Culprit Plaque Research Articles

Abstract 10450: Higher Body Mass Index is Associated with a Higher Prevalence of Thin-Cap Fibroatheroma in Younger Patients with Type 2 Diabetes Mellitus

Introduction: High body mass index (BMI) is associated with increased incidence of type 2 diabetes (T2D) and subsequent cardiovascular disease (CVD). However, the association between the BMI and the characteristics of coronary plaque in younger T2D patients with CVD remains to be elucidated. Hypothesis: Higher BMI is associated with a higher prevalence of vulnerable coronary plaque in younger T2D patients with CVD. Methods: A total of 140 consecutive younger (<65 years) T2D patients with CVD, who underwent optical coherence tomography (OCT) imaging of the culprit lesion were included. The patients were classified into either the higher BMI group (BMI ≥25.8 kg/m 2 , n=70) or the lower BMI group (BMI <25.8 kg/m 2 , n=70) according to the median of BMI. The characteristics of culprit plaque assessed by OCT were compared between the two groups. Results: The prevalence of thin-cap fibroatheroma (TCFA) (34.8 vs. 17.4%, p =0.020) and lipid-rich plaque (44.9 vs. 26.1%, p =0.021) was significantly higher in the higher BMI group than in the lower BMI group (Panel A). The prevalence of TCFA was further compared according to the tertile of LDL-C levels. A significant trend toward higher prevalence of TCFA according to the increase in LDL-C levels was observed in patients with higher BMI ( p =0.017) (Panel B), although the trend was not significant in patients with lower BMI ( p =0.487) (Panel C). Conclusions: Higher BMI was associated with a higher prevalence of TCFA in younger T2D patients with CVD. Higher LDL-C level was associated with a higher prevalence of TCFA among patients with higher BMI although the association was not significant among patients with lower BMI.

Abstract 10824: High Bleeding Risk is Associated with a Higher Prevalence of Severe Calcified Plaque in Patients Requiring Percutaneous Coronary Intervention

Introduction: Optimal revascularization strategy and shorter duration of dual antiplatelet are required in patients with coronary artery disease concomitant with high bleeding risk (HBR). More complex percutaneous coronary intervention (PCI) and subsequent high thrombotic risk in patients with HBR have been also demonstrated. However, the characteristics of culprit plaque in patients with HBR remains to be elucidated. Hypothesis: HBR is associated with more complex plaque in culprit lesion in patients requiring PCI. Methods: A total of 362 consecutive patients with stable coronary disease, who underwent optical coherence tomography (OCT) imaging of the culprit lesion during PCI were included. The characteristics of culprit plaque assessed by OCT were compared between the HBR group (n=196) and the non-HBR group (n=166), which were classified based on the Academic Research Consortium for High Bleeding Risk (ARC-HBR). Results: The prevalence of severe calcified plaque (angle >180 degee, thickness >0.5mm and length >5mm) was significantly higher in the higher HBR group than in the non-HBR group (48 vs. 35%, p =0.016), although other characteristics were comparable (Panel A). Among patients with HBR, the incremental prevalence of severe calcified plaque according to the number of major ARC-HBR criteria met was observed ( p <0.001) (Panel B). Conclusions: HBR was associated with a higher prevalence of severe calcified plaque in culprit lesion in patients with stable coronary disease requiring PCI. The greater number of major ARC-HBR criteria met was associated with a higher prevalence of severe calcified plaque among patients with HBR.

Plaque Rupture, Compared With Plaque Erosion, Is Associated With a Higher Level of Pancoronary Inflammation

ObjectivesThe aim of this study was to compare the level of coronary inflammation between plaque rupture and plaque erosion using pericoronary adipose tissue (PCAT) attenuation. BackgroundVascular inflammation plays a key role in plaque rupture, while the role of inflammation in plaque erosion remains less well defined. PCAT attenuation determined using computed tomography has emerged as a marker specific for coronary artery inflammation. MethodsPatients with non–ST-segment elevation acute coronary syndromes who underwent preintervention coronary computed tomographic angiography and optical coherence tomographic culprit lesion imaging were enrolled. PCAT attenuation was measured around the culprit lesion and in the proximal 40 mm of all coronary arteries. ResultsAmong 198 patients, plaque rupture was the underlying mechanism in 107 (54.0%) and plaque erosion in 91 (46.0%). Plaque rupture had higher PCAT attenuation than plaque erosion both at the culprit plaque level (−65.8 ± 7.5 HU vs −69.5 ± 11.4 HU; P = 0.010) and at the culprit vessel level (−67.1 ± 7.1 HU vs −69.6 ± 8.2 HU; P = 0.024). The mean PCAT attenuation of all 3 coronary arteries was also significantly higher in patients with plaque rupture than in plaque erosion, indicating a higher level of inflammation (−67.9 ± 5.7 HU vs −69.9 ± 6.8 HU; P = 0.030). In multivariable analysis, plaque rupture was significantly associated with high PCAT attenuation. ConclusionsPCAT attenuation in culprit plaque, culprit vessel, and all 3 coronary arteries was higher in plaque rupture than in plaque erosion. The results suggest that pancoronary inflammation plays a more significant role in plaque rupture than in plaque erosion. (Massachusetts General Hospital and Tsuchiura Kyodo General Hospital Coronary Imaging Collaboration; NCT04523194)

Gender-based in vivo comparison of culprit plaque characteristics and plaque microstructures using optical coherence tomography in acute coronary syndrome.

Introduction: Women perform worse after acute coronary syndrome (ACS) than men. The reason for these differences is unclear. The aim was to ascertain gender differences in the culprit plaque characteristics in ACS. Methods: Patients with ACS undergoing percutaneous coronary intervention for the culprit vessel underwent optical coherence tomography (OCT) imaging. Culprit plaque was identified as lipid rich,fibrous, and calcific plaque. Mechanisms underlying ACS are classified as plaque rupture, erosion,or calcified nodule. A lipid rich plaque along with thin-cap fibroatheroma (TCFA) was a vulnerable plaque. Plaque microstructures including cholesterol crystals, macrophages, and microvessels were noted. Results: A total of 52 patients were enrolled (men=29 and women=23). Baseline demographic features were similar in both the groups except men largely were current smokers (P <0.001). Plaque morphology,men vs. women: lipid rich 88.0% vs. 90.5%; fibrous 4% vs 0%; calcific 8.0% vs. 9.5% (P = 0.64). Of the ACS mechanisms in males versus females; plaque rupture (76.9 % vs. 50 %), plaque erosion (15.4 % vs.40 %) and calcified nodule (7.7 % vs. 10 %) was noted (P = 0.139). Fibrous cap thickness was (50.19 ±11.17 vs. 49.00 ± 10.71 mm, P = 0.71) and thin-cap fibroatheroma (96.2% vs. 95.0%, P = 1.0) in men and women respectively. Likewise no significant difference in presence of macrophages (42.3 % vs. 30%, P = 0.76), microvessels (73.1% vs. 60 %, P = 0.52) and cholesterol crystals (92.3% vs. 80%, P = 0.38). Conclusion: No significant gender-based in-vivo differences could be discerned in ACS patients’ culprit plaques morphology, characteristics, and underlying mechanisms.

Abstract 1122‐000188: 3D Analysis of Atherosclerotic Plaque Enhancement and the Parent Vessel

Introduction : High resolution vessel wall imaging (HR‐VWI) is a promising tool in studying intracerebral atherosclerotic disease. The analysis of the interplay between the patterns of enhancement between the plaque and its parent vessel can generate further insights on the biology of these lesions. We have developed a 3D method of plaque and parent vessel analysis. Methods : Images from fifty‐five plaques were obtained using 7T HR‐VWI. T1 and T1+Gd sequences were performed. 3D reconstructions of the plaque and its parent vessel were generated with 3D Slicer. Using an in‐house code, probes were orthogonally extended from the lumen of the vessel into the vessel wall and the plaque. Signal intensity values were then normalized to the corpus callosum. 3D heat maps and histograms were generated from hundreds of data points. A detailed analysis of the morphology of the histograms was performed to determine the uptake of gadolinium (Gd) by the parent vessel and the plaque. Variations in the width of the histogram were measured with the standard deviation. Results : Forty‐one patients with 55 plaques (41 culprit and 15 non culprit) were included. There was no difference in enhancement in T1‐pre between culprit and non‐culprit plaques when compared to the parent vessel (width = 0.14 ± 0.05 and 0.14 ± 0.03, respectively; p = 0.91). On the T1+Gd culprit plaques were significantly more enhancing compared to the parent vessel (0.26 ± 0.10) than non‐culprit plaques (0.20 ± 0.06) (p = 0.02). The presence of an enhancing plaque creates a bimodal distribution that increases the width of the histogram curve (figure). Conclusions : Culprit plaques exhibit different patterns of enhancement relative to the parent vessel compared to non‐culprit plaques. Histogram analysis of the parent vessel and its plaques provides a new set of metrics that may be used as a biomarker of disease progression.

A Novel Monocyte Subset as a Unique Signature of Atherosclerotic Plaque Rupture.

The evaluation of monocyte subset distribution among acute coronary syndrome (ACS) patients according to culprit coronary plaque morphology has never been explored. We evaluated whether there were significant differences in frequency of circulating monocyte subsets isolated from ACS patients according to optical coherence tomography (OCT) investigation of plaque erosion and rupture. We enrolled 74 patients with non-ST-elevation ACS (NSTE-ACS), 21 of them underwent OCT investigation of the culprit coronary plaque and local macrophage infiltration (MØI) assessment. As control, we enrolled 30 chronic coronary syndrome (CCS) patients. We assessed the frequency of monocyte subsets in the whole study population, in reliance on their CD14 and CD16 expression (classical, CM: CD14++CD16–; intermediates, IM: CD14++CD16+; non-classical, NCM: CD14+CD16++). Then, we tested the effect of lipopolysaccharide (LPS) (a CD14 ligand) on peripheral blood mononuclear cells (PBMCs) of NSTE-ACS patients, quantifying the inflammatory cytokine levels in cell-culture supernatants. Our data proved that monocyte subsets isolated from NSTE-ACS patients represent a peculiar biological signature of the pathophysiological mechanism lying beneath atherosclerotic plaque with a ruptured fibrous cap (RFC) as compared with plaque erosion. Moreover, the magnitude of LPS-mediated effects on IL-1β, IL-6, and IL-10 cytokine release in cell-culture supernatants appeared to be greater in NSTE-ACS patients with RFC. Finally, we described a fourth monocyte population never explored before in this clinical setting (pre-classical monocytes, PCM: CD14+CD16–) that was prevalent in NSTE-ACS patients as compared with CCS and, especially, in patients with RFC and culprit plaque with MØI.

Impact of wall shear stress affected by anatomical difference between acute and chronic coronary syndrome in patients with LAD proximal disease

Abstract Recent hemodynamic studies have demonstrated that progression of coronary atherosclerosis occurs at low wall share-stress site, whereas plaque rupture frequently occurs at high share stress site. It is well recognized that wall shear stress is relatively low along the outer walls of the bifurcation. We investigated consecutive 140 patients (77 with acute coronary syndrome (ACS) and 63 with chronic coronary syndrome (CCS) performed PCI for LAD proximal lesions (AHA seg.6) from January 2016 to December 2019. In CCS group, entry criteria included stenosis of at least 90% in the LAD proximal lesion or at least 70% in the LAD proximal lesion and objective evidence of myocardial ischemia (inducible ischemia with either exercise or pharmacologic vasodilator stress or with pressure wire). Exclusion criteria were patients with maintenance dialysis, chronic total occlusion lesions, in-stent restenosis, and clinically diagnosed unstable angina without troponin I elevation. We measured the distance from LMT distal carina to the culprit site (Distance) and plaque location (Location) with intravascular ultrasound and angle between LMT and LAD with cardiovascular angiography analysis system (CAAS) (Angle). The two groups were generally well balanced with regard to baseline clinical characteristics. The mean (±SD) age of the patients was 69.0±11.8 years, and 75% were men. Medication at baseline was also similar between two groups except higher prevalence of statin prescription in CCS group. The Distance was shorter and Angle was steeper in CCS group than in ACS group. The number of patients with Angle less than 150 degrees and with Location in the lateral wall side was much more in CCS group. In this study, plaques in CCS were frequently observed at low shear stress site, whereas those in ACS at high shear stress site. Plaque progression in CCS may be associated with low wall shear stress, and high shear stress may play key role in plaque rupture in ACS. This anatomical difference can partly explain the different mechanisms of onset between of ACS and CCS. Funding Acknowledgement Type of funding sources: None. Anatomical differenceCharacteristics and results

Impact of nodular calcification on the outcomes of patients with acute coronary syndrome (ACS) treated with primary percutaneous coronary intervention (PCI)

Abstract Background Calcified plaque is thought to adversely impact clinical outcomes but the impact of nodular calcification after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) remains unclear. Purpose This study sought to explore the impact of nodular calcification on the outcomes of patients undergoing percutaneous coronary intervention for acute coronary syndromes. Methods Five-hundred culprit plaque with calcification were analysed from 495 ACS patients in whom PCI was performed. Plaques were divided into nodular calcification group (n=238) and non-nodular calcification group (n=262). Calcification is defined as an area with low back-scattering signal and a sharp border. Nodular calcification was defined as a protruding mass with an irregular surface, high backscattering, and signal attenuation on optical coherence tomography (OCT). Results Patients with nodular calcification were older (p&amp;lt;0.001) and had lower left ventricular ejection fraction (p=0.006) compared to patients with non-nodular calcification. Lesion length (31 (25.2, 38.5) vs. 29 (22.8, 34.1), p&amp;lt;0.001) was longer in plaques with nodular calcification. A higher prevalence of superficial calcium (p&amp;lt;0.001) was observed in plaques with nodular calcification compared with non-nodular calcification group. Minimum stent area (MSA) (5.0 (3.9, 6.3) vs. 5.4 (4.2, 6.7), p=0.011) and stent expansion (70 (62.7, 81.8) vs. 75 (65.2, 86.6), p=0.004) were significantly smaller in the nodular calcification group than in the non-nodular calcification group. Independent predictors of nodular calcification were age (p&amp;lt;0.001) lesion length (p=0.002) and calcium depth (p&amp;lt;0.001). Conclusion This study demonstrated that the presence of nodular calcification is associated with unfavourable outcomes with smaller minimum stent area and higher incidence of stent under expansion in patients with ACS treated with primary PCI. Funding Acknowledgement Type of funding sources: None.

Comparison of peripheral artery plaque characteristics between ACS patients with plaque rupture and plaque erosion in culprit coronary artery: an OCT and ultrasound study

Abstract Background Recent research has found that the characteristics of peripheral arterial plaque are related to the increased risk of cardiovascular disease, however, the relationship of plaque characteristics between peripheral artery and coronary is still unknown. Purpose To assess the correlation between coronary plaque characteristics assessed by optical coherence tomography (OCT) and peripheral artery plaque characteristics assessed by ultrasound. Methods 150 patients with acute coronary syndrome (ACS) underwent coronary angiography were prospectively enrolled. OCT imaging of culprit vessel were performed during the procedure and ultrasound examination of bilateral carotid, iliofemoral and popliteal arteries was performed during hospitalization after procedure. Panvascular disease was defined as the presence of observable plaques in two or more vascular beds. Patients were divided into plaque rupture (PR) group and plaque erosion (PE) group according to culprit plaque characteristics on OCT. Results There were 132 (88%) ACS patients had panvascular disease in which 36 (24%) with generalized atherosclerosis (4 sites) and the prevalence of panvascular atherosclerosis in PR group was significantly higher than in PE group especially in carotid arteries and iliofemoral arteries (Figure 1, Figure 2). Compared to PE group, PR group had higher carotid plaque score (p=0.001) which indicates more plaques and severer atherosclerosis. Moreover, there were larger intima-media thickness (IMT) of iliofemoral arteries (6.9±1.4mm vs. 6.5±1.1mm, p=0.036) and more calcified plaques in PR group. Conclusions Panvascular disease is highly prevalent in ACS patients especially in patients with plaque rupture in culprit vessel, in which more than half of the patients had plaques in more than 3 sites of vascular beds. In addition, patients with plaque rupture had thicker iliofemoral IMT and higher panvascular atherosclerosis burden, which indicates that characteristics of coronary plaques are the focal expression of plaques in the whole panvcascular system. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): National Key R&amp;D Program of China Figure 1. Prevalence of panvascular disease in ACSFigure 2. Comparison of peripheral artery plaques

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

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). 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. 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. 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.

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. 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.

Association between apolipoprotein B/A1 ratio and coronary plaque vulnerability in patients with atherosclerotic cardiovascular disease: an intravascular optical coherence tomography study

BackgroundApolipoprotein (Apo) A1 and Apo B are strongly associated with the risk of atherosclerotic cardiovascular disease (ASCVD). However, the relationship between the Apo B/A1 ratio and the morphology of coronary vulnerable plaques has not been fully elucidated in patients with ASCVD.MethodsA total of 320 patients with ASCVD undergoing percutaneous coronary intervention were enrolled and assigned into acute coronary syndrome (ACS) or chronic coronary syndrome (CCS) group. The morphology of culprit plaque was analyzed by intravascular optical coherence tomography. Association between the Apo B/A1 ratio and coronary vulnerable plaques were evaluated using logistic regression models and receiver operator characteristic (ROC) curve analyses.ResultsThe Apo B/A1 ratio was higher in ACS patients than CCS patients (0.77 ± 0.28 vs. 0.64 ± 0.22, P < 0.001) and it was also higher in patients with plaque rupture, erosion or thrombus than those without culprit plaques. The high Apo B/A1 ratio was associated with high percent of vulnerable plaques compared with low ratio group. The Apo B/A1 ratio was negatively related to fibrous cap thickness in lipid-rich plaque (r = − 0.228, P = 0.043). Univariate and multivariate logistic regression analyses revealed that the Apo B/A1 ratio was an independent factor of plaque rupture, erosion, and thrombus. The area under the ROC curve of the Apo B/A1 ratio for plaque rupture, erosion, and thrombus were 0.632, 0.624, and 0.670 respectively (P < 0.001 for all), which were higher than that of low-density lipoprotein cholesterol.ConclusionsThe Apo B/A1 ratio is an independent predictor for plaque rupture, erosion, and thrombus in patients with ASCVD.

Focal Geometry and Characteristics of Erosion-Prone Coronary Plaques in vivo Angiography and Optical Coherence Tomography Study.

Objective: This study compared focal geometry and characteristics of culprit plaque erosion (PE) vs. non-culprit plaques in ST-segment elevated myocardial infarction (STEMI) patients in whom optical coherence tomography (OCT) identified PE as the cause of the acute event.Background: Culprit PE is a distinct clinical entity with specific coronary risk factors and its own tailored management strategy. However, not all plaques develop erosion resulting in occlusive thrombus formation.Methods: Between January 2017 and July 2019, there were 484 STEMI patients in whom OCT at the time of primary percutaneous intervention identified culprit lesion PE to be the cause of the event; 484 culprit PE were compared to 1,132 non-culprit plaques within 1,196 imaged vessels.Results: Culprit PE were highly populated at “hot spots” within the proximal 40 mm in the left anterior descending artery (LAD) and tended to cluster proximal to a nearby bifurcation mainly in the LAD. Minimal lumen area (MLA) <2.51 mm2 and AS (area stenosis) >64.02% discriminated culprit PE from non-culprit plaques. In the multivariable analysis, focal geometry (LAD location, distance from coronary ostium <40 mm, and location proximal to a nearby bifurcation), luminal narrowing (MLA <2.51 mm2, AS > 64.02%), and TCFA phenotype were independent predictors of culprit PE overall. Cholesterol crystals were predictive of culprit PE with underlying LRP morphology while the absence of calcification and microchannels were risk factors for culprit PE with an underlying non-LRP. Similarities and differences in predictors of culprit PE were found between males and females; distance from coronary ostium <40 mm, MLA <2.51 mm2, TCFA, and less spotty calcium were risk factors of culprit PE in males, but not in females while smaller RVD was associated with culprit PE only in females.Conclusions: Irrespective of underlying lesion substrates and patient risk factors, there are lesion-specific and OCT-identifiable predictors of developing culprit PE in erosion-prone vulnerable patients.

Coronary plaque and clinical characteristics of South Asian (Indian) patients with acute coronary syndromes: An optical coherence tomography study

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

Intravascular ultrasound insights into the unstable features of the coronary atherosclerotic plaques: A systematic review and meta‐analysis

There is a lack of a comprehensive picture of plaque geometry and composition of unstable atherosclerotic lesions as observed with intravascular ultrasound techniques. We analysed through a systematic review with meta-analysis 39 characteristics of atherosclerotic plaques in three scenarios involving culprit and non-culprit lesions from acute coronary syndromes vs stable angina pectoris patients, and culprit vs non-culprit lesions in acute coronary syndromes patients. A systematic search of PubMed and EMBASE, from inception to April 2020 was performed. The combined odds ratios or mean differences of all IVUS characteristics were calculated with random-effects models. Twenty-eight studies involving 5434 subjects, and 5618 lesions were included. Culprit lesions in acute coronary syndromes have larger plaque areas and remodeling indexes (MD=0.13 [0.08; 0.17], p<0.001) and contained larger necrotic cores (MD=0.67 (95% CI 0.19;1.15), p=0.006) that stable angina culprit lesions. In acute patients, culprit plaques were also more remodeled, had larger necrotic cores and had more frequently a Thin-Cap Fibroatheroma morphology (OR=1.79 (95% CI 1.21; 2.65), p=0.004) than non-culprit lesions. Non-culprit lesions in acute syndromes were more often ruptured (OR=2.25 (95% CI:1.05; 4.82), p=0.037) or Thin-Cap Fibroatheromas than in stable angina. Culprit lesions from acute coronary patients are larger, more positively remodeled and contained more lipids as compared to stable angina lesions or non-culprit in acute patients. Non culprit lesions are also more often complicated or vulnerable in acute than stable patients.

Impact of Low Body Mass Index on Features of Coronary Culprit Plaques and Outcomes in Patients With Acute Coronary Syndrome

The mechanisms behind poorer cardiac outcomes in underweight patients with acute coronary syndrome (ACS) are not understood and features of coronary culprit lesions in underweight ACS patients have not been fully examined. A total of 1,683 patients with ACS were divided into 4 groups according to body mass index (BMI): <18.5 (n=73), 18.5 to 24.9 (n=995), 25 to 29.9 (n=488), and ≥30 (n=117). Angiography and optical coherence tomography (OCT) images were analyzed for 1,428 of these patients who had primary percutaneous coronary intervention (PCI) and 838 who had primary PCI with OCT guidance, respectively. Diabetes (p <0.001), hypertension (p <0.001), and dyslipidemia (p <0.001) were less prevalent in BMI <18.5. Statin prescription at discharge was less frequent in the BMI <18.5 group (p <0.001). Quantitative coronary angiography analyses revealed smaller reference vessel (p=0.001) and minimum lumen diameters after PCI (p=0.019) and OCT revealed longer lipidic plaque length (p=0.029) in the BMI <18.5 group. Kaplan-Meier analyses revealed higher rates of cardiac mortality (p <0.001) and major bleeding (p=0.034) during the 2-year follow-up in the BMI <18.5 group. After adjusting for traditional cardiovascular risk factors, BMI <18.5 independently predicted 2-year cardiac mortality (hazard ratio 1.917 [95% confidence interval [1.082 to 3.397], p=0.026). In conclusion, being underweight contributed to poorer cardiac outcomes in established ACS population. Smaller minimum lumen diameter after PCI and further progressed atherosclerosis at the culprit lesions despite their lower prevalence of comorbid metabolic risk factors may be related partly to poorer cardiac outcomes.

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.

Morphological Plaque Characteristics and Clinical Outcomes in Patients With Acute Coronary Syndrome and a Cancer History

BackgroundAlthough patients with a cancer history have a 2 to 3 times higher risk for acute coronary syndrome (ACS), the morphological characteristics of ACS culprit plaque in those patients and their relations with clinical outcomes remain unknown.Methods and ResultsThis retrospective, multicenter, observational cohort study included consecutive patients with ACS who underwent optical coherence tomography‐guided emergent percutaneous coronary intervention. Patients were categorized into those without a cancer history, those with a cancer history, and those currently receiving cancer treatment. ACS culprit lesions were classified as plaque rupture, plaque erosion, or calcified nodule using optical coherence tomography. Plaque erosion frequency was significantly higher in culprit lesions of patients with current cancer and patients with cancer history than in those of patients without cancer history (56.3% versus 61.7% versus 36.5%). Calcified nodule incidence was significantly higher in patients without cancer history than in patients with current cancer and patients without cancer history (patients with current cancer: 12.4% versus patients without cancer history: 25.5% versus patients without cancer history: 12.6%, P<0.001). Cancer history was independently associated with nonplaque rupture (plaque erosion or calcified nodule) in ACS culprit lesions (odds ratio, 4.00; P<0.001). Cancer history was independently associated with major adverse cardiovascular events (hazard ratio [HR], 1.98; P=0.002). Nonplaque rupture in ACS culprit lesions was independently associated with major adverse cardiovascular events (HR, 1.60; P=0.011).ConclusionsPatients with a cancer history had significantly worse clinical outcomes after ACS than those without a cancer history. Those with a cancer history had significantly higher plaque erosion and calcified nodule incidences in the ACS culprit lesions, which might partly explain their worse clinical outcomes.RegistrationURL: www.umin.ac.jp/ctr/index.htm. Unique Identifier: UMIN000038442.

Cardio-ankle vascular index is associated with coronary plaque composition assessed with iMAP-intravascular ultrasound in patients with coronary artery disease

BackgroundThe cardio-ankle vascular index (CAVI) is an indicator of arterial stiffness and has been reported to be associated with the severity of coronary artery disease and cardiovascular events. However, whether CAVI can predict the composition of coronary plaques remains unclear. MethodsWe enrolled 208 patients who underwent percutaneous coronary intervention (PCI) for culprit lesions evaluated with iMAP-intravascular ultrasound (IVUS), a radiofrequency imaging system for characterizing tissues. iMAP-IVUS classified the culprit plaque composition as fibrotic, lipidic, necrotic, or calcified, and the respective absolute volumes [fibrotic volume (FV), lipidic volume (LV), necrotic volume NV, and calcified volume] and their ratios (%) within the total plaque volume were calculated. A plaque with a median %NV of ≥ 33.2% was defined as a larger NV (LNV) plaque. We measured CAVI and divided the patients into two groups according to CAVI ≥8 (high CAVI, n = 164) or <8 (low CAVI, n = 44). ResultsCulprit plaques had significantly greater absolute NV (p = 0.016), %NV (p = 0.01), and smaller %FV (p = 0.02) in patients with high CAVI than in those with low CAVI. Patients with high CAVI had a higher prevalence of LNV plaques in culprit lesions than those with low CAVI (54% vs. 34%, p = 0.026). CAVI correlated significantly and positively with absolute NV, LV, and negatively with %FV. In logistic regression analysis after adjustment for the classic coronary risk factors and possible variables associated with vulnerable plaques, high CAVI had an independent and significant association with the presence of LNV plaques (OR, 3.37; 95% CI, 1.45–7.79; p = 0.0032). ConclusionsA high CAVI is associated with the composition of coronary culprit plaques, particularly increased amount of necrotic tissue, in patients with coronary artery disease undergoing PCI .

Understanding the Clinical Implications of Intracranial Arterial Calcification Using Brain CT and Vessel Wall Imaging.

Background and Purpose: Intracranial arterial calcification (IAC) has been the focus of much attention by clinicians and researchers as an indicator of intracranial atherosclerosis, but correlations of IAC patterns (intimal or medial) with the presence of atherosclerotic plaques and plaque stability are still a matter of debate. Our study aimed to assess the associations of IAC patterns identified on computed tomography (CT) with the presence of plaque detected on vessel wall magnetic resonance imaging and plaque stability.Materials and Methods: Patients with stroke or transient ischemic attack and intracranial artery stenosis were recruited. IAC was detected and localized (intima or media) on non-contrast CT images. Intracranial atherosclerotic plaques were identified using vessel wall magnetic resonance imaging and matched to corresponding CT images. Associations between IAC patterns and culprit atherosclerotic plaques were assessed by using multivariate regression.Results: Seventy-five patients (mean age, 63.4 ± 11.6 years; males, 46) were included. Two hundred and twenty-one segments with IAC were identified on CT in 66 patients, including 86 (38.9%) predominantly intimal calcifications and 135 (61.1%) predominantly medial calcifications. A total of 72.0% of intimal calcifications coexisted with atherosclerotic plaques, whereas only 10.2% of medial calcifications coexisted with plaques. Intimal calcification was more commonly shown in non-culprit plaques than culprit plaques (25.9 vs. 9.4%, P = 0.008). The multivariate mixed logistic regression adjusted for the degree of stenosis showed that intimal calcification was significantly associated with non-culprit plaques (OR, 2.971; 95% CI, 1.036–8.517; P = 0.043).Conclusion: Our findings suggest that intimal calcification may indicate the existence of a stable form of atherosclerotic plaque, but plaques can exist in the absence of intimal calcification especially in the middle cerebral artery.