Plaque Vulnerability In Patients Research Articles

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<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<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.

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

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

Impact of glucose variability on coronary plaque vulnerability in patients with dysglycemia: A whole coronary analysis with multislice computed tomography

BackgroundDysglycemia is associated with an increased risk of acute coronary syndrome caused by the disruption of vulnerable plaques. The relationship between glycemic variability (GV), which is a component of impaired glucose metabolism, and coronary plaque vulnerability has not been fully elucidated. This study investigated the impact of GV on whole coronary plaque vulnerability using multislice computed tomography (MSCT). MethodsWe analyzed 88 patients with dysglycemia who underwent 24 h blood glucose monitoring and MSCT. The mean amplitude of glycemic excursion (MAGE) was calculated as an index of the GV. We defined a CT-derived vulnerable plaque as a plaque with a remodeling index > 1.10 and a mean CT density < 30 HU. We calculated the percentage of low-attenuation plaque (% LAP) as the ratio of the low-attenuation component (CT density < 30HU) volume to the total vessel volume. ResultsVulnerable plaques were detected in 27 patients (31%). Patients with vulnerable plaques had higher MAGE (110.0 ± 40.7 vs. 71.7 ± 21.7, p < 0.01) than patients without vulnerable plaques. A univariate logistic regression analysis showed that vulnerable plaques were associated with the MAGE [odds ratio (OR) 1.04, 95% confidence interval (CI), 1.02–1.07, p < 0.01]. In a multivariate model, the MAGE (OR 1.05, 95% CI 1.02–1.07) remained a significant predictor of vulnerable plaque presence. Patients with multivessel-vulnerable plaques had higher MAGE values than those with single-vessel involvement or no vulnerable plaques (132.3 ± 39.4 vs. 102.2 ± 39.7, vs. 71.7 ± 21.7, p < 0.01). The regression analysis showed a positive correlation between MAGE levels and the % LAP (r = 0.55, p < 0.01). In a multiple linear regression analysis, the MAGE was independently associated with the % LAP (β = 0.42, p < 0.01). ConclusionsIncreased GV is associated with the presence and extent of vulnerable plaques.

Evaluation of Plaque Characteristics and Inflammation Using Magnetic Resonance Imaging.

Atherosclerosis is an inflammatory disease of large and medium-sized arteries, characterized by the growth of atherosclerotic lesions (plaques). These plaques often develop at inner curvatures of arteries, branchpoints, and bifurcations, where the endothelial wall shear stress is low and oscillatory. In conjunction with other processes such as lipid deposition, biomechanical factors lead to local vascular inflammation and plaque growth. There is also evidence that low and oscillatory shear stress contribute to arterial remodeling, entailing a loss in arterial elasticity and, therefore, an increased pulse-wave velocity. Although altered shear stress profiles, elasticity and inflammation are closely intertwined and critical for plaque growth, preclinical and clinical investigations for atherosclerosis mostly focus on the investigation of one of these parameters only due to the experimental limitations. However, cardiovascular magnetic resonance imaging (MRI) has been demonstrated to be a potent tool which can be used to provide insights into a large range of biological parameters in one experimental session. It enables the evaluation of the dynamic process of atherosclerotic lesion formation without the need for harmful radiation. Flow-sensitive MRI provides the assessment of hemodynamic parameters such as wall shear stress and pulse wave velocity which may replace invasive and radiation-based techniques for imaging of the vascular function and the characterization of early plaque development. In combination with inflammation imaging, the analyses and correlations of these parameters could not only significantly advance basic preclinical investigations of atherosclerotic lesion formation and progression, but also the diagnostic clinical evaluation for early identification of high-risk plaques, which are prone to rupture. In this review, we summarize the key applications of magnetic resonance imaging for the evaluation of plaque characteristics through flow sensitive and morphological measurements. The simultaneous measurements of functional and structural parameters will further preclinical research on atherosclerosis and has the potential to fundamentally improve the detection of inflammation and vulnerable plaques in patients.

Familial hypercholesterolemia and vulnerability of coronary plaque in patients with coronary artery disease

ObjectivesPatients with familial hypercholesterolemia (FH) are at a very high risk of coronary artery diseases. The aim of the present study was to clarify the characteristics of coronary plaque in patients with FH. Designand Methods: A total of 569 patients who underwent optical coherence tomography (OCT) imaging of culprit plaque were included. The characteristics of culprit plaque were compared between patients with and without FH. ResultsA total of 38 patients (6.7%) were clinically diagnosed with FH. The location of the culprit plaque was significantly different (p ​< ​0.001) with a trend toward higher frequency of left main lesion in the FH group than in the group with no FH (7.9 vs. 0%). Culprit plaque was significantly shorter in patients with FH than those without FH (28.1 vs. 33.2 ​mm, p ​= ​0.016). A trend toward higher prevalence of plaque with macrophage accumulation in patients with FH than those without FH (50.0 vs. 34.7%, p ​= ​0.056) was observed, although the prevalence of other vulnerable characteristics including thin-cap fibroatheroma (TCFA) was comparable between patients with and without FH. Among patients with FH, significant increases in the prevalence of lipid-rich plaque (p ​= ​0.028) and TCFA (p ​= ​0.003) were observed according to the increase in low-density lipoprotein cholesterol (LDL-C) levels. ConclusionsPatients with FH had shorter culprit plaque without significant difference in the prevalence of vulnerable plaque components compared with patients without FH. A higher LDL-C level was associated with higher prevalence of vulnerable plaque in patients with FH.

Predictors of Coronary Plaque Vulnerability in Patients with Stable Coronary Artery Disease

Aim To identify new predictors for vulnerability of atherosclerotic coronary plaques in patients with stable ischemic heart disease (sIHD).Material and methods This prospective, single-center study included 58 patients with sIHD. Unstable plaques were detected with virtual histology intravascular ultrasound of proximal and medium segments of a coronary artery without significant lesions according to coronarography data. Indexes of inflammation, dyslipidemia and carbohydrate metabolism were considered as candidate predictors for coronary plaque vulnerability.Results In 56 coronary arteries, 58 plaques were detected, 12 of which (20.7 %) were unstable. Vulnerable plaques differed morphologically from stable ones by a greater size of the necrotic core (35.1±8.5 % vs. 24.0±13.2 %; р=0.008), calcified nodules (2.0 [1.0; 5.0] % vs. 1.0 [0; 2.0] %; р=0.006), and a lower content of fibrous components (54.9±10.2 % vs. 66.4±15.8 %; р=0.02). In addition, vulnerable plaques more frequently narrowed the arterial lumen by &gt;70 % of the lumen area (33.3 % vs. 2.2 %; р=0.0006). Correlation analysis showed a negative correlation between the level of high-density lipoproteins (HDL) and calcium volume (r= -0.4104; р=0.023); a positive correlation between the blood glucose level as determined by the oral glucose tolerance test and the lipid component (r=0.48198; р=0.033); and a negative correlation between the apolipoprotein A level and the calcium volume (r= -0.4297; р=0.008).Conclusion The study demonstrated a high prevalence of vulnerable plaques in nontarget coronary arteries in patients with sIHD. In this process, dyslipidemia indexes (LDL, apolipoproteins A) correlate with the calcium volume whereas blood glucose, as measured in the oral glucose tolerance test, correlates with the lipid component of coronary plaque.

Platelet-Derived Growth Factor Predicts Vulnerable Plaque in Patients with Non-ST Elevation Acute Coronary Syndrome

BackgroundIdentifying a novel biomarker may contribute to detection of vulnerable plaque in patients with non-ST-elevation acute coronary syndrome (NSTE-ACS). The aim of this study was to investigate the relationship between serum platelet-derived growth factor (PDGF) and vulnerable plaque in patients with moderate and low risk of NSTE-ACS. MethodsA total of 65 moderate- and low-risk NSTE-ACS patients with 50–90% coronary stenosis were divided into a vulnerable plaque group (n=46) and a stable plaque group (n=19) according to intravascular ultrasound (IVUS) examinations. Total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C) and serum PDGF were measured. Plaque characteristics and components were analyzed using gray-scale and iMap-IVUS. Correlation was performed between plaque characteristics and ACS markers. Logistic regression analysis was applied to determine risk factors. Receiver operating characteristic (ROC) curve was used to evaluate the predictive value. ResultsPatients with vulnerable plaque had visible higher levels of TG, LDL-C and PDGF (P < 0.05). There were significant differences in minimal lumen area (MLA), plaque area, plaque burden, fibrotic (FI), clipidic (LI) and necrotic core (NC) between the two groups (P < 0.05). PDGF was weakly correlated with plaque burden (R = 0.428, P < 0.05), as well as moderately correlated with NC (R = 0.669, P < 0.05). Multivariate analysis showed that serum PDGF (OR 4.751, [95% CI 1.534–9.543], P = 0.05) was an independent risk factor of vulnerable plaque. The area under the curve (AUC) was 0.876 (95% CI 0.804–0.948, P=0.001). ConclusionsSerum PDGF could potentially predict vulnerable plaque in moderate and low risk of NSTE-ACS patients.

Intracoronary polarimetry for characterizing coronary plaque vulnerability in patients with coronary artery disease

Abstract Background Intracoronary polarimetry with polarization-sensitive (PS-) optical frequency domain imaging (OFDI) measures polarization properties, including birefringence and depolarization, in parallel with structural features of conventional OFDI (Figure 1A). Collagen, which imparts mechanical integrity to fibrous caps, and collagen-synthesizing smooth muscle cells exhibit elevated birefringence. Depolarization is increased by the presence of macrophages and lipid/necrotic cores. Purpose This study aimed to compare conventional OFDI and polarimetric signatures of coronary lesions between patients with acute coronary syndrome (ACS) and chronic coronary syndrome (CCS). Furthermore, we aimed to determine a birefringence cut-off value for identifying which fibrous caps belong to ACS culprit lesions. Methods This study consisted of 37 patients with ACS (n=23) or CCS (n=14). ACS culprit lesions (ACS-lesions) and CCS stenotic lesions (CCS-lesions) were included in the analysis (820 mm). Qualitative and quantitative conventional OFDI analysis included the presence of plaque rupture, macrophage infiltration, micro-vessels, thrombus, stenosis severity, fibrous cap thickness (FCT), lipid arc, lipid-burden and calcium-burden index. Birefringence and depolarization of the coronary lesions and fibrous caps were measured in the cross-sectional images showing the minimum FCT or minimum luminal area. Predictors of ACS-lesions were investigated by multivariate regression analysis. Receiver operating characteristic (ROC) analysis was used to determine the birefringence cut-off value identifying ACS fibrous caps (ACS-caps). Results There were no significant differences in clinical characteristics between the two groups, except for previous history of coronary artery disease. Compared to CCS-lesions, ACS-lesions featured higher lipid-burden index and maximum lipid arc (both p&amp;lt;0.05). ACS-lesions featured lower birefringence and higher depolarization than CCS-lesions (p&amp;lt;0.05). Multivariable regression demonstrated an independent association of birefringence with ACS-lesions (p&amp;lt;0.05), even after adjusting for the conventional OFDI findings. Limiting the analysis to the fibrous caps, ACS-caps exhibited significantly lower birefringence (p&amp;lt;0.05) and higher depolarization (p&amp;lt;0.05) that CCS-caps. ROC analysis for differentiating ACS-caps from CCS-caps found that a birefringence value of 0.0004 results in a sensitivity and specificity of 88% and 82%, respectively (Figure 1B, AUC = 0.82). Conclusions Intracoronary polarimetry provides quantitative assessment of coronary lesions related to their composition. Birefringence was an independent robust predictor of ACS-lesions. Decreased birefringence and pronounced depolarization within the ACS-caps may indicate increased collagenolytic activity and macrophage infiltration, respectively. These results suggest that polarization properties may serve as quantitative imaging markers for assessing plaque vulnerability. Figure 1 Funding Acknowledgement Type of funding source: Other. Main funding source(s): This work was supported by the National Institutes of Health and by Terumo Corporation.

Optical coherence tomography findings in healed vulnerable plaques in patients with coronary artery disease

Abstract Background Histopathological analysis or intracoronary image assessment of healed plaques (HPs) has been reported both in acute coronary syndrome (ACS) and stable angina pectoris (SAP) patients. However, background characteristics or lesion morphologies of HPs could not be fully clarified and their differences according to the clinical status remain undetermined. Purpose We sought to investigate the clinical and morphological characteristics and compare their differences among ACS and SAP patients in order to clarify the clinical significance in HPs lesions. Methods We enrolled consecutive 201 patients with 213 native coronary artery lesions (139 lesions with SAP, 42 ST elevation-ACS (STE-ACS) and 32 non-ST elevation ACS (NSTE-ACS) undergoing pre-intervention optical coherence tomography (OCT). HPs was defined as layered phenotype on OCT. Clinical and angiography characteristics and lesion morphologies on OCT were assessed. Results HPs were observed in 110 lesions (51.6%) and their prevalence were not different according to the clinical status (SAP:55.1%, STE-ACS:38.1%, NSTE-ACS:56.3%, p=0.14). Lesions with HPs had higher frequencies of angiography-eccentric lesions (62.7% vs. 35.9%, p&amp;lt;0.001) and OCT-macrophages (65.5% vs. 43.1%, p&amp;lt;0.001), and greater OCT-lumen area stenosis (%-AS) (77.1±10.2% vs. 73.6±10.6%, p=0.01) than those without HPs. Of lesions with HPs, OCT-thin-cap fibroatheroma (SAP 14.4%, STE-AC43.8%, NSTE-ACS 16.7%, p=0.03), plaque rupture (5.3%; 37.5%; 11.1%, p&amp;lt;0.001) and thrombus (6.6%, 75.0%, 22.2%, p=0.007) were more frequently observed in STE-ACS than in SAP patients, whereas OCT-microvessels were more frequent in SAP than in ACS patients (19.7%, 0.0%, 0.0%, p=0.02). Other OCT findings such as macrophages, cholesterol crystal, multiple layered phenotype, and %-AS were not significantly different according to the clinical status. Multivariate logistic regression analysis identified the angiography-eccentric lesions (odds ratio (OR): 2.97, 95% confidence intervals (CI): 1.68–5.25, p&amp;lt;0.001) and OCT macrophages (OR 2.41, 95% CI 1.36–4.27, p=0.003) as independent related factors for the existence of HPs. Conclusions The present study showed that HPs lesions had eccentric and large plaque burden, and persistent plaque inflammations regardless of clinical status, which might lead to future coronary events. Funding Acknowledgement Type of funding source: None

Impact of macrophage infiltration in patients with st-segment elevation myocardial infarction caused by plaque erosion: an in vivo optical coherence tomography study

Abstract Background Chronic inflammatory infiltration is a common process for atherosclerosis development. However, autopsy studies reveal that incidence rate of inflammatory infiltrates are less abundant in plaque erosion compared with plaque rupture. Purpose Studies performed by optical coherence tomography (OCT) have allowed to establish the severity of plaque inflammation by assessing macrophage infiltration (MØI). In this study, we aimed at assessing the impaction of MØI in plaque erosion among patients with STEMI by using OCT. Methods A total of 1561 patients with ST-segment elevation myocardial infarctions (STEMI) who underwent OCT imaging were enrolled in this study. According to the exclusion criteria, 312 patients with STEMI exhibiting plaque erosion were classified as MØI or no MØI. Results 163 (52.2%) patients had MØI at the site of plaque erosion, whereas 149 (47.8%) patients had no evidence of MØI and patients of MØI group were significantly older (P=0.015). The result of angiography showed the prevalence of multi-vessel disease appeared more frequency (P=0.021) and diameter stenosis% were higher (P=0.031) in MØI group. OCT results showed the minimum fibrous-cap thickness was thinner (P&amp;lt;0.001) and the maximum lipid arc was larger (P=0.005) in MØI group. Some patients underwent imaging follow-up at 1 year. There was no significant difference in the culprit plaque morphology progress among two groups (Figure 1A-1D). Conclusions This study demonstrated that plaque inflammation can increase culprit lesion severity and plaque vulnerability in patients with STEMI caused by plaque erosion. Figure 1 Funding Acknowledgement Type of funding source: None

Association Between Plasma Lipoprotein-Associated Phospholipase A2 and Plaque Vulnerability in TIA Patients With Unilateral Middle Cerebral Artery Stenosis.

Background: Plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) has emerged as a novel biomarker for coronary atherosclerosis. However, the association between Lp-PLA2 and plaque vulnerability in atherosclerosis of cervicocerebral arteries remains poorly defined, especially for intracranial atherosclerotic stenosis (ICAS). We aimed to investigate the association between Lp-PLA2 and plaque vulnerability in transient ischemic attack (TIA) patients with unilateral middle cerebral artery stenoses (MCAs).Methods: In this study, a total of 207 patients were enrolled from April 2017 to April 2020. Clinical data were collected, and MCA plaques were examined with high-resolution magnetic resonance imaging (HRMRI). Baseline characteristics of patients were collected during hospitalization. Statistical comparisons were performed using Pearson's chi-squared test, Mann–Whitney U test, and the Breslow–Day/Tarone's test for the determination of heterogeneity in different age strata. Multivariate binary logistic analysis was used to investigate the potential independent predictors that were highly correlated to plaque vulnerability.Results: The results showed that a high Lp-PLA2 level (>221 ng/ml) was associated with plaque vulnerability in TIA patients with unilateral MCAs. High Lp-PLA2 was independently associated with plaque vulnerability in patients ≤ 60 years old [multivariate adjusted odds ratio (OR) = 9.854; 95% CI, 2.458–39.501] but not in patients >60 years old (multivariate adjusted OR = 1.901; 95% CI, 0.640–5.650). Predictors of plaque vulnerability in different age strata were also different.Conclusion: Lp-PLA2 levels may be correlated to plaque vulnerability in TIA patients with unilateral MCAs and might be a diagnostic biomarker for plaque vulnerability in this kind of patients, especially for ones aged ≤ 60 years old.

Relationship between monocyte/lymphocyte ratio and non-culprit plaque vulnerability in patients with acute coronary syndrome: An optical coherence tomography study.

The importance of monocyte/lymphocyte ratio (MLR) has been indicated in the initiation and progression of coronary artery disease. However, few previous researches demonstrated the relationship between MLR and plaque vulnerability. We aimed to investigate coronary non-culprit plaque vulnerability in patients with acute coronary syndrome (ACS) by optical coherence tomography (OCT).A total of 72 ACS patients who underwent coronary angiography and OCT test in Beijing Anzhen Hospital were included in this retrospective study. The plaque vulnerability and plaque morphology were assessed by OCT.The non-culprit plaque in high MLR group exhibited more vulnerable features, characterizing as thinner thickness of fibrous cap (P = .013), greater maximum lipid core angle (P = .010) and longer lipid plaque length (P = .041). A prominently negative liner relation was found between MLR and thickness of fibrous cap (R = –0.225, P = .005). Meanwhile, the proportion of OCT-detected thin cap fibro-atheroma (TCFA) (P = .014) and plaque rupture (P = .017) were higher in high MLR group. Most importantly, multivariable logistic regression analysis showed MLR level was identified as an independent contributor to the presence of TCFA (OR:3.316, 95%: 1.448–7.593, P = .005). MLR could differentiate TCFA with a sensitivity of 60.0% and a specificity of 85.1%.Circulating MLR level has potential value in identifying the presence of vulnerable plaque in patients with ACS. MLR, as a non- invasive biomarker of inflammation, may be valuable in revealing plaque vulnerability.

Association between food and nutrients intakes and coronary plaque vulnerability in patients with coronary heart disease: An optical coherence tomography study

Background and aimsDietary intakes play important roles in the prevention and treatment of coronary heart disease (CHD). Coronary plaque vulnerability is the key mechanism leading to CHD progression. We aimed to explore the association between dietary intakes and plaque vulnerability via optical coherence tomography (OCT). Methods and resultsA total of 314 CHD patients were included in this study. Dietary intake status was assessed by semi-quantitative food frequency questionnaire and plaque vulnerability was measured by OCT. The results showed that vegetables were negatively associated with macrophage infiltration, thin cap fibroatheroma (TCFA) and thrombus [odds ratio (OR) = 0.48, 0.38, 0.38, 95% confidence interval (95% CI) = 0.24–0.93, 0.17–0.84, 0.15–0.94, all P < 0.05]; fruits were negatively associated with lipid plaque, TCFA, rupture and thrombus (OR = 0.17, 0.11, 0.12, 0.20, 95% CI = 0.07–0.39, 0.04–0.29, 0.05–0.28, 0.08–0.55, all P < 0.05); salt was positively associated with lipid plaque and TCFA (OR = 2.59, 2.83, 95% CI = 1.14–5.90, 1.23–6.51, all P < 0.05). Regarding nutrients intakes, dietary fiber was negatively associated with macrophage infiltration (OR = 0.34, 95% CI = 0.14–0.85, P = 0.021); folate was negatively associated with lipid plaque, TCFA and rupture (OR = 0.22, 0.16, 0.20, 95% CI = 0.09–0.58, 0.06–0.41, 0.08–0.51, all P < 0.05); vitamin C was negatively associated with TCFA, rupture and thrombus (OR = 0.26, 0.22, 0.05, 95% CI = 0.07–0.95, 0.07–0.65, 0.01–0.25, all P < 0.05); sodium was positively associated with lipid plaque, TCFA, rupture and thrombus (OR = 3.43, 3.96, 2.73, 4.84, 95% CI = 1.51–7.80, 1.66–9.45, 1.18–6.27, 1.76–9.28, all P < 0.05). ConclusionSalt and sodium were dietary risk factors for plaque vulnerability, whereas vegetables, fruits, dietary fiber, folate and vitamin C were dietary protective factors for plaque vulnerability.

Human cytomegalovirus infection is correlated with atherosclerotic plaque vulnerability in carotid artery.

Several studies have suggested that human cytomegalovirus (CMV) infection is closely related to the pathogenesis of atherosclerosis. The present study aimed to investigate the association between human CMV infection and carotid atherosclerotic plaque vulnerability in a Chinese population. In total, 42 patients with carotid atherosclerosis (observation group) and 30 healthy volunteers (control group) were recruited in our study from October 2016 to January 2018. Statistical analysis was carried out to calculate the infection rate of CMV in subjects. Spearman's rank analysis was performed to evaluate the correlation between CMV infection and atherosclerotic plaque vulnerability. The positive rate of CMV was significantly higher in the observation group compared to the control group, and matrix metalloproteinase 9 (MMP-9), tumor necrosis factor-α (TNF-α) and lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) expression levels were also elevated in the observation group compared to those in the control group. In carotid atherosclerotic patients, the detection rate of unstable plaques and the Crouse scores in vulnerable plaque were significantly higher in the CMV-positive group compared to those in the CMV-negative group. As revealed by correlation analysis, CMV infection was significantly positively correlated with plaque vulnerability and expression levels of MMP-9, TNF-α and LOX-1 in carotid atherosclerotic patients. Human CMV infection might be a potential risk factor for increased plaque vulnerability in patients with carotid atherosclerosis.

Endothelial glycocalyx and severity and vulnerability of coronary plaque in patients with coronary artery disease

Background and aimsEndothelial glycocalyx covers the endothelium and maintains vascular integrity. However, its association with the severity and vulnerability of coronary artery disease (CAD) remains to be elucidated. MethodsA total of 259 consecutive patients with stable CAD requiring percutaneous coronary intervention (PCI) were prospectively enrolled. Patients were classified into 2 groups according to the median value of serum syndecan-1, which is a core component of the endothelial glycocalyx (lower syndecan-1 group [syndecan-1 <99.0 ng/mL], n = 130; higher syndecan-1 group [syndecan-1 ≥99.0 ng/mL], n = 129). Severity of CAD and focal plaque vulnerability in culprit lesion were evaluated using angiography and optical coherence tomography. ResultsThere was no significant difference in clinical characteristics between the lower syndecan-1 group and the higher syndecan-1 group other than the prevalence of family history of CAD (19 vs. 32%, p = 0.022), prior PCI history (45 vs. 60%, p = 0.015) and estimated glomerular filtration rate (57.8 ± 17.2 vs. 50.9 ± 25.6 ml/min/1.73 m2, p = 0.011). Although disease severity on angiogram was comparable between the 2 groups, the prevalence of lipid-rich plaque (40 vs. 19%, p = 0.004) and thin-cap fibroatheroma (20 vs. 6%, p = 0.006) was significantly higher in the lower syndecan-1 group than the higher syndecan-1 group. Lower syndecan-1 level was independently associated with higher prevalence of lipid-rich plaque (odds ratio 3.626, 95% confidence interval 1.535–8.566, p = 0.003). ConclusionsLower syndecan-1 level was associated with higher prevalence of vulnerable plaque in patients with CAD. This finding suggests the association between impaired endothelial glycocalyx and the development of vulnerable plaque.

Progression of ultrasound plaque attenuation and low echogenicity associates with major adverse cardiovascular events.

Intravascular ultrasound (IVUS) imaging can visualize vulnerable plaque features including attenuation (AP) and echolucency (ELP). While IVUS-derived vulnerable plaque features associate with microvascular obstruction during percutaneous coronary intervention, the relationship between these plaque features and clinical outcomes has not been established. This analysis aimed to evaluate the association of AP/ELP with cardiovascular events. Serial IVUS imaging was reviewed in 1497 patients, followed for 18-24 months, with coronary artery disease from two clinical trials. Attenuated plaque and ELP were identified to measure each characteristics (AP arc, ELP area, and lengths), which permitted calculation of an AP index (API) and ELP volume. Attenuated plaque/ELP progression was defined as patients with any increase of API or ELP volume on serial imaging. The major cardiovascular events (MACEs) were defined as death, myocardial infarction, stroke, and coronary revascularization. AP or ELP was identified in 282 patients (18.8%) at baseline and 160 (10.7%) patients demonstrated an increase in AP or ELP at follow-up. The incidence of MACE was higher in patients with baseline AP/ELP than those without (8.2% vs. 3.9%, P = 0.002). Patients with AP/ELP progression were more likely to be acute coronary syndrome (41.9 vs. 33.2%, P = 0.03) and have greater baseline percent atheroma volume (40.0% vs. 35.8%, P < 0.001) than those without. On multivariable analysis, AP/ELP progression was more strongly associated with MACE [baseline AP/ELP: hazard ratio (HR) 1.76, 95% confidence interval (CI) 1.05-2.97, AP/ELP progression: HR 2.19, 95% CI 1.24-3.86]. Attenuation/ELP progression was associated with a higher prevalence of cardiovascular events, supporting a potential role for the identification of high-risk vulnerable plaques in patients with coronary artery disease.

Sequential Surgical Procedures in Vascular Surgery Patients Are Associated With Perioperative Adverse Cardiac Events.

Patients at elevated cardiovascular risk are prone to perioperative cardiovascular complications, like myocardial injury after non-cardiac surgery (MINS). We have demonstrated in a mouse model of atherosclerosis that perioperative stress leads to an increase in plaque volume and higher plaque vulnerability. Regulatory T cells (Tregs) play a pivotal role in development and destabilization of atherosclerotic plaques. For this exploratory post-hoc analysis we identified 40 patients recruited into a prospective perioperative biomarker study, who within the inclusion period underwent sequential open vascular surgery. On the basis of protein markers measured in the biomarker study, we evaluated the perioperative inflammatory response in patients' plasma before and after index surgery as well as before and after a second surgical procedure. We also analyzed available immunohistochemistry samples to describe plaque vulnerability in patients who underwent bilateral carotid endarterectomy (CEA) in two subsequent surgical procedures. Finally, we assessed if MINS was associated with sequential surgery. The inflammatory response of both surgeries was characterized by postoperative increases of interleukin-6,−10, Pentraxin 3 and C-reactive protein with no clear-cut difference between the two time points of surgery. Plaques from CEA extracted during the second surgery contained less Tregs, as measured by Foxp3 staining, than plaques from the first intervention. The 2nd surgical procedure was associated with MINS. In conclusion, we provide descriptive evidence that sequential surgical procedures involve repeat inflammation, and we hypothesize that elevated rates of cardiovascular complications after the second procedure could be related to reduced levels of intraplaque Tregs, a finding that deserves confirmatory testing and mechanistic exploration in future populations.

Systemic atherosclerotic plaque vulnerability in patients with Coronary Artery Disease with a single Whole Body FDG PET-CT scan.

Cardiovascular disease is a leading cause of morbimortality with over half cardiovascular events occurring in the asymptomatic population by traditional risk stratification. This preliminary study aimed to evaluate systemic plaque vulnerability in patients with prior Coronary Artery Disease (CAD) with a single Whole Body [FDG] PET-CT scan in terms of plaque inflammation and calcifications. Twenty-two patients referred for oncological evaluation and with prior history of advanced CAD or age and gender matched controls without cardiovascular disease, underwent a Whole Body PET-CT scan 90 min after injection of 18F-FDG. A total of 975 transaxial PET images were retrospectively analysed to assess plaque inflammation using a standardized method of analysis with averaged Target-to-Background Ratios (TBRs) at different levels, in the thoracic and abdominal aorta, carotids, LAD, common iliac and femoral arteries, and were correlated with calcium scores from the CT images. TBRs from the thoracic aorta were higher in male patients than controls (1.49±0.11, p<0.05) and a gradient was observed (ascending > descending > aortic arch), and were also higher in the carotids in female patients (1.43±0.07) versus controls (p<0.05). A tendency for higher levels of plaque inflammation in the abdominal aorta was noted in all groups, but no significant FDG uptake was found either in the iliac or femoral arteries in any group. Plaque inflammation was also higher in the LAD in males but with large variations. Higher levels of calcifications were noted in the LAD, infra-renal abdominal aorta and common iliac arteries, but without significant correlation with plaque inflammation except sporadic overlapping. Patients with advanced CAD are at risk for vulnerable inflamed atheromas in other territories such as the thoracic aorta and carotid arteries, underpinning the systemic nature of the atherosclerotic disease. Coexistence with calcifications is rare, suggesting a different functional status of the plaques and different stages of the disease. Evaluation of subclinical systemic plaque vulnerability in CAD with a Whole Body [FDG] PET-CT scan is feasible and a potentially useful biomarker to assess subclinical vascular risk for risk stratification and treatment optimization, but further studies are needed.

569 Association between periodontal disease, coronary calcium score and markers of subclinical atherosclerosis in patients with unstable angina-a CT-based sub-study from the ATHERODENT clinical trial

Abstract Funding Acknowledgements PlaqueImage financed by the National Authority of Scientific Research and Innovation and the Romanian Ministry of European Funding Background The relationship between periodontal disease (PD) and chronic inflammation is well established. PD leads to increased cardiovascular risk and favours development of acute coronary syndromes; however, the association between PD and markers of subclinical atherosclerosis has not been elucidated so far. Purpose To evaluate the interrelation between severity of PD, coronary calcium, subclinical atherosclerosis and plaque vulnerability in patients with unstable angina, who underwent coronary computed tomography angiography (CCTA). Methods Fifty-two patients with unstable angina were enrolled in the ATHERODENT clinical trial (NCT03395041). All patients underwent: (1) complex dental examination for assessment of periodontal status, expressed by the total periodontal index (PI) evaluating the following indices: gingival index, plaque index, tantrum index, furcation index, mobility, loss of attachment, pocket depth and papillary bleeding index, (2) CCTA for analysis of morphology, composition and vulnerability features of the culprit plaques causing myocardial schema. For each patient, coronary calcium score, body mass index, neck circumference, abdominal circumference and Intima-media thickness of the carotid artery were calculated. According to the median value of the total PI (set by 22) the study population was divided into two groups: group 1 included 26 patients with low PI (normal gum or gingivitis) and group 2 included 26 patients with high PI (periodontitis and severe PD). Results In patients with high PI the plaque volume (p = 0.019) and the non-calcified volume (p = 0.002) were more increased compared with patients with low PI. In patients with high risk features in the culprit coronary plaques (positive remodelling, low density atheroma, spotty calcification and napkin ring sign) the severity of PD was more expressed compared with those with low risk plaques (28.20+/-13.34 vs. 18.71+/-11.31, p = 0.001). From all PI indices, loss of gingival attachments (3.6 +/-2.91 vs. 1.66 +/- 1.8, p = 0.009) and papillary bleeding index (4.5 +/-3.06 vs. 2.04+/-1.96, p = 0.002) were significantly correlated with the plaque vulnerability. there was no significant correlation between PI and the markers of subclinical atherosclerosis expressed by the neck circumference, abdominal circumference and IMT of the carotid artery. However, total PI presented significantly correlation with the total coronary artery calcium score (r = 0.45, p = 0.0008). A higher calcium score was identified in patients with high PI compared with those with low PI (505.29 +/-478.64 vs. 93.82+/-233.0, p = 0.0001). Conclusions In patients with vulnerable coronary plaques, subclinical atherosclerosis is not correlated with PI. However, the severity of PD is directly associated with the total calcium score and with a more vulnerable phenotype of the atheromatous coronary plaques.

P6416Lower serum syndecan-1 level is associated with higher prevalence of vulnerable plaque in patients with coronary artery disease

Abstract Introduction Syndecan-1 is a component of endothelial glycocalyx which maintains vascular integrity. Thus, it may be impaied in patients with coronary artery disease (CAD). Purpose To assess the association between serum syndecan-1 level and the severity and vulnerability of CAD. Methods A total of 259 consecutive patients with stable angina requiring percutaneous coronary intervention (PCI) were prospectively enrolled. Patients were classified into 2 groups according to the median syndecan-1 value (Lower syndecan-1 group [syndecan-1 &lt;99.0], n=130; Higher syndecan-1 group [syndecan-1 ≥99.0], n=129). Severity of CAD and focal plaque vulnerability in target lesion was evaluated using findings of angiography and optical coherence tomography (OCT), respectively. Thin-cap fibroatheroma (TCFA) was defined as a lipid-rich plaque covered with thin fibrous cap (&lt;65 μm). Results There was no significant difference in baseline clinical characteristics between the lower syndecan-1 group and the higher syndecan-1 group other than the prevalence of family history of ischemic heart disease (19 vs. 32%, p=0.022) and prior PCI history (45 vs. 60%, p=0.015). The prevalence of multivessel disease (70 vs. 68%, p=0.627), left main disease (4 vs. 5%, p=0.748) and chronic total occlusion (15 vs. 15%, p=0.959) was comparable between the 2 groups. On the other hand, the prevalence of lipid-rich plaque (40 vs. 19%, p=0.004) and TCFA (20 vs. 6%, p=0.006) was significantly higher in the lower syndecan-1 groupthan the higher syndecan-1 group (Figure). The lower syndecan-1 was independently associated with the higher prevalence of lipid-rich plaque (Table). Table 1. Multivariate analysis for lipid-rich plaque Odds ratio 95% CI pvalue Lower syndecan-1 2.981 1.448–6.411 0.003 Dyslipidemia 1.693 0.738–4.142 0.218 Chronic kidney disease 1.354 0.669–2.765 0.400 Smoking 0.975 0.453–2.154 0.951 Diabetes mellitus 0.819 0.400–1.661 0.580 Conclusions Lower syndecan-1 level was associated with higher prevalence of vulnerable plaque in patients with CAD. Serum syndecan-1 may have a potential as a marker for the presence of vulnerable coronary plaque.