Prevalence Of Thin-cap Fibroatheroma Research Articles

Higher Noncalcified Plaque Volume Is Associated With Increased Plaque Vulnerability and Vascular Inflammation.

Recently, it was reported that noncalcified plaque (NCP) volume was an independent predictor for cardiac events. Pericoronary adipose tissue (PCAT) attenuation is a marker of vascular inflammation and has been associated with increased cardiac mortality. The aim of this study was to evaluate the relationships between NCP volume, plaque vulnerability, and PCAT attenuation. Patients who underwent preintervention coronary computed tomography angiography and optical coherence tomography were enrolled. Plaque volume was measured by computed tomography angiography, plaque vulnerability by optical coherence tomography, and the level of coronary inflammation by PCAT attenuation. The plaques were divided into 2 groups of high or low NCP volume based on the median NCP volume. Among 704 plaques in 454 patients, the group with high NCP volume had a higher prevalence of lipid-rich plaque (87.2% versus 75.9%; P<0.001), thin-cap fibroatheroma (38.1% versus 20.7%; P<0.001), macrophage (77.8% versus 63.4%; P<0.001), microvessel (58.2% versus 42.9%; P<0.001), and cholesterol crystal (42.0% versus 26.7%; P<0.001) than the group with low NCP plaque volume. The group with high NCP volume also had higher PCAT attenuation than the group with low NCP volume (-69.6±10.0 versus -73.5±10.6 Hounsfield unit; P<0.001). In multivariable analysis, NCP volume was significantly associated with thin-cap fibroatheroma and high PCAT attenuation. In the analysis of the combination of PCAT attenuation and NCP volume, the prevalence of thin-cap fibroatheroma was the highest in the high PCAT attenuation and high NCP volume group and the lowest in the low PCAT attenuation and low NCP volume group. Higher NCP volume was associated with higher plaque vulnerability and vascular inflammation. The combination of PCAT attenuation and NCP volume may help identify plaque vulnerability noninvasively. URL: https://www.clinicaltrials.gov; Unique identifier: NCT04523194.

Body mass index and characteristics of coronary plaque in younger patients with type 2 diabetes

Background and aimsThe association between the body mass index (BMI) and the characteristics of coronary plaque in younger type 2 diabetes (T2D) patients with coronary artery disease (CAD) remains to be elucidated. Methods and resultsA total of 138 consecutive younger (<65 years) T2D patients with CAD, who underwent optical coherence tomography imaging of the culprit lesion were included. The patients were classified into either the higher BMI group (n = 68) or the lower BMI group (n = 70) according to the median of BMI (25.9 kg/m2). The prevalence of thin-cap fibroatheroma (TCFA) (35.3 vs. 17.1 %, p = 0.015) was significantly higher in the higher BMI group than in the lower BMI group. The prevalence of TCFA was significantly higher in patients with higher BMI than in those with lower BMI among patients with hemoglobin A1c (HbA1c) ≥7.0 % (odds ratio [OR] 5.40, 95 % confidence interval [CI] 1.72–17.0, p = 0.003) although the significant difference was not observed among patients with HbA1c <7.0 % (OR 0.89, 95 % CI 0.25–3.13, p = 0.851). ConclusionHigher BMI was associated with a higher prevalence of TCFA in younger T2D patients with CAD, particularly in patients with HbA1c ≥ 7.0 %.

Abstract 14321: High Sensitivity C-Reactive Protein is Associated With Plaque Vulnerability and Increased Incidence of Adverse Events in Patients With Stable Coronary Disease

Introduction: Higher level of high sensitivity C-reactive protein (hsCRP) is associated with an increased risk of cardiovascular events in patients with coronary artery disease (CAD). However, the pathogenesis of the worse clinical outcomes in CAD patients with high hsCRP remains to be elucidated. Hypothesis: Higher hsCRP is associated with a higher prevalence of vulnerable characteristics in coronary plaques and an increased incidence of adverse events in patients with CAD. Methods: A total of 793 consecutive patients with stable CAD, who underwent intra coronary optical coherence tomography (OCT) imaging of the culprit vessel during percutaneous coronary intervention were included. Patients were classified into the higher hsCRP group (hsCRP ≥ 0.2 mg/dL, n=247) or the lower hsCRP group (hsCRP &lt; 0.2 mg/dL, n=546). OCT characteristics and clinical outcomes were investigated according to the level of hsCRP. Results: The prevalence of thin-cap fibroatheroma (TCFA) (32.0% vs. 20.9%, p &lt;0.001) and plaque with macrophage (53.9% vs. 46.2%, p =0.045) was significantly higher in the higher hsCRP group than in the lower hsCRP group (Panel A). The incidence of myocardial infarction was significantly higher in the higher hsCRP group than in the lower hsCRP group (log-rank p =0.006) during a median 938 days follow-up (Panel B) although the incidence of the composite of major adverse cardiac events was comparable (log-rank p =0.282). Among the four groups classified by the hsCRP level and the presence of TCFA, the incidence of myocardial infarction was the highest in the group with higher hsCRP and TCFA (log-rank p =0.017). Conclusions: Higher level of hsCRP was associated with a higher prevalence of vulnerable characteristics in coronary plaques and worse clinical outcomes in patients with stable CAD. The risk of recurrent myocardial infarction in patients with high hsCRP levels was further increased by the presence of TCFA.

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.

Abstract 11923: High Sensitivity C-Reactive Protein is Associated With Vulnerable Characteristics in Coronary Plaques in Patients With Stable Coronary Disease

Introduction: Higher level of high sensitivity C-reactive protein (hsCRP) is associated with an increased risk of cardiovascular events in patients with coronary artery disease (CAD). However, the association between hsCRP and the characteristics of coronary plaques in patients with CAD remains to be elucidated. Hypothesis: Higher hsCRP is associated with a higher prevalence of vulnerable characteristics in coronary plaques in patients with CAD. Methods: A total of 793 consecutive patients with stable coronary disease (SCD), who underwent optical coherence tomography (OCT) imaging of coronary plaques were included. The characteristics of culprit or non-culprit plaque assessed by OCT were compared between the higher hsCRP group (hsCRP ≥ 0.2 mg/dL, n=247) and the lower hsCRP group (hsCRP &lt; 0.2 mg/dL, n=546). Results: In culprit plaques, the prevalence of thin-cap fibroatheroma (TCFA) was significantly higher in the higher hsCRP group than in the lower hsCRP group (23.8% vs. 14.9%, p=0.003) (Panel A). In non-culprit plaques, the prevalence of TCFA (28.6 vs. 18.2%, p=0.014) and plaque with marcophages (56.4 vs. 45.1%, p=0.029) was significantly higher in the higher hsCRP group than in the lower hsCRP group (Panel B). Conclusions: Higher level of hsCRP is associated with a higher prevalence of vulnerable characteristics in culprit and non-culprit plaques in patients with CAD. The present results may partly explain the pathogenesis of an increased incidence of ​recurrent cardiovascular events in patients with CAD.

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.

The association of leukocyte telomere length and intermediate coronary lesions-a retrospective study.

Intermediate coronary lesions (40-70% stenosis) present a higher risk for future cardiovascular events for instability of plaques. Shortened telomere is an indicator of cellular senescence, which is associated with age-related diseases. However, the relationship between telomere length and severity of intermediate coronary lesions remains largely unknown. A total of 121 lesions of 121 patients with intermediate coronary disease that underwent intravascular optical coherence tomography were enrolled. These patients were retrospectively divided into two groups according to whether accept percutaneous coronary intervention (PCI) treatment: non-PCI group and PCI group. Leukocyte telomere length (LTL) in patients of PCI group were significantly shorter (12.54±2.70 vs. 15.32±3.72 kb, P<0.001) than non-PCI group. The PCI group had longer lipid length (17.17±9.94 vs. 12.21±10.15 mm, P=0.01) and greater lipid index (4,286.82±3,012.54 vs. 2,444.87±2,677.59 °*mm, P<0.001). There was a significant difference in the prevalence of thin-cap fibroatheroma (36.6% vs. 16.0%, P=0.013), macrophages (56.3% vs. 38.0%, P=0.047), plaque rupture (23.9% vs. 6.0%, P=0.009), cholesterol crystal (49.3% vs. 30.0%, P=0.034), dissection (23.9% vs. 4.0%, P=0.003) between PCI and non-PCI group. Logistic regression revealed that LTL was independently associated with PCI after adjusting for confounding factors (OR 0.952, CI: 0.930-0.974, per 1unit increase, P<0.001). Receiver operating characteristic (ROC) analysis revealed a LTL area under the ROC curve (AUC) of 0.714 (95% CI: 0.619-0.808, P<0.001) in the study population. Furthermore, LTL was inversely correlated with lipid length (r =-0.190, P=0.037), lipid arc (r =-0.301, P=0.001), lipid index (r =-0.182, P=0.046), and positive correlation with FCT (r =0.213, P=0.034). LTL was independently associated with possibility of receiving PCI in intermediate coronary lesion patients and LTL is also significantly related to plaque instability features that evaluated by optical coherence tomography. LTL may be as an indicator to assess the necessity of PCI in intermediate coronary lesion patients.

Predictors of Near-Infrared Spectroscopy-Detected Lipid-Rich Plaques by Optical Coherence Tomography-Defined Morphological Features in Patients With Acute Coronary Syndrome.

BackgroundNear-infrared spectroscopy (NIRS) provides the localization of lipid-rich components in coronary plaques. However, morphological features in NIRS-detected lipid-rich plaques (LRP) are unclear.MethodsA total of 140 de novo culprit lesions in 140 patients with the acute coronary syndrome (ACS) who underwent NIRS and optical coherence tomography (OCT) examinations for the culprit lesions at the time of percutaneous coronary interventions were investigated. We defined a NIRS-LRP as a lesion with a maximum lipid core burden index of 4 mm [LCBI4mm] > 500 in the culprit plaque. Clinical demographics, angiographic, and OCT findings were compared between the patients with NIRS-LRP (n = 54) vs. those without NIRS-LRP (n = 86). Uni- and multivariable logistic regression analyses were performed to examine the independent OCT morphological predictors for NIRS-LRP.ResultsClinical demographics showed no significant differences between the two groups. The angiographic minimum lumen diameter was smaller in the NIRS-LRP group than in the non- NIRS-LRP group. In OCT analysis, the minimum flow area was smaller; lipid angle, lipid length, the prevalence of thin-cap fibroatheroma, and cholesterol crystals were greater in the NIRS-LRP group than in the non-NIRS-LRP group. Plaque rupture and thrombi were more frequent in the NIRS-LRP group, albeit not significant. In a multivariable logistic regression analysis, presence of thin-cap fibroatheroma [odds ratio (OR): 2.56; 95% CI: 1.12 to 5.84; p = 0.03] and cholesterol crystals (OR: 2.90; 95% CI: 1.20 to 6.99; p = 0.02) were independently predictive of NIRS-LRP.ConclusionsIn ACS culprit lesions, OCT-detected thin-cap fibroatheroma and cholesterol crystals rather than plaque rupture and thrombi were closely associated with a great lipid-core burden.

Abstract 10456: Direct Oral Anticoagulant is Associated with a Lower Prevalence of Thin-Cap Fibroatheroma in Patients with Coronary Artery Disease

Introduction: The reduced incidence of cardiovascular events in patients with direct oral anticoagulant (DOAC) has been demonstrated. However, the association between taking DOAC and the characteristic of coronary plaque remains to be elucidated. Hypothesis: Taking DOAC is associated with a lower prevalence of vulnerable plaque in patients with coronary artery disease (CAD). Methods: A total of 2168 coronary plaques in consecutive 1439 patients who underwent optical coherence tomography imaging of the culprit or non-culprit lesion were analyzed. The prevalence of thin-cap fibroatheroma (TCFA) were compared between patients with DOAC (149 plaques in 105 patients) and those without (2019 plaques in 1334 patients). Results: The prevalence of TCFA was significantly lower in patients with DOAC than those without in both culprit lesion (27.3% vs. 15.4%, p=0.002) and non-culprit lesion (22.1% vs. 5.2%, p&lt;0.001) (Panel A). In addition to P2Y12 inhibitor intake (odds ratio: 0.941 [95% confidence interval: 0.890-0.995], p=0.034), taking DOAC was independently associated with a lower prevalence of TCFA at any lesion (odds ratio: 0.891 [95% confidence interval: 0.837-0.949], p&lt;0.001) after adjustment of confounders. The prevalence of TCFA at any lesion was significantly lower in patients with a combination of DOAC and P2Y12 inhibitor than those on either DOAC or P2Y12 inhibitor and those without (Panel B). Conclusions: Taking DOAC was associated with a lower prevalence of TCFA in patients with CAD. The present results may partly explain the efficacy of DOAC on the reduced incidence of cardiovascular events in patients with CAD.

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 (&lt;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 &lt;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.

Plasma Ceramides in Relation to Coronary Plaque Characterization Determined by Optical Coherence Tomography.

Plasma ceramides (Cer), a subset of bioactive lipids, have mechanistic links to development of atherosclerosis and are related to major adverse cardiovascular events (MACEs). Previous researches have demonstrated vulnerable plaques contribute to acute cardiovascular events and poor prognosis. This study aimed to explore the associations between Cer and culprit plaque characterizations evaluated by optical coherence tomography (OCT). It was found that plasma Cer are associated with culprit plaque vulnerability evaluated by OCT, providing evidence supporting proatherogenic roles and potential to act as markers for plaque vulnerability of Cer. Graphical Abstract With increasing plasma ceramide levels, the prevalence of thin-cap fibroatheroma (TCFA) and plaque rupture (PR) is higher, that is, culprit plaques are more vulnerable.

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

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

Optical coherence tomography-defined plaque vulnerability in relation to functional stenosis severity stratified by fractional flow reserve and quantitative flow ratio.

We sought to investigate that the quantitative flow ratio (QFR) might be associated with optical coherence tomography (OCT)-defined plaque vulnerability. Both functional stenosis severity and plaque instability are related to adverse clinical outcomes in patients with coronary artery disease. Recent studies have shown an association between physiological stenosis severity and the presence of thin-cap fibroatheroma (TCFA). Measurement of QFR is a novel method for rapid computational estimation of fractional flow reserve (FFR). We investigated 327 de novo intermediate-to-severe coronary lesions in 295 stable patients who underwent OCT, FFR, and QFR computation. The lesions were divided into tertiles based on either the FFR or QFR. The OCT findings were compared among these tertiles of FFR and QFR. Each tertile was defined as follows: FFR-T1 (FFR < 0.72), FFR-T2 (0.72 ≤ FFR ≤ 0.79), and FFR-T3 (FFR > 0.79) and QFR-T1 (QFR < 0.73), QFR-T2 (0.73 ≤ QFR ≤ 0.78), and QFR-T3 (QFR > 0.78). The prevalence of OCT-defined TCFA showed graded differences in proportion to the QFR tertiles (25.0% vs. 12.8% vs. 6.6%, p = .003). An overall significant difference in the prevalence of TCFA was found among FFR tertiles (p = .048), although pairwise comparison did not show statistical significance. Compared with FFR-based classifications, the model that integrated the FFR and QFR categorization improved the incremental reclassification efficacy (relative integrated discrimination improvement, 0.069; p = .002; continuous net reclassification improvement, 0.356; p = .022) for predicting the presence of TCFA. OCT-defined plaque instability was associated with the QFR in angiographically intermediate-to-severe lesions. Compared with the FFR alone, the QFR can provide incremental efficacy in predicting the presence of TCFA.

Lipoprotein (a) level is associated with plaque vulnerability in patients with coronary artery disease: An optical coherence tomography study

BackgroundHigh lipoprotein (a) [Lp(a)] levels are an independent factor for worse prognosis in patients with coronary artery disease (CAD). However, the association between serum Lp(a) level and coronary plaque vulnerability remains to be determined. MethodsA total of 255 consecutive patients with CAD who underwent optical coherence tomography imaging of culprit lesions were included. Patients were divided into 2 groups according to their Lp(a) levels (the higher Lp(a) group [≥25 mg/dL], n = 87; or the lower Lp(a) group [<25 mg/dL], n = 168). ResultsThe prevalence of thin-cap fibroatheroma (TCFA) was significantly higher in the higher Lp(a) group than in the lower Lp(a) group (23% [n = 20] vs. 11% [n = 19], p = 0.014). Although the prevalence of TCFA was comparable between the 2 groups among patients with a lower LDL cholesterol (LDL-C) level (<100 mg/dL), TCFA was significantly more prevalent in the higher Lp(a) group than in the lower Lp(a) group (39% [14/36] vs. 10% [5/50], p = 0.001) among patients with a higher LDL-C level (≥100 mg/dL). ConclusionsA higher Lp(a) level was associated with a higher frequency of TCFA, particularly in patients with a higher LDL-C level.

TCT-46 Prevalence of thin-cap fibroatheroma and plaque rupture in fractional flow reserve negative lesions in diabetic patients with or without acute coronary syndrome - Insights from the COMBINE Study

TCT-46 Prevalence of thin-cap fibroatheroma and plaque rupture in fractional flow reserve negative lesions in diabetic patients with or without acute coronary syndrome - Insights from the COMBINE Study

Intracoronary Imaging, Cholesterol Efflux, and Transcriptomics after Intensive Statin Treatment in Diabetes

Residual atherothrombotic risk remains higher in patients with versus without diabetes mellitus (DM) despite statin therapy. The underlying mechanisms are unclear. This is a retrospective post-hoc analysis of the YELLOW II trial, comparing patients with and without DM (non-DM) who received rosuvastatin 40 mg for 8–12 weeks and underwent intracoronary multimodality imaging of an obstructive nonculprit lesion, before and after therapy. In addition, blood samples were drawn to assess cholesterol efflux capacity (CEC) and changes in gene expression in peripheral blood mononuclear cells (PBMC). There was a significant reduction in low density lipoprotein-cholesterol (LDL-C), an increase in CEC and beneficial changes in plaque morphology including increase in fibrous cap thickness and decrease in the prevalence of thin cap fibro-atheroma by optical coherence tomography in DM and non-DM patients. While differential gene expression analysis did not demonstrate differences in PBMC transcriptome between the two groups on the single-gene level, weighted gene coexpression network analysis revealed two modules of coexpressed genes associated with DM, Collagen Module and Platelet Module, related to collagen catabolism and platelet function respectively. Bayesian network analysis revealed key driver genes within these modules. These transcriptomic findings might provide potential mechanisms responsible for the higher cardiovascular risk in DM patients.

Chronic kidney disease predicts coronary plaque vulnerability

The addition of cystatin C to creatinine in calculating the estimated glomerular filtration rate (eGFR) is known to improve the risk prediction for cardiovascular events. We sought to investigate the associations between eGFRs calculated by three Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equations and coronary plaque phenotype by optical coherence tomography. We analyzed 181 nonculprit plaques from 116 coronary artery disease patients. For each patient, the eGFR was calculated using the CKD-EPIcreatinine, CKD-EPIcystatin C, and CKD-EPIcombination equations. Patients were divided into three categories according to the eGFR calculated by each equation (≥90, 60-89, and <60 ml/min/1.73 m). The prevalence of thin-cap fibroatheroma (TCFA) was correlated inversely with eGFR calculated using CKD-EPIcystatin C and CKD-EPIcombination equations, but not using the CKD-EPIcreatinine equation. The best cut-off values of eGFR calculated by these two equations for differentiating TCFA were 83 and 84 ml/min/1.73 m, respectively. Compared with the CKD-EPIcreatinine equation, patients who were reclassified upward or downward categories by the CKD-EPIcystatin C equation were associated with consistently lower [adjusted odds ratio=0.27, 95% confidence interval (CI), 0.08-0.86] and higher (adjusted odds ratio=2.41, 95% CI, 1.08-5.41) prevalence for TCFA, respectively. The net reclassification improvement with cystatin C, compared with creatinine, was 0.45 (95% CI, 0.20-0.69) for TCFA, 0.38 (95% CI, 0.09-0.67) for thrombus, and 0.21 (95% CI, 0.00-0.42) for cholesterol crystals. Results were generally similar for the CKD-EPIcombination equation. The use of cystatin C alone or in combination with creatinine, compared with creatinine alone, for GFR estimation strengthens the associations between the eGFR and prevalence of vulnerable plaque characteristics.

Prevalence of Thin-Cap Fibroatheroma in Relation to the Severity of Anatomical and Physiological Stenosis.

The relationship between the features of morphologically unstable plaque and physiological lesion severity remains elusive. We aimed to investigate this relationship using optical coherence tomography (OCT)-derived high-risk plaque characteristics and fractional flow reserve (FFR) as the degree of anatomical and physiological stenosis severity.Methods and Results:We investigated 286 de novo intermediate and severe coronary lesions in 248 patients who underwent OCT and FFR examinations. Lesions were divided into tertiles based on either FFR or quantitative coronary angiographic diameter stenosis (QCA-%DS). The OCT findings were compared among the tertiles of FFR and QCA-%DS. FFR and QCA tertiles were defined as follows: FFR-T1 (FFR <0.74), FFR-T2 (0.74≤FFR≤0.81), and FFR-T3 (FFR >0.81); and QCA-T1 (%DS ≥61%), QCA-T2 (51%≤%DS<61%), and QCA-T3 (%DS <51%). The prevalence of thin-cap fibroatheroma (TCFA) was significantly greater in FFR-T1 (20.0%) than in FFR-T2 and FFR-T3 (7.0%, P=0.03 and 7.7%, P=0.04, respectively), although no significant differences were observed among the QCA tertiles. Physiological severity of coronary stenosis evaluated by FFR correlated with plaque instability in terms of TCFA. Preferable clinical outcomes for lesions with negative FFR based on the existing clinical evidence might be attributable to less likelihood of TCFA.

Comparison of Intensive Versus Moderate Lipid-Lowering Therapy on Fibrous Cap and Atheroma Volume of Coronary Lipid-Rich Plaque Using Serial Optical Coherence Tomography and Intravascular Ultrasound Imaging

Despite marked clinical benefit, reduction in atheroma volume with statin therapy is minimal. Changes in plaque composition may explain this discrepancy. We aimed in the present study to assess the effect of statin therapy on coronary plaque composition and plaque volume using serial multimodality imaging. From an open-label, single-blinded study, patients with angiographically mild-to-moderate lesion were randomized to receive atorvastatin 60 (AT 60) mg or atorvastatin 20 (AT 20) mg for 12 months. Optical coherence tomography was used to assess fibrous cap thickness (FCT) and intravascular ultrasound to assess atheroma burden at 3 time points: baseline, at 6 months, and at 12 months. Thirty-six lipid-rich plaques in 27 patients with AT 60 mg and 30 lipid-rich plaques in 19 patients with AT 20 mg were enrolled in this study. Low-density lipoprotein cholesterol level was significantly decreased at 6 months without further reduction at 12 months. AT 60 mg induced greater reduction in low-density lipoprotein cholesterol compared with AT 20 mg. Optical coherence tomography revealed continuous increase in FCT from baseline to 6 months and to 12 months in both groups. AT 60 mg induced greater increase in FCT compared with AT 20 mg at both follow-up points. The prevalence of thin-cap fibroatheroma and the presence of macrophage at 6 months were significantly lower in AT 60 mg compared with AT 20 mg. Plaque burden did not change significantly in both groups. In conclusion, both intensive and moderate statin therapy stabilizes coronary plaques, with a greater benefit in the intensive statin group. However, no significant changes in plaque volume were observed over time regardless of the intensity of statin therapy.

Association between daily glucose fluctuation and coronary plaque properties in patients receiving adequate lipid-lowering therapy assessed by continuous glucose monitoring and optical coherence tomography.

BackgroundGlucose fluctuation has been recognized as a residual risk apart from dyslipidemia for the development of coronary artery disease (CAD). This study aimed to investigate the association between glucose fluctuation and coronary plaque morphology in CAD patients.MethodsThis prospective study enrolled 72 consecutive CAD patients receiving adequate lipid-lowering therapy. They were divided into 3 tertiles according to the mean amplitude of glycemic excursions (MAGE), which represents glucose fluctuation, measured by continuous glucose monitoring (tertile 1; <49.1, tertile 2; 49.1 ~ 85.3, tertile 3; >85.3). Morphological feature of plaques were evaluated by optical coherence tomography. Lipid index (LI) (mean lipid arc × length), fibrous cap thickness (FCT), and the prevalence of thin-cap fibroatheroma (TCFA) were assessed in both culprit and non-culprit lesions.ResultsIn total, 166 lesions were evaluated. LI was stepwisely increased according to the tertile of MAGE (1958 ± 974 [tertile 1] vs. 2653 ± 1400 [tertile 2] vs. 4362 ± 1858 [tertile 3], p <0.001), whereas FCT was the thinnest in the tertile 3 (157.3 ± 73.0 μm vs. 104.0 ± 64.1 μm vs. 83.1 ± 34.7 μm, p <0.001, respectively). The tertile 3 had the highest prevalence of TCFA. Multiple linear regression analysis showed that MAGE had the strongest effect on LI and FCT (standardized coefficient β = 0.527 and −0.392, respectively, both P <0.001). Multiple logistic analysis identified MAGE as the only independent predictor of the presence of TCFA (odds ratio 1.034; P <0.001).ConclusionsGlucose fluctuation and hypoglycemia may impact the formation of lipid-rich plaques and thinning of fibrous cap in CAD patients with lipid-lowering therapy.