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      Soluble Urokinase‐Type Plasminogen Activator Receptor and High‐Sensitivity Troponin Levels Predict Outcomes in Nonobstructive Coronary Artery Disease

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          Abstract

          Background

          Multiple biomarkers have been independently and additively associated with major adverse cardiovascular events in patients with coronary artery disease. We investigated the prognostic value of suPAR (soluble urokinase‐type plasminogen activator receptor) and hsTnI (high‐sensitivity troponin I) levels in symptomatic patients with no obstructive coronary artery disease. We hypothesized that high levels of these biomarkers will be associated with the risk of future adverse outcomes.

          Methods and Results

          Plasma levels of suPAR and hsTnI were measured in 556 symptomatic patients with no obstructive coronary artery disease. A biomarker risk score was calculated by counting the number of biomarkers above the median in this cohort (suPAR>2523 pg/mL and hsTnI>2.7 pg/mL). Survival analyses were performed with models adjusted for traditional risk factors. All‐cause death and major adverse cardiovascular events (cardiovascular death, myocardial infarction, stroke, and heart failure) served as clinical outcomes over a median follow‐up of 6.2 years. Mean age was 57±10 years, 49% of the cohort patients were female, and 68% had a positive stress test. High suPAR and hsTnI levels were independent predictors of all‐cause death (hazard ratio=3.2 [95% CI, 1.8–5.7] and 1.3 [95% CI, 1.0–1.7], respectively; both P<0.04) and major adverse cardiovascular events (hazard ratio=2.7 [95% CI, 1.4–5.4] and 1.5 [95% CI, 1.2–2.0], respectively; both P<0.002). Compared with a biomarker risk score of 0, biomarker risk scores of 1 and 2 were associated with 19‐ and 14‐fold increased risk of death and development of major adverse cardiovascular events, respectively.

          Conclusions

          Among symptomatic patients with no obstructive coronary artery disease, higher levels of suPAR and hsTnI were independently and additively associated with an increased risk of adverse events. Whether modification of these biomarkers will improve risk in these patients needs further investigation.

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          Most cited references 40

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          Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women.

          C-reactive protein (CRP) predicts risk of myocardial infarction (MI) and stroke among apparently healthy men, but in women, virtually no data are available. CRP was measured in baseline blood samples from 122 apparently healthy participants in the Women's Health Study who subsequently suffered a first cardiovascular event and from 244 age- and smoking-matched control subjects who remained free of cardiovascular disease during a 3-year follow-up period. Women who developed cardiovascular events had higher baseline CRP levels than control subjects (P=0.0001), such that those with the highest levels at baseline had a 5-fold increase in risk of any vascular event (RR=4.8; 95% CI, 2.3 to 10.1; P=0.0001) and a 7-fold increase in risk of MI or stroke (RR=7.3; 95% CI, 2.7 to 19.9; P=0.0001). Risk estimates were independent of other risk factors, and prediction models that included CRP provided a better method to predict risk than models that excluded CRP (all P values <0.01). In stratified analyses, CRP was a predictor among subgroups of women with low as well as high risk as defined by other cardiovascular risk factors. In these prospective data among women, CRP is a strong independent risk factor for cardiovascular disease that adds to the predictive value of risk models based on usual factors alone. (Circulation. 1998;98:731-733.)
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            Insights from the NHLBI-Sponsored Women's Ischemia Syndrome Evaluation (WISE) Study: Part II: gender differences in presentation, diagnosis, and outcome with regard to gender-based pathophysiology of atherosclerosis and macrovascular and microvascular coronary disease.

            Coronary heart disease is the leading cause of death and disability in the U.S., but recent advances have not led to declines in case fatality rates for women. The current review highlights gender-specific issues in ischemic heart disease (IHD) presentation, evaluation, and outcomes with a special focus on the results derived from the National Institutes of Health-National Heart, Lung, and Blood Institute-sponsored Women's Ischemia Syndrome Evaluation (WISE) study. In the second part of this review, we will assess new evidence on gender-based differences in vascular wall or metabolic alterations, atherosclerotic plaque deposition, and functional expression on worsening outcomes of women. Additionally, innovative cardiovascular imaging techniques will be discussed. Finally, we identify critical areas of further inquiry needed to advance this new gender-specific IHD understanding into improved outcomes for women.
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              Stable angina pectoris with no obstructive coronary artery disease is associated with increased risks of major adverse cardiovascular events.

              Patients with chest pain and no obstructive coronary artery disease (CAD) are considered at low risk for cardiovascular events but evidence supporting this is scarce. We investigated the prognostic implications of stable angina pectoris in relation to the presence and degree of CAD with no obstructive CAD in focus. We identified 11 223 patients referred for coronary angiography (CAG) in 1998-2009 with stable angina pectoris as indication and 5705 participants from the Copenhagen City Heart Study for comparison. Main outcome measures were major adverse cardiovascular events (MACE), defined as cardiovascular death, myocardial infarction, stroke or heart failure, and all-cause mortality. Significantly more women (65%) than men (32%) had no obstructive CAD (P< 0.001). In Cox's models adjusted for age, body mass index, diabetes, smoking, and use of lipid-lowering or antihypertensive medication, hazard ratios (HRs) associated with no obstructive CAD were similar in men and women. In the pooled analysis, the risk of MACE increased with increasing degrees of CAD with multivariable-adjusted HRs of 1.52 (95% confidence interval, 1.27-1.83) for patients with normal coronary arteries and 1.85 (1.51-2.28) for patients with diffuse non-obstructive CAD compared with the reference population. For all-cause mortality, normal coronary arteries and diffuse non-obstructive CAD were associated with HRs of 1.29 (1.07-1.56) and 1.52 (1.24-1.88), respectively. Patients with stable angina and normal coronary arteries or diffuse non-obstructive CAD have elevated risks of MACE and all-cause mortality compared with a reference population without ischaemic heart disease.
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                Author and article information

                Contributors
                aquyyum@emory.edu
                Journal
                J Am Heart Assoc
                J Am Heart Assoc
                10.1002/(ISSN)2047-9980
                JAH3
                ahaoa
                Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
                John Wiley and Sons Inc. (Hoboken )
                2047-9980
                17 April 2020
                21 April 2020
                : 9
                : 8 ( doiID: 10.1002/jah3.v9.8 )
                Affiliations
                [ 1 ] Division of Cardiology Department of Medicine Emory University School of Medicine Atlanta GA
                [ 2 ] Departments of Biostatistics and Bioinformatics Emory University School of Medicine Atlanta GA
                [ 3 ] Department of Epidemiology and Rollins School of Public Health Emory University Atlanta GA
                [ 4 ] Diagnostics Division Abbott Laboratories North Chicago IL
                Author notes
                [* ]Correspondence to: Arshed A. Quyyumi, MD, FACC Professor of Medicine, Division of Cardiology, Department of Medicine, Emory University School of Medicine, 1462 Clifton Rd NE, Suite 507, Atlanta, GA 30322. E‐mail: aquyyum@ 123456emory.edu
                Article
                JAH34995
                10.1161/JAHA.119.015515
                7428519
                32301366
                © 2020 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

                Page count
                Figures: 5, Tables: 3, Pages: 11, Words: 7260
                Product
                Funding
                Funded by: American Heart Association Postdoctoral Fellowship Award Grant
                Award ID: 18POST34080330
                Funded by: Abraham J. & Phyllis Katz Foundation
                Funded by: National Institute on Aging , open-funder-registry 10.13039/100000049;
                Award ID: AG051633
                Funded by: National Institutes of Health , open-funder-registry 10.13039/100000002;
                Award ID: 5P01HL101398‐02
                Award ID: 1P20HL113451‐01
                Award ID: 1R56HL126558‐01
                Award ID: 1RF1AG051633‐01
                Award ID: R01 NS064162‐01
                Award ID: R01 HL89650‐01
                Award ID: HL095479‐01
                Award ID: 1U10HL110302‐01
                Award ID: 1DP3DK094346‐01
                Award ID: 2P01HL086773‐06A1
                Funded by: Abbott Labs and Cardiorisk
                Categories
                Original Research
                Original Research
                Coronary Heart Disease
                Custom metadata
                2.0
                21 April 2020
                Converter:WILEY_ML3GV2_TO_JATSPMC version:5.8.5 mode:remove_FC converted:06.07.2020

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