CRP and CD14 polymorphisms correlate with coronary plaque volume in patients with coronary artery disease – IVUS substudy of the ENCORE trials

Background and Purpose: We aim to determine, in healthy high-risk adults, the association between subclinical coronary artery disease and white matter hyperintensity (WMH) volume and location, independent of atherosclerotic risk factors. Methods: Seven hundred eighty-two asymptomatic first-degree relatives of index cases with early-onset coronary artery disease (<60 years old) from GeneSTAR (Genetic Study of Atherosclerosis Risk) with contemporaneous coronary computed tomography angiography and brain magnetic resonance imaging were analyzed. Multilevel mixed-effects linear regression models, accounting for family structure, evaluated the association of total WMH volume and 3 regions (deep WMH, periventricular WMH [PVWMH], or borderzone [cuff]) with markers of coronary artery disease. Separate models were created for total WMH, deep WMH, PVWMH, and cuff volumes, each, as dependent variables, across coronary computed tomography angiography variables, adjusted for covariates. Results: Mean age was 51 years ±10, with 58% women and 39% African American people. Participants with any coronary plaque had 52% larger WMH volumes than those without plaque (95% CI, 0.24–0.59). Per 1% greater coronary plaque volume, total WMH volumes were 0.07% larger (95% CI, 0.04–0.10). Every 1% higher total coronary plaque volume was associated with 5.03% larger deep WMH volume (95% CI, 4.67–5.38), 5.10% PVWMH larger volume (95% CI, 4.72–5.48), and 2.74% larger cuff volume (95% CI, 2.38–3.09) with differences in this association when comparing deep WMH to PVWMH ( P interaction, 0.001) or cuff ( P interaction, <0.001), respectively. Conclusions: In healthy, high-risk individuals, the presence and volume of coronary artery plaque are associated with larger WMH volumes, appearing the strongest for PVWMH. These findings in high-risk families suggest a disease relationship in 2 different vascular beds, beyond traditional risk factors, possibly due to genetic predisposition.

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Quantified coronary plaque volume provides superior risk stratification up to 10 years

European Heart Journal ◽

10.1093/ehjci/ehaa946.0179 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

S Deseive ◽

R Straub ◽

M Kupke ◽

P Kitslaar ◽

A Broersen ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

High Risk ◽

Cardiac Death ◽

Coronary Plaque ◽

Suspected Coronary Artery Disease ◽

Plaque Volume ◽

Risk Patients ◽

Artery Disease ◽

Coronary Plaque Volume

Abstract Background Automated plaque quantification derived from coronary CT angiogragphy datasets provides exact and reliable assessment of coronary atherosclerosis burden. Purpose To investigate the potential for category based reclassification of patients based upon quantified coronary plaque volume in patients with 10 years of follow-up. Methods Coronary PV was quantified with dedicated software in 1577 patients with suspected coronary artery disease. Cardiac death and acute coronary syndrome were defined as endpoint. Patients were initially classified as low, intermediate or high risk based upon the Morise score. Quantified PV was used to reclassify patients as shown in Figure 1 Panel A. The applied cutoffs (PV=0, PV0–110.5 mm3 and PV>110.5mm3) were established by previous work of our group. Categorical net reclassification improvement was used to compare the initial and updated patient stratification. Results Patients were followed for 10.4 years. The combined endpoint occurred in 59 patients, of whom 36 suffered from cardiac death, 18 had non-fatal myocardial infarction and 5 presented with unstable angina requiring recascularisation. The Morise score classified the majority of patients as intermediate risk patients (71%) and smaller proportions as low risk (21.9%) or high risk (7.1%). Quantified PV based reclassification resulted in reclassification of 800 (51%) patients. Of those, the majority was classified into a lower risk category (n=502). Calculation of the categorical NRI proved a significantly superior risk stratification when compared to the initial risk groups (0.48 with 95% CI 0.13 and 0.68, p<0.001). The reclassification matrix is shown in Figure 1 Panel B. After reclassification, the estimated 10-year event rates for low, intermediate and high risk patients were 0.6% (95% CI 0 and 1.3%), 4.8% (95% CI 2.4 and 7.2%) and 11.3% (95% CI 6.6 and 13.9%) respectively. Conclusion Quantified coronary PV permits an effective and useful approach to reclassify patients with suspected coronary artery disease into superior risk categories. Funding Acknowledgement Type of funding source: None

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Diastolic blood pressure predicts coronary plaque volume in patients with coronary artery disease

Atherosclerosis ◽

10.1016/j.atherosclerosis.2018.07.031 ◽

2018 ◽

Vol 277 ◽

pp. 34-41 ◽

Cited By ~ 2

Author(s):

Mohamad Saleh ◽

Abdulhamied Alfaddagh ◽

Tarec K. Elajami ◽

Hasan Ashfaque ◽

Huzifa Haj-Ibrahim ◽

...

Keyword(s):

Blood Pressure ◽

Coronary Artery Disease ◽

Coronary Artery ◽

Diastolic Blood Pressure ◽

Coronary Plaque ◽

Plaque Volume ◽

Artery Disease ◽

Coronary Plaque Volume

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

Journal of Cardiology ◽

10.1016/j.jjcc.2021.05.015 ◽

2021 ◽

Author(s):

Ryohei Akashi ◽

Seiji Koga ◽

Tsuyoshi Yonekura ◽

Satoshi Ikeda ◽

Hiroaki Kawano ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Intravascular Ultrasound ◽

Coronary Plaque ◽

Plaque Composition ◽

Artery Disease

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Abstract P049: Serum Uric Acid Levels Are Associated With Non-Calcified Coronary Plaque Independent of Traditional Cardiovascular Risk Factors in Patients With Psoriasis

Circulation ◽

10.1161/circ.137.suppl_1.p049 ◽

2018 ◽

Vol 137 (suppl_1) ◽

Author(s):

Youssef A Elnabawi ◽

Amit K Dey ◽

Agastya D Belur ◽

Aditya Goyal ◽

Jacob W Groenendyk ◽

...

Keyword(s):

Risk Factors ◽

Coronary Artery Disease ◽

Uric Acid ◽

Coronary Artery ◽

Serum Uric Acid ◽

Coronary Plaque ◽

Chronic Inflammatory Disease ◽

Human Model ◽

Plaque Burden ◽

Artery Disease

Introduction: Serum uric acid (sUA), a known inflammosome-inducer, is associated with prospective risk of coronary artery disease in a dose-dependent fashion. Psoriasis (PSO), a chronic inflammatory disease associated with elevated burden of systemic inflammation and subclinical coronary artery disease, provides a reliable human model to study how sUA may relate to non-calcified coronary plaque burden (NCB) measured by computed coronary tomography angiography (CCTA). Hypothesis: We hypothesized that sUA would directly associate with NCB beyond traditional cardiovascular (CV) risk factors. Methods: 103 consecutive PSO patients and 47 healthy volunteers (HV) underwent CCTA (320 detector row, Toshiba) for coronary plaque burden quantification using QAngio (Medis). PSO severity was assessed by Psoriasis Area Severity Score (PASI) and divided into severe PSO (PASI>10) and mild-moderate PSO (PASI<10). All patients had fasting blood draws for the measurement of sUA at a certified clinical lab. Results: PSO patients were older than HV and had a higher CV risk by Framingham risk score (FRS) (Table 1). We observed a significant trend towards increase in sUA among severe PSO, mild-moderate PSO, and HV groups (mean 6.4, 5.9, 5.4 respectively, p=0.02 for trend). A positive association was observed between sUA and NCB, which was stronger in severe PSO after adjustment for traditional CV risk, alcohol, statins, and systemic/biologic PSO treatment (Severe PSO: β=0.27, p<0.001; Mild-moderate PSO: β=0.18, p=0.03), not significant in HV (β=0.18, p=0.12). Conclusions: sUA is independently associated with NCB in states of chronic inflammation such as PSO, and as such, may potentially serve as a biomarker for subclinical coronary atherosclerosis. However, larger prospective studies of CV outcomes in chronic inflammatory diseases are needed to confirm these results.

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P5508Impact of CD14++CD16+ monocytes on coronary plaque vulnerability assessed by optical coherence tomography in coronary artery disease patients

European Heart Journal ◽

10.1093/eurheartj/ehz746.0458 ◽

2019 ◽

Vol 40 (Supplement_1) ◽

Author(s):

H Yamamoto ◽

H Otake ◽

T Shinke ◽

T Yamashita ◽

H Kawamori ◽

...

Keyword(s):

Coronary Artery Disease ◽

Coronary Artery ◽

Coronary Plaque ◽

Lipid Lowering ◽

Lipid Lowering Therapy ◽

Plaque Vulnerability ◽

Glucose Fluctuation ◽

Fibrous Cap ◽

Lipid Rich Plaque ◽

Artery Disease

Abstract Background Diabetes mellitus has been known as an important factor of coronary artery disease (CAD) progression despite of widespread with lipid-lowering therapy. Although we have reported that large glucose fluctuation is associated with the development of cardiovascular disease in both diabetes mellitus (DM) and non-DM patients, the underlying mechanisms remain unclear. Monocytes play a key role for atherosclerotic plaque formation. Monocytes in human peripheral blood are divided into three subsets: CD14++CD16− monocytes, CD14++CD16+ monocytes, and CD14+CD16++ monocytes. The CD14++CD16+ monocyte subset has recently received attention because it is reported to be associated with future cardiovascular events such as acute myocardial infarction. However, their impact on coronary plaque vulnerability in coronary artery disease (CAD) patients with or without DM remains unclear. Purpose The aim of this study was to investigate the impact of CD14++CD16+ monocyte levels on coronary plaque vulnerability and glucose fluctuation in stable CAD patients with well-regulated lipid levels. Methods This prospective observational study included 50 consecutive patients with CAD (DM [n=22], Non-DM [n=28]), receiving lipid-lowering therapy and undergoing coronary angiography and optical coherence tomography (OCT). Patients were divided into 3 tertiles according to the CD14++CD16+ monocyte percentages assessed by flow cytometry. Standard OCT parameters including lipid arc, lipid length, fibrous cap thickness (FCT) on lipid rich plaque, were assessed for 97 angiographically intermediate lesions (diameter stenosis: 30–70%). The presence of thin-cap fibroatheroma (TCFA), defined as a thin fibrous cap (<65μm) overlying a lipid-rich plaque (>90°), was also assessed. Daily glucose fluctuation assessed by using continuous glucose monitoring system was analyzed by measuring the mean amplitude of glycemic excursion (MAGE). Results CD14++CD16+ monocytes negatively correlated with FCT on lipid rich plaque (r=0.508, p<0.01) (Figure. 1). The presence of thin-cap fibroatheroma (TCFA) was increased stepwise according to the tertile of CD14++CD16+ monocytes (0 [tertile 1] vs. 5 [tertile 2] vs. 10 [tertile 3], p<0.01). CD14++CD16+ monocytes were a significant determinant of TCFA (OR 1.279, p=0.001). Although CD14++CD16+ monocytes were not significantly correlated with MAGE in DM patients (r=0.259, p=0.244), a significant relationship was found between CD14++CD16+ monocytes and MAGE in non-DM patients (r=0.477, p=0.018) (Figure 2). Conclusions CD14++CD16+ monocytes were associated with coronary plaque vulnerability in CAD patients with well-regulated lipid levels both in DM and non-DM patients. Cross-talk between glucose fluctuation and CD14++CD16+ monocytes may enhance plaque vulnerability, particularly in non-DM patients. CD14++CD16+ monocytes could be a possible therapeutic target for coronary plaque stabilization.

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