque rupture (PR) patients, 238 from plaque erosion (PE) patients. NCPs of CP patients had greater maximal calcium thickness, wider calcium arc, longer calcium length, and greater calcium index, compared to PR or PE patients (CP vs. PR: all p < .001, CP vs. PE: all p < .001). Thin-cap fibroatheroma was less prevalent (p = .023), fibrous cap was thicker (p = .035), and mean lipid arc was narrower in CP than in PR (p < .001). In conclusion, NCPs of CP patients had greater calcium burden and less vulnerability. This information may help to better understand the underlying mechanisms of ACS and to develop strategy for tailored management.

Characteristics of non-culprit plaques in acute coronary syndrome patients with layered culprit plaque

Layered plaques represent signs of previous plaque destabilization. A recent study showed that acute coronary syndrome (ACS) patients with layered culprit plaque have more vulnerability at the culprit lesion and systemic inflammation. We aimed to compare the characteristics of non-culprit plaques between patients with or without layered plaque at the culprit lesion. We also evaluated the characteristics of layered non-culprit plaques, irrespective of culprit plaque phenotype. We studied ACS patients who had undergone pre-intervention optical coherence tomography (OCT) imaging. The number of non-culprit lesions was evaluated on coronary angiogram and morphological characteristics of plaques were studied by OCT. In 349 patients, 99 (28.4%) had layered culprit plaque. The number of non-culprit plaques in patients with or without layered culprit plaque was similar (3.2 ± 0.8 and 2.8 ± 0.8, P = 0.23). Among 465 non-culprit plaques, 145 from patients with layered culprit plaque showed a higher prevalence of macrophage infiltration (71.0% vs. 60.9%, P = 0.050). When analysed irrespective of culprit plaque phenotype, layered non-culprit plaques showed higher prevalence of lipid (93.3% vs. 86.0%, P = 0.028), thin cap fibroatheroma (29.7% vs. 13.7%, P < 0.001), and macrophage infiltration (82.4% vs. 54.0%, P < 0.001) than non-layered plaques. Plaques with layered phenotype at both culprit and non-culprit lesions had the highest vulnerability. In ACS patients, those with layered phenotype at the culprit lesion demonstrated greater macrophage infiltration at the non-culprit sites. Layered plaque at the non-culprit lesions was associated with more features of plaque vulnerability, particularly when the culprit lesion also had a layered pattern.

Gender differences in plaque characteristics of nonculprit lesions in patients with coronary artery disease

BackgroundAlthough numerous reports suggest sex-related differences in atherosclerosis, limited data describing gender-associated differences in plaque morphology and composition are currently available. The aim of the present study was to compare coronary nonculprit plaque characteristics in women and men with coronary artery disease (CAD) by optical coherence tomography (OCT).MethodsThis was a retrospective study. A total of 187 nonculprit plaques were identified in 103 patients with CAD who underwent OCT imaging of all 3 coronary arteries. These patients included 77 (74.8%) men and 26 (25.2%) women.ResultsFemale patients were significantly older than males (mean age, 70.8 ± 7.3 vs 60.8 ± 9.8 years; P < 0.001) and less likely to be current smokers (P = 0.007). OCT analysis included the presence of lipid-rich plaque, maximum lipid arc, lipid-core length, lipid index (LI), fibrous cap thickness, and the incidence of thin-cap fibroatheroma (TCFA). Nonculprit plaques in men exhibited greater lipid-core length and LI compared with those of women (9.4 ± 4.5 vs. 7.3 ± 4.3 mm, P = 0.024; 1615.1 ± 893.8 vs. 1237.8 ± 859.8, P = 0.035, respectively). In the univariate linear regression model, sex and current smoker were all associated with a larger LI, whereas only use of statin was independent risk factor for a larger LI in multivariate analysis.ConclusionsCoronary nonculprit plaques in male patients with CAD contain larger lipid cores than those of female patients.

Coronary Plaque Characteristics in Patients With Diabetes Mellitus Who Presented With Acute Coronary Syndromes.

BackgroundDiabetes mellitus (DM) is a major risk factor for cardiovascular events. We aimed to investigate the coronary plaque phenotype of diabetic patients who presented with acute coronary syndromes by optical coherence tomography.Methods and ResultsA total of 322 patients with acute coronary syndromes who underwent preintervention optical coherence tomography imaging of the culprit lesion were included. Culprit plaque characteristics were compared between patients with DM (n=95) and those without DM (n=227). In the subgroup of 250 patients in whom sufficient length of nonculprit region in the culprit vessel was imaged by optical coherence tomography, the characteristics of nonculprit plaques were also evaluated. Patients with DM had a higher prevalence of lipid‐rich plaque (58.9% versus 44.9%, P=0.030) and macrophage accumulation (60.0% versus 44.9%, P=0.019) in the culprit lesion compared with patients without DM. The prevalence of plaque rupture (33.7% versus 30.4%, P=0.896) and plaque erosion (21.1% versus 22.0%, P=0.458) was similar. In the nonculprit lesions, the DM group had greater maximal lipid arc (248.9°±83.9° versus 179.9°±58.3°, P=0.006), thinner fibrous cap thickness (103.3±56.2 μm versus 140.7±70.0 μm, P=0.013), and a higher prevalence of thin‐cap fibroatheroma (17.2% versus 6.3%, P=0.031), compared with the non‐DM group.ConclusionsCompared with patients without DM, those with DM had more vulnerable features in both culprit and nonculprit lesions, thus indicating a higher level of panvascular instability.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01110538.

Non-culprit plaque characteristics in acute coronary syndrome patients with raised hemoglobinA1c: an intravascular optical coherence tomography study

BackgroundRaised hemoglobinA1c (HbA1c) is an indicator of pre-diabetes, which is associated with increased risk of coronary artery disease. However, the detailed morphological characteristics of non-culprit plaques in acute coronary syndrome (ACS) patients remain largely unknown.MethodsA total of 305 non-culprit plaques from 216 ACS patients were analyzed by intravascular optical coherence tomography. These patients were divided into three groups according to the serum glycosylated hemoglobin level: normal HbA1c (< 5.7%), pre-diabetes with raised HbA1c (5.7–6.4%) and diabetes mellitus (DM).ResultsPlaques in patients with raised HbA1c had a longer lipid length (17.0 ± 8.3 mm vs. 13.9 ± 7.2 mm, P = 0.004) and greater lipid index (2775.0 ± 1694.0 mm° vs. 1592.1 ± 981.2 mm°, P = 0.001) than those with normal HbA1c but were similar to DM. The prevalence of calcification in patients with raised HbA1c was significantly higher (38.7% vs. 26.3%, P = 0.048) than normal HbA1c but was similar to DM. The percentage of macrophage infiltration in the DM group was higher than that in the normal HbA1c group (20.5% vs. 7.4%, P = 0.005).ConclusionsCompared to patients with normal HbA1c, the non-culprit plaques in ACS patients with raised HbA1c had more typical vulnerable features but were similar to DM.

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.