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      High-Sensitivity Cardiac Troponin Concentration and Risk of First-Ever Cardiovascular Outcomes in 154,052 Participants

      research-article
      , MD, MPhil, PhD a , b , , , PhD c , , MBChB b , d , , Dipl-Ing, BSc a , , BSc c , , MD, PhD e , , PhD f , , PhD g , , MD c , , MD, PhD h , , MD, PhD g , , MD a , , MD, MSc, PhD b , i , j , k , , MD, PhD c
      Journal of the American College of Cardiology
      Elsevier Biomedical
      biomarker, cardiovascular disease, coronary heart disease, primary prevention, stroke, systematic review, CHD, coronary heart disease, CI, confidence interval, CRP, C-reactive protein, CVD, cardiovascular disease, eGFR, estimated glomerular filtration rate, HDL-C, high-density lipoprotein cholesterol, HR, hazard ratio, hs-cTnI, high-sensitivity cardiac troponin I, hs-cTnT, high-sensitivity cardiac troponin T, MI, myocardial infarction, NRI, net reclassification index, NT-proBNP, N-terminal pro–B-type natriuretic peptide, RR, relative risk

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          Abstract

          Background

          High-sensitivity assays can quantify cardiac troponins I and T (hs-cTnI, hs-cTnT) in individuals with no clinically manifest myocardial injury.

          Objectives

          The goal of this study was to assess associations of cardiac troponin concentration with cardiovascular disease (CVD) outcomes in primary prevention studies.

          Methods

          A search was conducted of PubMed, Web of Science, and EMBASE for prospective studies published up to September 2016, reporting on associations of cardiac troponin concentration with first-ever CVD outcomes (i.e., coronary heart disease [CHD], stroke, or the combination of both). Study-specific estimates, adjusted for conventional risk factors, were extracted by 2 independent reviewers, supplemented with de novo data from PROSPER (Pravastatin in Elderly Individuals at Risk of Vascular Disease Study), then pooled by using random effects meta-analysis.

          Results

          A total of 28 relevant studies were identified involving 154,052 participants. Cardiac troponin was detectable in 80.0% (hs-cTnI: 82.6%; hs-cTnT: 69.7%). In PROSPER, positive associations of log-linear shape were observed between hs-cTnT and CVD outcomes. In the meta-analysis, the relative risks comparing the top versus the bottom troponin third were 1.43 (95% confidence interval [CI]: 1.31 to 1.56) for CVD (11,763 events), 1.67 (95% CI: 1.50 to 1.86) for fatal CVD (7,775 events), 1.59 (95% CI: 1.38 to 1.83) for CHD (7,061 events), and 1.35 (95% CI: 1.23 to 1.48) for stroke (2,526 events). For fatal CVD, associations were stronger in North American studies (p = 0.010) and those measuring hs-cTnT rather than hs-cTnI (p = 0.027).

          Conclusions

          In the general population, high cardiac troponin concentration within the normal range is associated with increased CVD risk. This association is independent of conventional risk factors, strongest for fatal CVD, and applies to both CHD and stroke.

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          Most cited references37

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          Pravastatin in elderly individuals at risk of vascular disease (PROSPER): a randomised controlled trial.

          Although statins reduce coronary and cerebrovascular morbidity and mortality in middle-aged individuals, their efficacy and safety in elderly people is not fully established. Our aim was to test the benefits of pravastatin treatment in an elderly cohort of men and women with, or at high risk of developing, cardiovascular disease and stroke. We did a randomised controlled trial in which we assigned 5804 men (n=2804) and women (n=3000) aged 70-82 years with a history of, or risk factors for, vascular disease to pravastatin (40 mg per day; n=2891) or placebo (n=2913). Baseline cholesterol concentrations ranged from 4.0 mmol/L to 9.0 mmol/L. Follow-up was 3.2 years on average and our primary endpoint was a composite of coronary death, non-fatal myocardial infarction, and fatal or non-fatal stroke. Analysis was by intention-to-treat. Pravastatin lowered LDL cholesterol concentrations by 34% and reduced the incidence of the primary endpoint to 408 events compared with 473 on placebo (hazard ratio 0.85, 95% CI 0.74-0.97, p=0.014). Coronary heart disease death and non-fatal myocardial infarction risk was also reduced (0.81, 0.69-0.94, p=0.006). Stroke risk was unaffected (1.03, 0.81-1.31, p=0.8), but the hazard ratio for transient ischaemic attack was 0.75 (0.55-1.00, p=0.051). New cancer diagnoses were more frequent on pravastatin than on placebo (1.25, 1.04-1.51, p=0.020). However, incorporation of this finding in a meta-analysis of all pravastatin and all statin trials showed no overall increase in risk. Mortality from coronary disease fell by 24% (p=0.043) in the pravastatin group. Pravastatin had no significant effect on cognitive function or disability. Pravastatin given for 3 years reduced the risk of coronary disease in elderly individuals. PROSPER therefore extends to elderly individuals the treatment strategy currently used in middle aged people.
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            Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease: meta-analyses of prospective studies.

            A large number of epidemiologic studies have reported on associations between various "inflammatory" factors and coronary heart disease (CHD). To assess the associations of blood levels of fibrinogen, C-reactive protein (CRP), and albumin and leukocyte count with the subsequent risk of CHD. Meta-analyses of any long-term prospective studies of CHD published before 1998 on any of these 4 factors. Studies were identified by MEDLINE searches, scanning of relevant reference lists, hand searching of cardiology, epidemiology, and other relevant journals, and discussions with authors of relevant reports. All relevant studies identified were included. The following information was abstracted from published reports (supplemented, in several cases, by the authors): size and type of cohort, mean age, mean duration of follow-up, assay methods, degree of adjustment for confounders, and relationship of CHD risk to the baseline assay results. For fibrinogen, with 4018 CHD cases in 18 studies, comparison of individuals in the top third with those in the bottom third of the baseline measurements yielded a combined risk ratio of 1.8 (95% confidence interval [CI], 1.6-2.0) associated with a difference in long-term usual mean fibrinogen levels of 2.9 pmol/L (0.1 g/dL) between the top and bottom thirds (10.3 vs 7.4 pmol/L [0.35 vs 0.25 g/dL]). For CRP, with 1053 CHD cases in 7 studies, the combined risk ratio of 1.7 (95% CI, 1.4-2.1) was associated with a difference of 1.4 mg/L (2.4 vs 1.0 mg/L). For albumin, with 3770 CHD cases in 8 studies, the combined risk ratio of 1.5 (95% CI, 1.3-1.7) was associated with a difference of 4 g/L (38 vs 42 g/L, ie, an inverse association). For leukocyte count, with 5337 CHD cases in the 7 largest studies, the combined risk ratio of 1.4 (95% CI, 1.3-1.5) was associated with a difference of 2.8 x 10(9)/L (8.4 vs 5.6 x 10(9)/L). Each of these overall results was highly significant (P<.0001). The published results from these prospective studies are remarkably consistent for each factor, indicating moderate but highly statistically significant associations with CHD. Hence, even though mechanisms that might account for these associations are not clear, further study of the relevance of these factors to the causation of CHD is warranted.
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              Troponin I and cardiovascular risk prediction in the general population: the BiomarCaRE consortium

              Aims Our aims were to evaluate the distribution of troponin I concentrations in population cohorts across Europe, to characterize the association with cardiovascular outcomes, to determine the predictive value beyond the variables used in the ESC SCORE, to test a potentially clinically relevant cut-off value, and to evaluate the improved eligibility for statin therapy based on elevated troponin I concentrations retrospectively. Methods and results Based on the Biomarkers for Cardiovascular Risk Assessment in Europe (BiomarCaRE) project, we analysed individual level data from 10 prospective population-based studies including 74 738 participants. We investigated the value of adding troponin I levels to conventional risk factors for prediction of cardiovascular disease by calculating measures of discrimination (C-index) and net reclassification improvement (NRI). We further tested the clinical implication of statin therapy based on troponin concentration in 12 956 individuals free of cardiovascular disease in the JUPITER study. Troponin I remained an independent predictor with a hazard ratio of 1.37 for cardiovascular mortality, 1.23 for cardiovascular disease, and 1.24 for total mortality. The addition of troponin I information to a prognostic model for cardiovascular death constructed of ESC SCORE variables increased the C-index discrimination measure by 0.007 and yielded an NRI of 0.048, whereas the addition to prognostic models for cardiovascular disease and total mortality led to lesser C-index discrimination and NRI increment. In individuals above 6 ng/L of troponin I, a concentration near the upper quintile in BiomarCaRE (5.9 ng/L) and JUPITER (5.8 ng/L), rosuvastatin therapy resulted in higher absolute risk reduction compared with individuals <6 ng/L of troponin I, whereas the relative risk reduction was similar. Conclusion In individuals free of cardiovascular disease, the addition of troponin I to variables of established risk score improves prediction of cardiovascular death and cardiovascular disease.
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                Author and article information

                Contributors
                Journal
                J Am Coll Cardiol
                J. Am. Coll. Cardiol
                Journal of the American College of Cardiology
                Elsevier Biomedical
                0735-1097
                1558-3597
                01 August 2017
                01 August 2017
                : 70
                : 5
                : 558-568
                Affiliations
                [a ]Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria
                [b ]Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom
                [c ]Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom
                [d ]Transplant Unit, Papworth Hospital NHS Foundation Trust, Papworth Everard, Cambridge, United Kingdom
                [e ]Department of Cardiology, Leiden University Medical Center, Leiden, the Netherlands
                [f ]Robertson Centre for Biostatistics, University of Glasgow, Glasgow, United Kingdom
                [g ]Department of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, the Netherlands
                [h ]Department of Epidemiology and Public Health, University College Cork, Cork, Ireland
                [i ]National Institute for Health Research Blood and Transplant Research Unit in Donor Health and Genomics, University of Cambridge, Cambridge, United Kingdom
                [j ]NHS Blood and Transplant, Cambridge, United Kingdom
                [k ]British Heart Foundation Cambridge Centre of Excellence, University of Cambridge, Cambridge, United Kingdom
                Author notes
                [] Address for correspondence: Dr. Peter Willeit, Department of Neurology, Medical University of Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria.Department of Neurology, Medical University of InnsbruckAnichstrasse 356020 InnsbruckAustria peter.willeit@ 123456i-med.ac.at
                Article
                S0735-1097(17)37687-8
                10.1016/j.jacc.2017.05.062
                5527070
                28750699
                b722ffd8-44a0-4c39-b8cf-1c3dc3b61c5d
                © 2017 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 6 April 2017
                : 30 May 2017
                : 30 May 2017
                Categories
                Original Investigation

                Cardiovascular Medicine
                biomarker,cardiovascular disease,coronary heart disease,primary prevention,stroke,systematic review,chd, coronary heart disease,ci, confidence interval,crp, c-reactive protein,cvd, cardiovascular disease,egfr, estimated glomerular filtration rate,hdl-c, high-density lipoprotein cholesterol,hr, hazard ratio,hs-ctni, high-sensitivity cardiac troponin i,hs-ctnt, high-sensitivity cardiac troponin t,mi, myocardial infarction,nri, net reclassification index,nt-probnp, n-terminal pro–b-type natriuretic peptide,rr, relative risk

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