Coronary Plaque Vulnerability Research Articles

Cardiac Computed Tomography Assessment in Acute Coronary Syndromes — Do We Have Time for It in Emergency Settings?

Abstract The diagnosis and treatment of acute coronary syndrome remain a challenge for clinicians in many clinical settings, especially in patients with previous low-to-intermediate risk. Due to its high specificity and sensitivity for detecting significant coronary artery stenoses, cardiac computed tomography angiography (CCTA) tends to be used more frequently in the emergency room (ER) in the last years. This technique has been associated with a higher rate of safe discharge in patients with chest pain, less time spent in the ER, and decreased costs related to further investigations. In cases positive for coronary artery stenosis, CCTA can accurately evaluate the indication for percutaneous coronary angioplasty and can offer relevant information related to the characteristics of the coronary plaques, being able to detect vulnerable coronary plaques. The aim of this manuscript is to highlight the possibility of using CCTA in the ER in the assessment of patients with chest pain and to show the benefits of the procedure regarding safety, costs, accuracy, and time.

The impact of blood pressure variability on coronary plaque vulnerability in stable angina: an analysis using optical coherence tomography.

Blood pressure variability (BPV), especially visit-to-visit BPV, has been reported to be a risk factor for cardiovascular disease. The impact of BPV on coronary plaque vulnerability remains uncertain. The aim of this study was to investigate the relationship between BPV and coronary plaque vulnerability. From August 2013 to May 2014, 36 patients with both hypertension and stable angina pectoris who underwent a percutaneous coronary intervention guided by frequency-domain optical coherence tomography were investigated retrospectively. The size of the lipid cores and the thickness of the fibrous cap covering the lipid core were measured by frequency-domain optical coherence tomography, and we calculated the blood pressure coefficient of variation (CV) and SD as intraindividual visit-to-visit BPV. Both SD and CV of systolic blood pressure (SBP) correlated positively with lipid arc (SBP-SD: r=0.68, P<0.01; SBP-CV: r=0.64, P<0.01) as well as average SBP (r=0.48, P<0.01). Fibrous cap thickness did not correlate with blood pressure variables or BPV. BPV is related to coronary plaque volume, but not to coronary plaque vulnerability. In addition to conventional coronary risk factors, BPV may be a therapeutic target for coronary atherosclerosis.

Early Detection and Treatment of the Vulnerable Coronary Plaque: Can We Prevent Acute Coronary Syndromes?

Early identification and treatment of the vulnerable plaque, that is, a coronary artery lesion with a high likelihood of rupture leading to an acute coronary syndrome, have gained great interest in the cardiovascular research field. Postmortem studies have identified clear morphological characteristics associated with plaque rupture. Recent advances in invasive and noninvasive coronary imaging techniques have empowered the clinician to identify suspected vulnerable plaques in vivo and paved the way for the evaluation of therapeutic agents targeted at reducing plaque vulnerability. Local treatment of vulnerable plaques by percutaneous coronary intervention and systemic treatment with anti-inflammatory and low-density lipoprotein-lowering drugs are currently being investigated in large randomized clinical trials to assess their therapeutic potential for reducing adverse coronary events. Results from these studies may enable a more patient-tailored strategy for the treatment of coronary artery disease.

Patients with vulnerable coronary plaques have higher serum metalloproteinase-1 levels

Most acute coronary syndromes are caused by the fracture of a vulnerable atherosclerotic plaque. These plaques are thin cap fibroatheromas, which can only be detected with invasive coronary imaging techniques. It is necessary to find a non-invasive biomarker of these vulnerable plaques in order to identify patients at risk without a coronary angiography. Metalloproteinase-1 is an enzyme involved in extracellular matrix metabolism which has been correlated with the rupture of atherosclerotic plaques. Its serum levels in patients with vulnerable plaques remain unknown. Patients with suspected stable coronary artery disease undergoing coronary angiography in our hospital were in-cluded. The coronary arteries were studied with optical coherence tomography to detect vulnerable plaques. Blood samples were taken from a peripheral vein and from the coronary sinus, to assess metalloproteinase-1 levels. Fifty-one patients were included, 13 of whom had at least one vulnerable plaque. There were not significant dif-ferences in clinical characteristics, lipid profile or C reactive protein levels, between patients with or without vulnerable plaques. Patients with vulnerable plaques had significant higher metalloproteinase-1 levels both in peripheral (7330±5541 vs 2894±1783 pg/ml, p=0.025) and coronary sinus serum (6012±3854 vs 2707±1252 pg/ml, p=0.047). Patients with vulnerable plaques had significantly higher metalloproteinase-1 serum levels. Further studies with clinical follow up are needed to assess the prognostic value of serum metalloproteinase-1.

Echolucency of the carotid artery is associated with short-term plaque progression and positive remodeling in the culprit coronary artery in AMI survivors

BackgroundRapid plaque progression and positive remodeling are recognized as vulnerable coronary plaque characteristics. This study examined whether serial carotid ultrasonography might be of value for assessment of coronary plaque progression and positive remodeling, measured by serial intravascular ultrasound (IVUS), in survivors of acute myocardial infarction (AMI). MethodsThirty-nine patients with AMI had repeated examinations by IVUS of culprit coronary arteries and echolucency of the coronary artery on admission (1st test) and 6 months later (2nd test). Plaque volume and external elastic membrane area of the native segment (15±9mm in length) beginning 5mm proximal to the stent edge in the culprit coronary artery were measured using volumetric IVUS. Echolucency of the carotid artery was assessed by integrated backscatter (IBS) analysis. Lower IBS reflects an echolucent and lipid-rich plaque. ResultsIncrease in coronary plaque volume and positive remodeling over 6 months occurred in 17 and 12 patients, respectively. The % change in carotid IBS value over 6 months was correlated with the % change in the coronary plaque volume (r=−0.69, p<0.001). The aggravated change in the carotid IBS was significantly associated with increase in the coronary plaque volume and positive remodeling over 6 months (OR 0.94 and 0.95, respectively, 95% CI 0.90–0.99, both p<0.05). ConclusionsSerial measurements of echolucency of the carotid artery may be of value for assessment of short-term progression and positive remodeling of coronary plaques in AMI survivors.

Positive Remodeling as a Biomarker of Plaque Vulnerability — at the Border Between Invasive and Noninvasive Assessment

AbstractSince the introduction of the new concepts of plaque vulnerability and patient vulnerability, many researchers have focused on different biomarkers that can represent predictors for coronary plaque instability. One of the features that characterize the vulnerable coronary plaque is positive remodeling, which can be easily identified by computed tomography angiography, a noninvasive procedure, or by other invasive methods such as intravascular ultrasound. This review aims to describe the assessment of positive remodeling as a marker of coronary plaque instability and the differences between computed tomography angiography and intravascular ultrasound in investigating this new biomarker.

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.

The Lipid-Rich Plaque Study of vulnerable plaques and vulnerable patients: Study design and rationale

It has been hypothesized that the outcome post-PCI could be improved by the detection and subsequent treatment of vulnerable patients and lipid-rich vulnerable coronary plaques (LRP). A near-infrared spectroscopy (NIRS) catheter capable of detecting LRP is being evaluated in The Lipid-Rich Plaque Study. The LRP Study is an international, multicenter, prospective cohort study conducted in patients with suspected coronary artery disease (CAD) who underwent cardiac catheterization with possible ad hoc PCI for an index event. Patient level and plaque level events were detected by follow-up in the subsequent 2 years. Enrollment began in February 2014 and was completed in March 2016; a total of 1,562 patients were enrolled. Adjudication of new coronary event occurrence and de novo culprit lesion location during the 2-year follow-up is performed by an independent clinical end-points committee (CEC) blinded to NIRS-IVUS findings. The first analysis of the results will be performed when at least 20 de novo events have occurred for which follow-up angiographic data and baseline NIRS-IVUS measurements are available. It is expected that results of the study will be announced in 2018. The LRP Study will test the hypotheses that NIRS-IVUS imaging to detect LRP in patients can identify vulnerable patients and vulnerable plaques. Identification of vulnerable patients will assist future studies of novel systemic therapies; identification of localized vulnerable plaques would enhance future studies of possible preventive measures.

Molecular Imaging of Vulnerable Coronary Plaque: A Pathophysiologic Perspective

Atherothrombotic events in coronary arteries are most often due to rupture of unstable plaque resulting in myocardial infarction. Radiolabeled molecular imaging tracers directed toward cellular targets that are unique to unstable plaque can serve as a powerful tool for identifying high-risk patients and for assessing the potential of new therapeutic approaches. Two commonly available radiopharmaceuticals-18F-FDG and 18F-NaF-have been used in clinical research for imaging coronary artery plaque, and ongoing clinical studies are testing whether there is an association between 18F-NaF uptake and future atherothrombotic events. Other, less available, tracers that target macrophages, endothelial cells, and apoptotic cells have also been tested in small groups of patients. Adoption of molecular imaging of coronary plaque into clinical practice will depend on overcoming major hurdles, ultimately including evidence that the detection of unstable plaque can change patient management and improve outcomes.

Analysis of Cardiovascular Tissue Components for the Diagnosis of Coronary Vulnerable Plaque from Intravascular Ultrasound Images.

The purpose of this study was to characterize cardiovascular tissue components and analyze the different tissue properties for predicting coronary vulnerable plaque from intravascular ultrasound (IVUS) images. For this purpose, sequential IVUS image frames were obtained from human coronary arteries using 20 MHz catheters. The plaque regions between the intima and media-adventitial borders were manually segmented in all IVUS images. Tissue components of the plaque regions were classified into having fibrous tissue (FT), fibrofatty tissue (FFT), necrotic core (NC), or dense calcium (DC). The media area and lumen diameter were also estimated simultaneously. In addition, the external elastic membrane (EEM) was computed to predict the vulnerable plaque after the tissue characterization. The reliability of manual segmentation was validated in terms of inter- and intraobserver agreements. The quantitative results found that the FT and the media as well as the NC would be good indicators for predicting vulnerable plaques in IVUS images. In addition, the lumen was not suitable for early diagnosis of vulnerable plaque because of the low significance compared to the other vessel parameters. To predict vulnerable plaque rupture, future study should have additional experiments using various tissue components, such as the EEM, FT, NC, and media.

Developing a Strategy for Interventional Molecular Imaging of Oxidized Low-Density Lipoprotein in Atherosclerosis.

The identification of vulnerable coronary artery atherosclerotic plaques offers the prospect of either localized or systematic therapeutic targeting in order to prevent myocardial infarction. Molecular imaging of atherosclerosis adds to morphological imaging by focusing on the immunobiology hidden in and behind the endothelium and therefore may be able to improve the identification of prospective culprit lesions. Our focus has been on identifying arterial accumulation of oxidized low-density lipoprotein (oxLDL) by exploiting advances in knowledge of vascular pathobiology. Here, we reflect on our work developing near-infrared fluorescence imaging of oxLDL using LO1, a monoclonal autoantibody generated in our laboratory. We detail progress to date and discuss our vision on taking the work through the early translational pipeline toward a multitargeted approach in imaging rupture-prone atherosclerotic plaques. Ultimately, molecular imaging of coronary arteries should be able to assess the regional risk that is specific to a lesion, which can then be used in concert with global risk factors to personalize the therapeutic strategy for patients in a way that goes beyond generalized population-based therapies.

Computed Tomography Biomarkers of Vulnerable Coronary Plaques

Abstract An unstable plaque has a high risk of thrombosis and at the same time for a fast progression of the stenosis degree. Also, “high-risk plaque” and “thrombosis-prone plaque” are used as synonym terms for characterization of a vulnerable plaque. The imaging biomarkers for vulnerable coronary plaques are considered to be spotty calcifications, active remodeling, low-density atheroma and the presence of a ring-like attenuation pattern, also known as the napkin-ring sign. Computed cardiac tomography can determine the plaque composition by assessing the plaque density, which is measured in Hounsfield units (HU). The aim of this manuscript was to provide an update about the most frequently used biomarkers of vulnerability in a vulnerable plaque with the help of computed cardiac tomography.

Rapid Fire Abstract: Cardiac imaging with computed tomography and radionuclide techniques: usefulness in miscellaneous patient subsets347A novel CT calcium-based approach for predicting mitral stenosis348Value of 18-fluoro-2-deoxyglucose positron emission tomography-computed tomography in the diagnosis of native, prosthetic and device related infective endocarditis349Pulmonary veins anatomy variants assessment using CT in patients with atrial fibrillation350Aortic valve area using cardiac CT to improve the

Rapid Fire Abstract: Cardiac imaging with computed tomography and radionuclide techniques: usefulness in miscellaneous patient subsets347A novel CT calcium-based approach for predicting mitral stenosis348Value of 18-fluoro-2-deoxyglucose positron emission tomography-computed tomography in the diagnosis of native, prosthetic and device related infective endocarditis349Pulmonary veins anatomy variants assessment using CT in patients with atrial fibrillation350Aortic valve area using cardiac CT to improve the

Assessment of Coronary Plaque Vulnerability in Acute Coronary Syndromes using Optical Coherence Tomography and Intravascular Ultrasound. A Systematic Review

Abstract The aim of this systematic review was to analyze studies characterizing vulnerable coronary plaques using optical coherence tomography (OCT) and intravascular ultrasound (IVUS), in order to identify the most efficient invasive technique permitting plaque characterization in patients with acute myocardial infarction. Method: A total number of 432 studies were identified, 420 through database searching and 12 through manual searching. Eight duplicate studies were removed, leaving a total number of 424 studies to be screened. Twenty-six studies only available in Abstract-only form were excluded, resulting in 398 studies checked for eligibility. Eleven studies fulfilled the eligibility criteria and were included in this systematic analysis. Plaque vulnerability was investigated in plaques with thin cap fibroatheroma (TCFA) versus those with thick cap fibroatheroma, in ruptured coronary plaques versus non-ruptured coronary plaques, in culprit versus non-culprit lesions and in lipid-rich versus non-lipid-rich plaques. Results: A total of 1,568 coronary plaques in 1,225 patients with acute coronary syndromes (ACS) who underwent both IVUS and OCT for analysis of plaque features were included in the final analysis. The review identified the following IVUS-derived features as significantly correlated with plaque vulnerability: plaque burden (p &lt;0.001), remodeling index (p &lt;0.001), external elastic membrane cross-sectional area (p &lt;0.001), and the amount of necrotic core (p &lt;0.001), while OCT-derived features characterizing unstable plaque were TCFA (p &lt;0.001), lipid arch (p &lt;0.001), accumulation of macrophages (p = 0.03), and presence of intracoronary thrombus (p &lt;0.001). Conclusion: Both IVUS and OCT are invasive imaging techniques able to provide relevant information on the vulnerability of coronary atheromatous plaques, identifying, as they do, various plaque features significantly associated with unstable plaques. Information provided by the two techniques is complementary, and both methods can serve as a useful clinical diagnostic tool, especially in cases of ACS patients undergoing a revascularization procedure.

Abstract 13236: Elevated Serum Proprotein Convertase Subtilisin/Kexin Type 9 Level Independently Predicts Long-Term Cardiovascular Outcomes in Patients With Chronic Coronary Artery Disease

Background: Proprotein convertase subtilisin/kexin type 9 (PCSK9) may directly promote atherosclerosis. However, the long-term impact of elevated serum PCSK9 levels on the risk of cardiovascular events has not been fully elucidated. We therefore analyzed the association of serum PCSK9 levels with major adverse cardiovascular events (MACE) in patients with chronic coronary artery disease (CAD). Methods: Serum PCSK9 levels were measured in 306 patients (171 men; mean age, 68.3 ± 10.5 years) who underwent coronary computed tomography (CT) angiography. Furthermore, 174 patients who were judged to have obstructive CAD were followed-up for a median period of 1584 days (interquartile range [IR] 1334-1790). MACE was defined as death, acute coronary syndrome, and cerebral stroke. Results: Serum levels of PCSK9 were higher in women (268 ng/mL, IR 211-325) than in men (218 ng/mL, IR 175-284, P&lt;0.001). In age- and gender-adjusted logistic regression analysis, serum PCSK9 levels had a significant association with obstructive CAD (odds ratio 1.63 per 100 ng/mL increase, 95% confidence interval [CI] 1.21-2.19, P=0.001). Among patients with obstructive CAD, 14 patients developed MACE during the follow-up period. Patients in the highest tertile of PCSK9 (≥288 ng/mL) had a significantly higher risk of MACE than those in the lower tertiles (log-rank, P=0.005). In Cox regression analysis using age, gender, estimated glomerular filtration rate (eGFR), hypertension, dyslipidemia, diabetes, smoking, and vulnerable coronary plaque characteristics assessed by CT, including low-density plaque, positive remodeling, and spotty calcification, as covariates, serum PCSK9 level was an independent predictor of MACE (hazard ratio 2.03 per 100 ng/mL increase, 95% CI 1.13-3.62, P=0.017). Conclusions: Baseline serum PCSK9 level significantly predicted MACE, as well as present coronary stenosis, independent of traditional cardiovascular risk factors and vulnerable plaques.

Potential contribution of the hepcidin-macrophage axis to plaque vulnerability in acute myocardial infarction in human

ObjectivesHepcidin-25 serves as a key peptide in the regulation of iron homeostasis and inflammation. It remains unknown whether hepcidin-25 plays an adverse role in atherosclerotic diseases. The aim of this study was to investigate whether hepcidin-25 is involved in the pathophysiology of coronary plaque vulnerability. Methods and resultsSerum hepcidin-25 levels were quantitatively determined by the LC–MS/MS assay system. Peripheral blood was collected from patients with acute myocardial infarction (MI, n=33) and patients with stable angina pectoris (sCAD, n=19). The levels of hepcidin-25, IL-6, and CRP were significantly higher in the patients with acute MI than in the patients with sCAD. Coronary blood was aspirated from the culprit arteries via a thrombectomy catheter in 16 of the MI patients. Serum from the aspirates contained higher levels of hepcidin-25 and IL-6 compared with the peripheral blood. In immunohistochemical staining, the macrophages of the plaques in the solid component of the aspirates were immunoreactive for hepcidin-25. To confirm the clinical observation, an in vitro study was performed using human macrophages and coronary endothelial cells. The hepcidin gene and protein were detected in the cultured macrophages but not in the endothelial cells. Hepcidin-25 exposure induced ferroportin degradation and reduced the survival rate of endothelial cells. ConclusionsThe results of the present study demonstrated that circulating hepcidin-25 and IL-6 were both elevated in the acute phase of MI and that hepcidin-25 released from plaque macrophages and other cell sources contributed to the plaque instability by inducing endothelial cell death.

Plaque Vulnerability as Assessed by Radiofrequency Intravascular Ultrasound in Patients with Valvular Calcification.

BackgroundCardiac valvular calcification is associated with the overall coronary plaque burden and considered an independent cardiovascular risk and prognostic factor. The purpose of this study was to evaluate the relationship between the presence of valvular calcification and plaque morphology and/or vulnerability.MethodsTransthoracic echocardiography was used to assess valvular calcification in 280 patients with coronary artery disease who underwent radiofrequency intravascular ultrasound (Virtual Histology IVUS, VH-IVUS). A propensity score–matched cohort of 192 patients (n = 96 in each group) was analyzed. Thin-capped fibroatheroma (TCFA) was defined as a necrotic core (NC) >10% of the plaque area with a plaque burden >40% and NC in contact with the lumen for ≥3 image slices. A remodeling index (lesion/reference vessel area) >1.05 was considered to be positive.ResultsPatients were divided into two groups: any calcification in at least one valve (152 patients) vs. no detectable valvular calcification (128 patients). Groups were similar in terms of age, risk factors, clinical diagnosis, and angiographic analysis after propensity score-matched analysis. Gray-scale IVUS analysis showed that the vessel size, plaque burden, minimal lumen area, and remodeling index were similar. By VH-IVUS, % NC and % dense calcium (DC) were greater in patients with valvular calcification (p = 0.024, and p = 0.016, respectively). However, only % DC was higher at the maximal NC site by propensity score-matched analysis (p = 0.029). The frequency of VH-TCFA occurrence was higher depending on the complexity (p = 0.0064) and severity (p = 0.013) of valvular calcification.ConclusionsThere is a significant relationship between valvular calcifications and VH-IVUS assessment of TCFAs. Valvular calcification indicates a greater atherosclerosis disease complexity (increased calcification of the coronary plaque) and vulnerable coronary plaques (higher incidence of VH-TCFA).

The Role of Virtual Histology Intravascular Ultrasound in the Identification of Coronary Artery Plaque Vulnerability in Acute Coronary Syndromes.

Markers of coronary plaque vulnerability, such as a high lipid burden, increased inflammatory activity, and a thin fibrous cap, have been identified in histological studies. In vivo, grayscale intravascular ultrasound (IVUS) provides more in-depth information on coronary artery plaque burden than conventional angiography but is unable to accurately distinguish between noncalcific tissue types within the plaque. An analysis of IVUS radiofrequency backscatter based on spectral pattern recognition, such as virtual histology IVUS, allows detailed scrutiny of plaque composition and classification of coronary lesions. This review discusses the virtual histology IVUS technology and its accuracy in identifying vulnerable plaque features, focusing on its use in predicting patient outcomes after acute coronary syndrome, and its limitations in clinical practice.

Soluble adhesion molecules in patients with acute coronary syndrome after percutaneous coronary intervention with drug-coated balloon, drug-eluting stent or bare metal stent

Adhesion molecules play an important role in inflammation, atherosclerosis and coronary artery disease (CAD). These molecules are expressed on the surface of dysfunctional endothelial cells, causing inflammatory cells from the circulation to adhere and migrate through the endothelium. Their expression is upregulated in acute coronary syndrome (ACS) and after percutaneous coronary intervention (PCI). The contact between stent struts and endothelium upregulates endothelial cell gene expression, endothelial cell activation and inflammation. The paclitaxel or sirolimus eluting stents inhibited expression of adhesion molecules in several studies and reduced the incidence of major adverse cardiac events (MACE) after drug-eluting stent (DES) over bare metal stent (BMS) implantation. Therefore, we propose that elevated serum levels of the soluble adhesion molecules after primary PCI in patients treated with BMS or DES implantation versus drug-coated balloon (DCB) application to the vulnerable coronary plaque might be a predictor of MACE and further adverse outcomes. Consequently, DCB-only strategy in patients with ACS might be a superior approach in comparison to BMS implantation and non-inferior approach when compared to DES implantation.

Coronary Plaque Characterization Assessed by Optical Coherence Tomography and Plasma Trimethylamine-N-oxide Levels in Patients With Coronary Artery Disease

Optical coherence tomography (OCT) has been considered as the ideal tool for the evaluation of atherosclerotic plaques. Circulating trimethylamine-N-oxide (TMAO), which is a metabolite of the dietary lipid phosphatidylcholine, has recently been linked to elevated coronary artery disease (CAD) risk. The objective of the study was to investigate the relation between circulating TMAO level and coronary plaque vulnerability assessed by OCT in patients with CAD. A total of 26 patients with CAD were recruited to assess coronary plaque using OCT and measure plasma TMAO level. According to plaque rupture status, patients were divided into plaque rupture group (n= 12) and nonplaque rupture group (n= 14). Plasma TMAO level was significantly higher in patients with plaque rupture than in those with nonplaque rupture (8.6 ± 4.8μmol/L vs 4.2 ± 2.4μmol/L, p=0.011). Moreover, positive correlations between plasma TMAO level and lipid arc (r=0.43, p= 0.031), lipid volume index (r= 0.39, p= 0.048) were also observed. In conclusion, circulating TMAO level may reflect coronary plaque vulnerability and progression.