Abstract P210: Calcified Atherosclerotic Plaque and All Cause Mortality in Diabetes: Diabetes Heart Study

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Subhashish Agarwal ◽  
David M Herrington ◽  
Amanda J Cox ◽  
Neal Jorgensen ◽  
Jianzhao Xu ◽  
...  

Introduction Coronary artery calcium (CAC), a measure of atherosclerosis predicts mortality in both diabetes and the general population. The incremental utility of measuring atherosclerosis across multiple vascular beds beyond CAC for the prediction of mortality has not been reported. In this study we derived a composite atherosclerosis score (CAS) from multiple vascular beds and compared it with CAC in predicting all-cause mortality. We hypothesized that this composite score will be significantly better than CAC in predicting mortality. Methods A total of 803 participants, ages 39–86, with complete data on diabetes and vascular imaging in the Diabetes Heart Study (DHS) were followed for an average of 7.4 years. Computed tomography (CT) scans were performed at baseline to obtain measures of carotid (CAAC), coronary (CAC) and abdominal aorta (AAC) Agatston scores. A principal component analysis using studentized residuals of log transformed (CAAC+1), (CAC+1), and (AAC+1) adjusting for age, race, and gender was performed. We selected the first principal component as the CAS. Seven-year risk estimates for mortality were obtained using logistic regression models. Model 1 included age, gender, smoking, systolic blood pressure, antihypertensive medication use, total and high-density lipoprotein cholesterol, and ethnicity and CAS. Model 2 included these risk factors plus CAC. We compared the estimation of mortality in Model 1 with CAS vs. Model 2 with CAC using chi-square values. Results Overall, 14% (116/803) of participants died during follow-up. CAS explained 70% of the variance, (eigenvalue of 2.1 with loading, CAAC, 0.57; CAC, 0.57; and AAC, 0.59). After adjusting for potential confounders, the odds ratio (95% CI) of all-cause mortality for 1-standard deviation (SD) increment was 2.12 (1.64–2.78) for CAS and 2.38 (1.77–3.35) for CAC. The area under the curve (chi-square value) with CAS or CAC to predict mortality was 0.76 (36) vs 0.76 (37) respectively. Conclusion Subclinical atherosclerosis, as measured by CT determined calcified plaque burden has increasing evidence supporting its role as a tool to stratify future risk for mortality. Here we demonstrated that the diagnostic accuracy between CAS and CAC are comparable and the predictive value of CAC alone for mortality is not further enhanced by inclusion of calcified plaque burden in carotid or abdominal aortic territories.

2018 ◽  
Vol 9 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Sameer Prasada ◽  
Cameron Oswalt ◽  
Phyllis Yeboah ◽  
Georgia Saylor ◽  
Donald Bowden ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Katharine A Kott ◽  
Marie-Christine Morel-Kopp ◽  
Stephen T Vernon ◽  
Yuki Takagi ◽  
Christopher Ward ◽  
...  

Introduction & Aim: Plaque micro-ruptures and associated thrombosis are a contributor to the progression of coronary artery disease (CAD). We sought to determine if disorders of haemostasis detectable by a global coagulation assay was a novel risk factor for CAD, or if hypercoagulation was associated with any of the traditional cardiac risk factors. Methods: Using the BioHEART biobank of clinical data, imaging data and pathology specimens, a cohort of patients (mean age 62.9 +/- 9.9 years, n=103 female, 103 male) had platelet poor plasma assessed by the overall haemostatic potential (OHP) assay. This assay measures the integrated effect of procoagulant, anticoagulant and fibrinolytic factors via calculation of area under a fibrin time curve. All patients had CT coronary angiograms scored; calcified plaque was identified by the coronary artery calcium score, and non-calcified plaque burden by a soft plaque score (SPS). Analysis was segregated by sex because of baseline differences in coagulation between males and females. Results: The OHP was found to be elevated in male patients who had non-calcified CAD [SPS>0 - 10.4 +/- 0.6 (n=62) vs SPS=0 - 8.78 +/- 0.5 (n=41), p=0.04], male patients with obesity [BMI >= 30 - 12.6 +/- 1.1 (n=26) vs BMI < 30 - 8.8 +/- 0.4 (n=77), p<0.01] and in female patients with hyperlipidaemia [hyperlipidaemic 11.8 +/- 0.6 (n=63) vs normolipidaemic 9.2 +/- 0.6 (n=40), p<0.01]. No differences were seen in OHP with calcified CAD, hypertension, diabetes mellitus, current or previous smoking history, or significant family history of CAD. Conclusions: These results indicate that hypercoagulation is associated with more biologically active non-calcified plaque, and that disordered coagulation is associated with two significant cardiac risk factors in a sex-discrepant manner. These findings underscore the importance of global coagulation assessments as potential novel, sex-specific biomarker for subclinical atherosclerosis.


Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Subhashish Agarwal ◽  
Amanda J Cox ◽  
David M Herrington ◽  
Neal Jorgensen ◽  
Jianzhao Xu ◽  
...  

Objective: Does coronary artery calcium (CAC) and C-reactive protein (CRP) improve discrimination and risk stratification of cardiovascular (CVD) and all-cause mortality in diabetes. Background: Inflammation is associated in the pathogenesis and progression of atherosclerosis. Since diabetes is characterized by both atherosclerosis and high CRP levels, we hypothesized that CAC and CRP will predict CVD and all-cause mortality in diabetes beyond Framingham risk factors (FRS). Method: A total of 961 participants, ages 39-86, with complete data on diabetes, vascular imaging, and inflammation in the Diabetes Heart Study were followed for an average of 7.4 years. CAC was assessed by CT at baseline. CRP was measured using enzyme-linked immunosorbent assay. Risk estimates for CVD and all-cause mortality were obtained using logistic regression models. Model 1 included FRS; age, gender, smoking, systolic blood pressure, antihypertensive medication use, total and HDL cholesterol, and ethnicity. Model 2 included FRS plus CRP or CAC. Model 3 included FRS plus CRP and CAC. Models for CVD and all-cause mortality were compared using c-statistics. Results: During follow-up there were 183 (19%) deaths of which 80 (8%) were CVD deaths. In FRS adjusted models both CRP and CAC were independently associated with all-cause mortality, however only CAC was associated with CVD mortality. The addition of CAC to a model with FRS and CRP improves discrimination for CVD and all-cause mortality (both p=0.001). However, the addition of CRP to a model with FRS and CAC only improves discrimination in all-cause mortality (p=0.001) ( Table 1 ). Conclusion: In participants with T2DM, measures of CAC and CRP are significantly associated with CVD (CAC only) and all-cause (CAC and CRP) mortality independent of the FRS; however, the improvement in CVD and all-cause mortality prediction was predominantly driven by CAC. Table 1 C-Statistics for the Combined Assessment of Framingham Risk Factors, CAC and CRP in Predicting Cardiovascular and All-Cause Mortality CVD Mortality All-Cause Mortality C-Statistic p-value C-Statistic p-value Model 1 FRS Only 0.715 -- 0.701 -- Model 2 vs. Model 1 Adding CRP to FRS Adding CAC to FRS 0.715 0.768 P=0.737 P=0.001 0.709 0.760 p=0.002 P=0.001 Model 3 vs. Model 2 Adding CAC to FRS + CRP Adding CRP to FRS + CAC 0.769 0.769 P=0.001 P=0.981 0.765 0.765 P=0.001 P=0.001


2018 ◽  
Vol 17 (1) ◽  
Author(s):  
Laura M. Raffield ◽  
Amanda J. Cox ◽  
Michael H. Criqui ◽  
Fang-Chi Hsu ◽  
James G. Terry ◽  
...  

Diabetes ◽  
2006 ◽  
Vol 55 (3) ◽  
pp. 651-658 ◽  
Author(s):  
K. P. Burdon ◽  
J. L. Bento ◽  
C. D. Langefeld ◽  
J. K. Campbell ◽  
J. J. Carr ◽  
...  

2021 ◽  
Vol 77 (18) ◽  
pp. 1452
Author(s):  
Parag Anilkumar Chevli ◽  
Nicholette Allred ◽  
Fang-Chi Hsu ◽  
John Parks ◽  
Barry Freedman ◽  
...  

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Kathryn P. Burdon ◽  
Megan E. Rudock ◽  
Allison B. Lehtinen ◽  
Carl D. Langefeld ◽  
Donald W. Bowden ◽  
...  

Aims. Genes of the 5-lipoxygenase pathway are compelling candidates for atherosclerosis. We hypothesize that polymorphisms inALOX12, ALOX15, ALOX5, andALOX5APgenes are associated with subclinical atherosclerosis in multiple vascular beds.Methods. Families with two or more siblings with type 2 diabetes and their nondiabetic siblings were studied as part of the Diabetes Heart Study (DHS). European American diabetic (n=828) and nondiabetic (n=170) siblings were genotyped for SNPs in theALOX12, ALOX15, ALOX5, andALOX5APgenes. Subclinical measures of atherosclerosis (IMT, coronary (CorCP), carotid (CarCP) and aortic (AorCP) calcified plaque) were obtained.Results. Associations were observed betweenALOX12with CorCP,ALOX5with CorCP, AorCP, and IMT, andALOX5APwith CorCP and CarCP, independent of known epidemiologic risk factors. Further, lipoxygenase pathway SNPs that were associated with measures of atherosclerosis were associated with markers of inflammation (CRP, ICAM-1) and calcification (MGP).Conclusions. Polymorphisms withinALOX12, ALOX5, andALOX5APare genetically associated with subclinical atherosclerosis and with biomarkers of disease in families with type 2 diabetes. These results suggest that variants in lipoxygenase pathway genes may have pleiotropic effects on multiple components that determine risk of cardiovascular disease.


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