Near-infrared Spectroscopy Intravascular Ultrasound Research Articles

Clinical Utility of Near-Infrared Spectroscopy Intravascular Ultrasound in the Assessment of Rapidly Progressive Cardiac Allograft Vasculopathy.

Clinical Utility of Near-Infrared Spectroscopy Intravascular Ultrasound in the Assessment of Rapidly Progressive Cardiac Allograft Vasculopathy.

Computed tomography versus near-infrared spectroscopy for the assessment of coronary atherosclerosis.

Coronary computed tomography angiography (CCTA) has been proposed as an alternative to intravascular imaging for assessing plaque pathology. We aimed to assess the efficacy of CCTA against near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) in evaluating atheroma burden and composition and for guiding coronary interventions. Seventy patients with a chronic coronary syndrome were recruited and underwent CCTA and NIRS-IVUS. The imaging data were matched, and the estimations of lumen, vessel wall and plaque dimensions and composition of the two modalities were compared. The primary endpoint of the study was the efficacy of CCTA in detecting lipid-rich plaques identified by NIRS-IVUS. Secondary endpoints included the performance of CCTA in evaluating coronary artery pathology in the studied segments and its value in stent sizing, using NIRS-IVUS as the reference standard. In total, 186 vessels were analysed. The attenuated plaque volume on CCTA had weak accuracy in detecting lipid-rich plaques (58%; p=0.029). Compared to NIRS-IVUS, CCTA underestimated the lumen volume (309.2 mm3 vs 420.4 mm3; p=0.001) and plaque dimensions (total atheroma volume 116.1 mm3 vs 292.8 mm3; p<0.001 and percentage atheroma volume 27.67% vs 41.06%; p<0.001) and overestimated the lipid component (lipid core burden index 48.6 vs 33.8; p=0.007). In the 86 lesions considered for revascularisation, CCTA underestimated the reference vessel area (8.16 mm2 vs 12.30 mm2; p<0.001) and overestimated the lesion length (23.5 mm vs 19.0 mm; p=0.029) compared to NIRS-IVUS. CCTA has limited efficacy in assessing plaque composition and quantifying lumen and plaque dimensions and tissue types, which may potentially impact revascularisation planning.

Evaluation of non-target lesions in femoropopliteal disease using near-infrared spectroscopy intravascular ultrasound imaging

Abstract Aim This study aims to assess the plaque morphology of non-target lesions, especially lipid-core-containing plaque (LCP), and compare it to target lesions using near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) in patients with femoropopliteal disease. Methods We conducted a single-center prospective observational study on 14 patients who underwent endovascular therapy for femoropopliteal disease between July 2022 and November 2023. NIRS-IVUS assessment was performed on the whole femoropopliteal arterial segment. Forty-one LCP lesions &amp;gt; maximum lipid-core burden index in any 4-mm region (max LCBI4mm) 100 were detected by NIRS-IVUS. We evaluated patient and lesion characteristics. In addition, the LCP lesions were divided into two groups, the target lesion group (n=18) and the non-target lesion group (n=23), and compared. Results Patient characteristics were notable for advanced age (76.8±6.6 years), high incidence of male (78.7%), hypertension (100%), dyslipidemia (78.6%), diabetes (64.3%), statin use (71.4%). Lipid profiles were as follows: LDL-cholesterol 85.9±26.7 mg/dl, HDL-cholesterol 48.9±12.7 mg/dl, triglyceride 138.9±80.3 mg/dl, lipoprotein(a) 19.6±16.3 mg/dl. Ten participants had LCPs in the non-target lesion (71.4%). For IVUS findings, the target lesion group had significantly longer lesion length (34.6±11.9 mm vs. 22.6±8.7 mm, p=0.001), smaller minimum lumen area (7.0±2.8 mm2 vs. 14.8±5.4 mm2, p&amp;lt;0.001), and larger plaque burden (78.0±5.0 % vs. 53.0±12.0 %, p&amp;lt;0.001) than those in the non-target lesion group. No significant differences were observed in the prevalence of calcification (target lesion group vs. non-target lesion group: 83.3 % vs. 91.3 %, p=0.64) and the extent of calcification (p=0.76). For NIRS findings, the target lesion group contained a significantly smaller proportion of LCP in the lesion length (25.9±15.7 % vs. 50.6±29.2 %, p=0.002) than the non-target lesion group. On the other hand, there were no significant differences in the value of max LCBI4mm (284.4±153.4 vs. 289.5±113.1, p=0.90) and the length of LCP lesion (9.8±9.7 mm vs. 10.7±6.9 mm, p=0.74) and distribution of LCP (p=0.08) between both groups. In addition, the number of LCPs in the target femoropopliteal artery was positively correlated with max LCBI4mm in the target femoropopliteal artery (r=0.671, p=0.008) Conclusion NIRS-IVUS findings in this study demonstrated that the non-target lesions contained LCPs to the same degree as the target lesions.

Evaluation of nontarget lesions in femoropopliteal disease using near-infrared spectroscopy intravascular ultrasound imaging.

In coronary artery disease (CAD), lipid-core-containing plaque (LCP) in nontarget lesions detected using near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) was related to increased major adverse cardiovascular events in patients with CAD. In the endovascular therapy field, few previous studies using NIRS-IVUS revealed the presence of LCPs in severe stenotic lesions of femoropopliteal disease. This study aimed to assess the plaque morphology of nontarget lesions, especially LCPs, and compare it with that of target lesions using NIRS-IVUS in patients with femoropopliteal disease. This single-center prospective observational study included 14 patients who underwent endovascular therapy for FP disease. NIRS-IVUS assessment was performed on the entire FP arterial segment. Forty-one LCP lesions with a maximum lipid-core burden index in any 4-mm region (max LCBI4mm) > 100 were detected using NIRS-IVUS. We evaluated the patient and lesion characteristics. LCP lesions were divided into the target (n = 18) and nontarget (n = 23) lesion groups for comparison. Patient characteristics were notable for advanced age (76.8 ± 6.6 years); high proportion of males (78.7%); and high incidence of hypertension (100%), dyslipidemia (78.6%), diabetes (64.3%). Regarding NIRS findings, the target lesion group exhibited a significantly smaller proportion of LCPs concerning the lesion length (25.9 ± 15.7% vs. 50.6 ± 29.2%, p = 0.002) than the nontarget lesion group. Conversely, there were no significant differences in the value of max LCBI4mm (284.4 ± 153.4 vs. 289.5 ± 113.1, p = 0.90), length of LCP lesion (9.8 ± 9.7 mm vs. 10.7 ± 6.9 mm, p = 0.74), and distribution of LCPs (p = 0.08) between the groups. In addition, the number of LCPs in the target FP artery positively correlated with max LCBI4mm in the target FP artery (r = 0.671, p = 0.008). NIRS-IVUS findings demonstrated the presence of LCPs in nontarget lesions in patients with FP disease. Moreover, the abundance of LCPs in nontarget lesions was similar to that in target lesions in FP disease.

Very short-term effects of a single dose of a proprotein convertase subtilisin/kexin 9 inhibitor before percutaneous coronary intervention: A single-arm study

Background and aimsThe short-term (within 6 weeks) effects of proprotein convertase subtilisin/kexin 9 (PCSK9) inhibitors on lipid plaques have not been adequately evaluated. We aimed to investigate whether a single dose of a PCSK9 inhibitor before percutaneous coronary intervention (PCI) could reduce the abundance of lipid-core plaques identified via near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) at target lesions within a very short period. MethodsThis prospective, single-arm, single-center interventional study enrolled 27 consecutive patients with coronary artery disease. These patients underwent NIRS-IVUS during coronary angiography and repeat NIRS-IVUS during PCI performed between 2 and 6 weeks after the single-dose administration of 420 mg evolocumab. Changes in lesion lipid-core burden index (LCBI) and maximal LCBI over any 4-mm segment (max-LCBI4mm) were assessed using NIRS at the target lesions, along with lipid profile. ResultsThe max-LCBI4mm significantly decreased from 387 before PCSK9 inhibitor administration to 315 after its administration (interquartile range [IQR]: 268–572 and 221–488, respectively; p = 0.02) within a very short period. The lesion LCBI also decreased from 161 to 117 (IQR: 105–263 and 65–226, respectively; p = 0.02). No significant changes were observed in the minimum lumen area and diameter. After PCSK9 inhibitor administration, low-density lipoprotein (LDL) cholesterol (p < 0.001), lipoprotein(a) (p = 0.001), and malondialdehyde-modified LDL (p < 0.001) levels decreased compared with those before its administration. ConclusionsA single dose of the PCSK9 inhibitor administered before PCI reduced the abundance of lipid-core plaques identified via NIRS-IVUS at target lesions within a very short period of 2–6 weeks.

Implications of coronary calcification on the assessment of plaque pathology: a comparison of computed tomography and multimodality intravascular imaging.

This study aimed to investigate the impact of calcific (Ca) on the efficacy of coronary computed coronary angiography (CTA) in evaluating plaque burden (PB) and composition with near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) serving as the reference standard. Sixty-four patients (186 vessels) were recruited and underwent CTA and 3-vessel NIRS-IVUS imaging (NCT03556644). Expert analysts matched and annotated NIRS-IVUS and CTA frames, identifying lumen and vessel wall borders. Tissue distribution was estimated using NIRS chemograms and the arc of Ca on IVUS, while in CTA Hounsfield unit cut-offs were utilized to establish plaque composition. Plaque distribution plots were compared at segment-, lesion-, and cross-sectional-levels. Segment- and lesion-level analysis showed no effect of Ca on the correlation of NIRS-IVUS and CTA estimations. However, at the cross-sectional level, Ca influenced the agreement between NIRS-IVUS and CTA for the lipid and Ca components (p-heterogeneity < 0.001). Proportional odds model analysis revealed that Ca had an impact on the per cent atheroma volume quantification on CTA compared to NIRS-IVUS at the segment level (p-interaction < 0.001). At lesion level, Ca affected differences between the modalities for maximum PB, remodelling index, and Ca burden (p-interaction < 0.001, 0.029, and 0.002, respectively). Cross-sectional-level modelling demonstrated Ca's effect on differences between modalities for all studied variables (p-interaction ≤ 0.002). Ca burden influences agreement between NIRS-IVUS and CTA at the cross-sectional level and causes discrepancies between the predictions for per cent atheroma volume at the segment level and maximum PB, remodelling index, and Ca burden at lesion-level analysis. Coronary calcification affects the quantification of lumen and plaque dimensions and the characterization of plaque composition coronary CTA. This should be considered in the analysis and interpretation of CTAs performed in patients with extensive Ca burden. Coronary CT Angiography is limited in assessing coronary plaques by resolution and blooming artefacts. Agreement between dual-source CT angiography and NIRS-IVUS is affected by a Ca burden for the per cent atheroma volume. Advanced CT imaging systems that eliminate blooming artefacts enable more accurate quantification of coronary artery disease and characterisation of plaque morphology.

Intracoronary Near-Infrared Spectroscopy to Predict No-Reflow Phenomenon During Percutaneous Coronary Intervention in Acute Coronary Syndrome

Near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) can identify the lipid-rich lesions, described as high lipid-core burden index (LCBI). The aim of this study was to investigate the relationship between lipid core plaque (LCP) in the infarct-related lesion detected using NIRS-IVUS and no-reflow phenomenon during percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS). We investigated 371 ACS patients who underwent NIRS-IVUS in the infarct-related lesions before PCI. The extent of LCP in the infarct-related lesion was calculated as the maximum LCBI for each of the 4-mm longitudinal segments (maxLCBI4mm) measured by NIRS-IVUS. The patients were divided into 2 groups using a maxLCBI4mm cut-off value of 400. The overall incidence of no-reflow phenomenon was 53/371 (14.3%). No-reflow phenomenon was more frequently occurred in patients with maxLCBI4mm ≥400 compared to those with maxLCBI4mm <400 (17.5% vs. 2.5%, p<0.001). After propensity score matching, multivariable logistic regression analysis demonstrated that maxLCBI4mm (odds ratio: 1.008; 95% confidence interval: 1.005 - 1.012, p<0.001) was independently associated with no-reflow phenomenon. The maxLCBI4mm of 719 in the infarct-related lesion had the highest combined sensitivity (69.8%) and specificity (72.1%) for the identification of no-reflow phenomenon. In conclusion, in patients with ACS, maxLCBI4mm in the infarct-related lesion assessed by NIRS-IVUS was independently associated with no-reflow phenomenon during PCI.

Efficacy of Coronary Calcium Score in Predicting Coronary Artery Morphology in Patients With Obstructive Coronary Artery Disease

BackgroundCoronary artery calcium score (CACS) is an established marker of coronary artery disease (CAD) and has been extensively used to stratify risk in asymptomatic individuals. However, the value of CACS in predicting plaque morphology in patients with advanced CAD is less established. The present analysis aims to assess the association between CACS and plaque characteristics detected by near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS) imaging in patients with obstructive CAD. MethodsSeventy patients with obstructive CAD underwent coronary computed tomography angiography (CTA) and 3-vessel NIRS-IVUS imaging were included in the present analysis. The CTA data were used to measure the CACS in the entire coronary tree and the segments assessed by NIRS-IVUS, and these estimations were associated with the NIRS-IVUS measurements at a patient and segment level. ResultsIn total, 65 patients (188 segments) completed the study protocol and were included in the analysis. A weak correlation was noted between the CACS, percent atheroma volume (r = 0.271, P = .002), and the calcific burden measured by NIRS-IVUS (r = 0.648, P < .001) at patient-level analysis. Conversely, there was no association between the CACS and the lipid content, or the incidence of high-risk plaques detected by NIRS. Linear regression analysis at the segment level demonstrated an association between the CACS and the total atheroma volume (coefficient, 0.087; 95% CI, 0.024-0.149; P = .008) and the calcific burden (coefficient, 0.117; 95% CI, 0.048-0.186; P = .001), but there was no association between the lipid content or the incidence of high-risk lesions. ConclusionsIn patients with obstructive CAD, the CACS is not associated with the lipid content or plaque phenotypes. These findings indicate that the CACS may have a limited value for screening or stratifying cardiovascular risk in symptomatic patients with a high probability of CAD.

NIRS-IVUS Assessment of OCT-Derived Healed Coronary Plaques.

Healed plaque (HP) is associated with rapid plaque growth and luminal narrowing. Thin-cap fibroatheroma (TCFA) is recognized as a precursor lesion to plaque rupture. The aim of the present study was to compare the lipid size among optical coherence tomography (OCT)-derived HP, TCFA, and thick-cap fibroatheroma (ThCFA) using near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS). The present study included 173 patients with acute myocardial infarction (AMI) who underwent percutaneous coronary intervention. Non-culprit lesions with angiographically intermediate stenosis were assessed by both OCT and NIRS-IVUS. The frequency of TCFA, HP, and ThCFA was 35 (20%), 53 (30%), and 85 (49%), respectively. Minimum lumen area was not significantly different between TCFA and HP, but was smaller in TCFA and HP than in ThCFA (4.6 [interquartile range {IQR}: 3.5-6.4] mm2 vs. 4.3 [3.4-5.3] mm2 vs. 6.5 [4.8-8.6] mm2, P＜0.001). Plaque burden was not significantly different between TCFA and HP, but was larger in TCFA and HP than in ThCFA (72 [IQR: 66-80] % vs. 75 [67-80] % vs. 62 [54-69] %, P＜0.001). Maximum lipid core burden index in 4mm (maxLCBI4mm) was largest in TCFA, followed by HP and ThCFA (493 [IQR: 443-606] vs. 446 [347-520] vs. 231 [161-302], P＜0.001). The frequency of lipid rich plaque with maxLCBI4mm ＞400 was highest in TCFA, followed by HP and ThCFA (89% vs. 60% vs. 7%, P＜0.001). Based on NIRS-IVUS findings, non-culprit coronary HP in AMI was associated with vulnerable plaque characteristics, but not as much as TCFA.

Mechanical wall stress and wall shear stress are associated with atherosclerosis development in non-calcified coronary segments

Background and aimsAtherosclerotic plaque onset and progression are known to be affected by local biomechanical factors. Whereas the role of wall shear stress (WSS) has been studied, the impact of another biomechanical factor, namely mechanical wall stress (MWS), remains poorly understood. In this study, we investigated the association of MWS, independently and combined with WSS, towards atherosclerosis in coronary arteries. MethodsThirty-four human coronary arteries were analyzed using near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) at baseline and after 12 months. Baseline WSS and MWS were calculated using computational models, and wall thickness (ΔWT) and lipid-rich necrotic core size (ΔLRNC) change were measured in non-calcified coronary segments. The arteries were further divided into 1.5 mm/45° sectors and categorized as plaque-free or plaque sectors. For each category, associations between the biomechanical factors (WSS & MWS) and changes in the coronary wall (ΔWT & ΔLRNC) were studied using linear mixed models. ResultsIn plaque-free sectors, higher MWS (p < 0.001) was associated with greater vessel wall growth. Plaque sectors demonstrated wall thickness reduction over time, likely due to the medical therapy, where higher levels of WSS and WMS, individually and combined, (p < 0.05) were associated with a greater reduction. Sectors with low MWS combined with high WSS demonstrated the highest LRNC increase (p < 0.01). ConclusionsIn this study, we investigated the association of the (largely-overlooked) biomechanical factor, MWS with coronary atherosclerosis, individually and combined with WSS. Our results demonstrated that both MWS and WSS significantly correlate with atherosclerotic plaque initiation and development.

Lowering apolipoprotein C-III associates with regression of lipidic plaque materials in type 2 DM patients with coronary artery disease: the pre-specified analysis from the OPTIMAL trial

Abstract Introduction Apolipoprotein CIII (ApoC-III) is a circulating lipoprotein which affects triglyceride-rich lipoprotein metabolism and functionality of high-density lipoproteins. These properties indicate ApoC-III as a potential contributor to atherosclerosis. The OPTIMAL randomized controlled trial (jRCT1052180152) compared the efficacy of continuous glucose monitoring guided versus HbA1c-guided glycemic control on coronary atherosclerosis in Type 2 Diabetes (T2DM) patients by using serial near-infrared spectroscopy/intravascular ultrasound (NIRS/IVUS). Given that NIRS/IVUS imaging enables to quantitatively evaluate plaque burden and its lipidic component in vivo, the OPTIMAL study provides an opportunity to elucidate the association of ApoC-III with change in quantity and quality of coronary plaques. Purpose To elucidate whether serial change in ApoC-III affects the degree of atheroma progression and lipidic plaque materials on NIRS/IVUS imaging. Methods The OPTIMAL trial has serially monitored non-culprit lesions in 94 T2DM patients receiving PCI by NIRS/IVUS imaging. Of these, 46 patients (73 lesions) were included into the current analysis. Circulating ApoC-III levels were measured at both baseline and 48 weeks. The relationships of serial change in ApoC-III with NIRS/IVUS-derived measures [total atheroma volume (TAV) and maximum lipid core burden index in a 4-mm segment (maxLCBI4mm)] were analyzed. Results All of study subjects received a statin, and high-intensity statin was used in 65.2% of them. On-treatment LDL-C and HbA1c levels were 1.9±0.5mmol/L and 7.2±0.7%, respectively. On NIRS/IVUS analysis, any regression of TAV and maxLCBI4mm was observed in 71.2 and 38.4% of analyzed lesions, respectively (Table). There was no significant relationship between change in ApoC-III and TAV regression (r=0.02, p=0.89). However, a reduction of ApoC-III was significantly associated with a greater regression of maxLCBI4mm (r=0.26, p=0.03) (Figure). Furthermore, multivariate analysis adjusting for LDL-C and high-intensity statin use demonstrated lowering ApoC-III level as an independent predictor of maxLCBI4mm regression (OR=0.83, 95%CI=0.69-0.99, p=0.04) (Table). Even in patients receiving high-intensity statin, the relationship of change in ApoC-III with regression of maxLCBI4mm still existed (Figure). Conclusion Serial NIRS/IVUS imaging revealed that a reduction of circulating ApoC-III was associated with a greater regression of maxLCBI4mm. Our findings suggest ApoC-III as an important therapeutic target to modulate lipidic plaque materials in T2DM receiving a statin.Tables

Plaque progression is dependent on the local hemodynamics (time-averaged wall shear stress and TSVI) in combination with the plaque phenotype

Abstract Objective To investigate the predictive power of TSVI for plaque growth in human coronary arteries in plaques with different phenotypes. Methods 38 non-stented, non-culprit coronary arteries (MPACT study) were imaged with near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) at the baseline and after 12 months [2]. Coronary reconstructions were based on fusion of the multimodality imaging and used as input for computational fluid dynamics. Vessel-specific flow was measured using Doppler wire and used as input to calculate TAWSS and TSVI [2]. The coronary arteries were subdivided into 1.5 mmx45º sectors and the TAWSS and TSVI were classified as low, mid and high based on the range per vessel. Per sector the plaque growth was quantified as plaque burden (Plaque area/total vessel area*100%) change over time (ΔPAV). Based on the NIRS and OCT data, the sectors were characterized as lipid rich plaque (wall thickness&amp;gt;0.5 mm &amp; NIRS+, lipid rich(OCT)) or plaque without lipid (wall thickness &amp;gt;0.5 mm &amp; NIRS-, fibrous (OCT)) or plaque free wall (wall thickness &amp;lt;0.5 mm &amp;NIRS-, PFW (OCT)). The effect of TAWSS, TSVI and the combination with plaque phenotype on plaque progression was evaluated using Linear Mixed Model in SPSS. Results TSVI at baseline was significantly associated with PAV increase, with high PAV for high TSVI (p&amp;lt;0.001). A clear trend emerged for TAWSS, with high PAV for low TAWSS at baseline (Figure 1B). The highest plaque progression at 1-year follow-up was observed for lipid rich plaques (both based on NIRS and OCT) exposed to either low TAWSS or high TSVI (figure 2). Also in the PFW sectors clear plaque progression was observed dependent on either TAWSS or TSVI. Conclusion Lipid rich regions exposed to either low TAWSS or high TSVI are at the highest risk for plaque progression. These data suggest that although TAWSS and TSVI have a different mechanism of action on the endothelium, but both actions are involved in plaque progression.Figure 1Figure 2

Influence of wall shear and structural stress on plaque progression of different phenotype in human coronary arteries

Abstract Introduction Atherosclerotic plaque progression is affected by local wall shear stress (WSS), .i.e. the frictional force of the blood at the vessel wall [1,2]. However, the blood pressure also induces stress inside the vessel wall (wall stress, WMS) and is mainly studied for plaque rupture [3]. Little is known on the impact of WMS on plaque progression. Purpose In order to have a comprehensive understanding of the involvement of the biomechanical factors (WSS and WMS) in atherosclerotic artery disease, we studied the individual and combined effects of WMS and WSS in plaque free as well as in atherosclerotic coronary segments. Methods Forty non-stented, non-culprit human coronary arteries (IMPACT study) were imaged with near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) at the baseline and after 12 months [3]. The 2D and 3D lumen, vessel wall and lipid-rich necrotic core (LRNC) geometries were reconstructed based on the co-registration of NIRS-IVUS and OCT. WSS was computed with Computational Fluid Dynamics [3]. The WMS on the peri-luminal region was calculated via ABAQUS with hyperelastic material models [4] using intraluminal pressure of 120mmHg. The vessels were divided into 1.5mm/45° sectors. In each sector wall growth was quantified as plaque burden (plaque area/total vessel area*100%) change over time. Plaque was defined as wall thickness &amp;gt; 0.5 mm. The sectors were categorized as "plaque with lipid rich necrotic core (LRNC)", "plaque w/o lipid rich necrotic core (LRNC)", or "plaque free wall". The individual and combined effect of WSS and WMS on plaque progression was evaluated using Linear Mixed Model in SPSS and all stress metrics were divided into artery-based tertiles. Results Vessel sectors exposed to low WSS at baseline demonstrated a higher plaque burden increase over the follow up period compared to the vessel sectors exposed to mid or high WSS (Fig.1), which was significantly different for all the 3 categories (Plaque free wall, Plaque without LRNC, Plaque with LRNC). Vessel sectors exposed to increasing WMS demonstrated increasing plaque progression (Fig.1) Sectors that were simultaneously exposed to low WSS and high WMS revealed the highest change in plaque size and in particular in plaque sectors that were lipid rich (Fig.2). Conclusion Our findings suggest that the local atherosclerotic disease progression in coronary arteries is not only associated with the well-known WSS, but also with WMS. Moreover, our results show that there is an complex interplay between WSS, WMS and plaque composition, such that lipid rich plaques exposed to low WSS and high WMS demonstrated the highest plaque progression.Figure 1Figure 2

Determination of lipid-rich plaques by artificial intelligence-enabled quantitative computed tomography using near-infrared spectroscopy as reference

Background and aimsArtificial intelligence quantitative CT (AI-QCT) determines coronary plaque morphology with high efficiency and accuracy. Yet, its performance to quantify lipid-rich plaque remains unclear. This study investigated the performance of AI-QCT for the detection of low-density noncalcified plaque (LD-NCP) using near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS). MethodsThe INVICTUS Registry is a multi-center registry enrolling patients undergoing clinically indicated coronary CT angiography and IVUS, NIRS-IVUS, or optical coherence tomography. We assessed the performance of various Hounsfield unit (HU) and volume thresholds of LD-NCP using maxLCBI4mm ≥ 400 as the reference standard and the correlation of the vessel area, lumen area, plaque burden, and lesion length between AI-QCT and IVUS. ResultsThis study included 133 atherosclerotic plaques from 47 patients who underwent coronary CT angiography and NIRS-IVUS The area under the curve of LD-NCP<30HU was 0.97 (95% confidence interval [CI]: 0.93–1.00] with an optimal volume threshold of 2.30 mm3. Accuracy, sensitivity, and specificity were 94% (95% CI: 88–96%], 93% (95% CI: 76–98%), and 94% (95% CI: 88–98%), respectively, using <30 HU and 2.3 mm3, versus 42%, 100%, and 27% using <30 HU and >0 mm3 volume of LD-NCP (p < 0.001 for accuracy and specificity). AI-QCT strongly correlated with IVUS measurements; vessel area (r2 = 0.87), lumen area (r2 = 0.87), plaque burden (r2 = 0.78) and lesion length (r2 = 0.88), respectively. ConclusionsAI-QCT demonstrated excellent diagnostic performance in detecting significant LD-NCP using maxLCBI4mm ≥ 400 as the reference standard. Additionally, vessel area, lumen area, plaque burden, and lesion length derived from AI-QCT strongly correlated with respective IVUS measurements.

Clinical outcomes of acute myocardial infarction arising from non-lipid-rich plaque determined by NIRS-IVUS

Acute myocardial infarction (AMI) can rarely arise from non-lipid-rich coronary plaques. This study sought to compare the clinical outcomes after percutaneous coronary intervention (PCI) between AMI showing maximum lipid-core burden index in 4 mm (maxLCBI4mm) < 400 and ≥ 400 in the infarct-related lesions assessed by near-infrared spectroscopy-intravascular ultrasound (NIRS-IVUS). We investigated 426 AMI patients who underwent NIRS-IVUS in the infarct-related lesions before PCI. Major adverse cardiovascular events (MACE) were defined as the composite of cardiac death, non-fatal MI, clinically driven target lesion revascularization (TLR), clinically driven non-TLR, and congestive heart failure requiring hospitalization. 107 (25%) patients had infarct-related lesions of maxLCBI4mm < 400, and 319 (75%) patients had those of maxLCBI4mm ≥ 400. The maxLCBI4mm < 400 group had a younger median age at onset (68 years [IQR: 57–78 years] vs. 73 years [IQR: 64–80 years], P = 0.007), less frequent multivessel disease (39% vs. 51%, P = 0.029), less frequent TIMI flow grade 0 or 1 before PCI (62% vs. 75%, P = 0.007), and less frequent no-reflow immediately after PCI (5% vs. 11%, P = 0.039). During a median follow-up period of 31 months [IQR: 19–48 months], the frequency of MACE was significantly lower in the maxLCBI4mm < 400 group compared with the maxLCBI4mm ≥ 400 group (4.7% vs. 17.2%, P = 0.001). MaxLCBI4mm < 400 was an independent predictor of MACE-free survival at multivariable analysis (hazard ratio: 0.36 [confidence interval: 0.13–0.98], P = 0.046). MaxLCBI4mm < 400 measured by NIRS in the infract-related lesions before PCI was associated with better long-term clinical outcomes in AMI patients.

Characterization of plaque phenotypes exhibiting an elevated pericoronary adipose tissue attenuation: insights from the REASSURE-NIRS registry.

Inflammation has been considered to promote atheroma instability. Coronary computed tomography angiography (CCTA) visualizes pericoronary adipose tissue (PCAT) attenuation, which reflects coronary artery inflammation. While PCAT attenuation has been reported to predict future coronary events, plaque phenotypes exhibiting high PCAT attenuation remains to be fully elucidated. The current study aims to characterize coronary atheroma with a greater vascular inflammation. We retrospectively analyzed culprit lesions in 69 CAD patients receiving PCI from the REASSURE-NIRS registry (NCT04864171). Culprit lesions were evaluated by both CCTA and near-infrared spectroscopy/intravascular ultrasound (NIRS/IVUS) imaging prior to PCI. PCAT attenuation at proximal RCA (PCATRCA) and NIRS/IVUS-derived plaque measures were compared in patients with PCATRCA attenuation ≥ and < -78.3 HU (median). Lesions with PCATRCA attenuation ≥ -78.3 HU exhibited a greater frequency of maxLCBI4mm ≥ 400 (66% vs. 26%, p < 0.01), plaque burden ≥ 70% (94% vs. 74%, p = 0.02) and spotty calcification (49% vs. 6%, p < 0.01). Whereas positive remodeling (63% vs. 41%, p = 0.07) did not differ between two groups. On multivariable analysis, maxLCBI4mm ≥ 400 (OR = 4.07; 95%CI 1.12-14.74, p = 0.03), plaque burden ≥ 70% (OR = 7.87; 95%CI 1.01-61.26, p = 0.04), and spotty calcification (OR = 14.33; 95%CI 2.37-86.73, p < 0.01) independently predicted high PCATRCA attenuation. Of note, while the presence of only one plaque feature did not necessarily elevate PCATRCA attenuation (p = 0.22), lesions harboring two or more features were significantly associated with higher PCATRCA attenuation. More vulnerable plaque phenotypes were observed in patients with high PCATRCA attenuation. Our findings suggest PCATRCA attenuation as the presence of profound disease substrate, which potentially benefits from anti-inflammatory agents.

Disparities among Black and White patients in plaque burden and composition and long-term impact

BackgroundBlack patients presenting to the catheterization laboratory have more risk factors and worse long-term outcomes. This sub-analysis of the Lipid Rich Plaque (LRP) study quantifies the plaque burden and composition of Black vs White patients and associated outcomes. MethodsPatients with a singular, self-reported race presenting for cardiac catheterization were enrolled if near-infrared spectroscopy/intravascular ultrasound (NIRS-IVUS) imaging of non-stented, non-culprit (NC) vessels was performed. Lipidic content was quantified at the 4-mm region with maximum Lipid Core Burden Index (maxLCBI4mm). NC major adverse cardiac events (NC-MACE) were defined as: cardiac death, cardiac arrest, non-fatal myocardial infarction, acute coronary syndrome, revascularization, and hospital readmission for angina with >20 % disease progression through 2 years. ResultsAmong 1346 patients with a singular, self-reported race, 182 were Black. Black vs White patients were more likely to be female, had higher rates of traditional risk factors, and were more likely to present acutely. Both patients and segments were more likely to have maxLCBI4mm > 400 (46.7 % vs 30.6 %, p < 0.001, respectively; 15.5 % vs 8.9 %, p < 0.001, respectively). Vessel size and plaque burden were larger for Black vs White patients. At 2 years, maxLCBI4mm > 400 and Black race were independently predictive of NC-MACE (hazard ratio [HR] maxLCBI4mm > 400: 2.37 [95 % confidence interval (CI) 1.50–3.76, p < 0.001], Black race: 2.8 [95 % CI 1.27–3.42, p = 0.004], pinteraction = 0.137). ConclusionsCompared to White patients, Black patients had more lipid-rich plaques with greater plaque burden. Both high lipidic burden and Black race were independently predictive of NC-MACE within 2 years. Clinical trial registrationhttps://clinicaltrials.gov/ct2/show/NCT02033694, NCT02033694

(466) Clinical Utility of Near-Infrared Spectroscopy Intravascular Ultrasound in the Assessment of Rapidly Progressive Cardiac Allograft Vasculopathy

(466) Clinical Utility of Near-Infrared Spectroscopy Intravascular Ultrasound in the Assessment of Rapidly Progressive Cardiac Allograft Vasculopathy

Relation of GRACE Risk Score to Coronary Lipid Core Plaques in Patients with Acute Coronary Syndrome.

The GRACE risk score is established to predict thrombotic events in patients with acute coronary syndrome (ACS). Although thrombotic events including myocardial infarction after ACS are mainly attributable to vulnerable plaque formation, whether the GRACE score correlates with coronary lipid-rich plaque is unclear. A total of 54 patients with ACS undergoing primary percutaneous coronary intervention under near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) guidance were included in a prospective manner. Patients were divided into two groups according to the median of the GRACE risk score. Coronary lipid plaques in the target vessel were assessed by NIRS-IVUS with lipid core burden index (LCBI) and a maximum LCBI in 4 mm (maxLCBI4mm). The receiver operating characteristics (ROC) curve analysis was performed based on the major adverse cardiovascular events as an exploratory analysis. The GRACE risk score was significantly and positively correlated with LCBI (r = 0.31, p = 0.03) and maxLCBI4mm (r = 0.38, p = 0.006). LCBI (111.7 ± 85.7 vs. 169.0 ± 83.5, p = 0.02) and maxLCBI4mm (428.5 ± 227.1 vs. 600.6 ± 227.7, p = 0.009) in the target vessel were significantly higher in the high GRACE risk score group than their counterpart. In the ROC curve analysis, LCBI and maxLCBI4mm were predictive for clinical events. In conclusion, the higher GRACE risk score may serve as a discriminator of risk comprising more lipid-rich plaques as an underlying mechanism of an increased risk of thrombotic events after ACS. In patients with ACS, the higher GRACE risk score was significantly and modestly associated with greater coronary lipid plaques in the target vessel.

Wall shear stress-related plaque growth of lipid-rich plaques in human coronary arteries: an near-infrared spectroscopy and optical coherence tomography study.

Low wall shear stress (WSS) is acknowledged to play a role in plaque development through its influence on local endothelial function. Also, lipid-rich plaques (LRPs) are associated with endothelial dysfunction. However, little is known about the interplay between WSS and the presence of lipids with respect to plaque progression. Therefore, we aimed to study the differences in WSS-related plaque progression between LRPs, non-LRPs, or plaque-free regions in human coronary arteries. In the present single-centre, prospective study, 40 patients who presented with an acute coronary syndrome successfully underwent near-infrared spectroscopy intravascular ultrasound (NIRS-IVUS) and optical coherence tomography (OCT) of at least one non-culprit vessel at baseline and completed a 1-year follow-up. WSS was computed applying computational fluid dynamics to a three-dimensional reconstruction of the coronary artery based on the fusion of the IVUS-segmented lumen with a CT-derived centreline, using invasive flow measurements as boundary conditions. For data analysis, each artery was divided into 1.5 mm/45° sectors. Plaque growth based on IVUS-derived percentage atheroma volume change was compared between LRPs, non-LRPs, and plaque-free wall segments, as assessed by both OCT and NIRS. Both NIRS- and OCT-detected lipid-rich sectors showed a significantly higher plaque progression than non-LRPs or plaque-free regions. Exposure to low WSS was associated with a higher plaque progression than exposure to mid or high WSS, even in the regions classified as a plaque-free wall. Furthermore, low WSS and the presence of lipids had a synergistic effect on plaque growth, resulting in the highest plaque progression in lipid-rich regions exposed to low shear stress. This study demonstrates that NIRS- and OCT-detected lipid-rich regions exposed to low WSS are subject to enhanced plaque growth over a 1-year follow-up. The presence of lipids and low WSS proves to have a synergistic effect on plaque growth.