High-Sensitivity Troponin I and Incident Coronary Events, Stroke, Heart Failure Hospitalization, and Mortality in the ARIC Study

We assessed whether plasma troponin I measured by a high-sensitivity assay (hs-TnI) is associated with incident cardiovascular disease (CVD) and mortality in a community-based sample without prior CVD. ARIC study (Atherosclerosis Risk in Communities) participants aged 54 to 74 years without baseline...

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Veröffentlicht in:Circulation (New York, N.Y.) Jg. 139; H. 23; S. 2642
Hauptverfasser: Jia, Xiaoming, Sun, Wensheng, Hoogeveen, Ron C, Nambi, Vijay, Matsushita, Kunihiro, Folsom, Aaron R, Heiss, Gerardo, Couper, David J, Solomon, Scott D, Boerwinkle, Eric, Shah, Amil, Selvin, Elizabeth, de Lemos, James A, Ballantyne, Christie M
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 04.06.2019
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ISSN:1524-4539, 1524-4539
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Abstract We assessed whether plasma troponin I measured by a high-sensitivity assay (hs-TnI) is associated with incident cardiovascular disease (CVD) and mortality in a community-based sample without prior CVD. ARIC study (Atherosclerosis Risk in Communities) participants aged 54 to 74 years without baseline CVD were included in this study (n=8121). Cox proportional hazards models were constructed to determine associations between hs-TnI and incident coronary heart disease (CHD; myocardial infarction and fatal CHD), ischemic stroke, atherosclerotic CVD (CHD and stroke), heart failure hospitalization, global CVD (atherosclerotic CVD and heart failure), and all-cause mortality. The comparative association of hs-TnI and high-sensitivity troponin T with incident CVD events was also evaluated. Risk prediction models were constructed to assess prediction improvement when hs-TnI was added to traditional risk factors used in the Pooled Cohort Equation. The median follow-up period was ≈15 years. Detectable hs-TnI levels were observed in 85% of the study population. In adjusted models, in comparison to low hs-TnI (lowest quintile, hs-TnI ≤1.3 ng/L), elevated hs-TnI (highest quintile, hs-TnI ≥3.8 ng/L) was associated with greater incident CHD (hazard ratio [HR], 2.20; 95% CI, 1.64-2.95), ischemic stroke (HR, 2.99; 95% CI, 2.01-4.46), atherosclerotic CVD (HR, 2.36; 95% CI, 1.86-3.00), heart failure hospitalization (HR, 4.20; 95% CI, 3.28-5.37), global CVD (HR, 3.01; 95% CI, 2.50-3.63), and all-cause mortality (HR, 1.83; 95% CI, 1.56-2.14). hs-TnI was observed to have a stronger association with incident global CVD events in white than in black individuals and a stronger association with incident CHD in women than in men. hs-TnI and high-sensitivity troponin T were only modestly correlated ( r=0.47) and were complementary in prediction of incident CVD events, with elevation of both troponins conferring the highest risk in comparison with elevation in either one alone. The addition of hs-TnI to the Pooled Cohort Equation model improved risk prediction for atherosclerotic CVD, heart failure, and global CVD. Elevated hs-TnI is strongly associated with increased global CVD incidence in the general population independent of traditional risk factors. hs-TnI and high-sensitivity troponin T provide complementary rather than redundant information.
AbstractList We assessed whether plasma troponin I measured by a high-sensitivity assay (hs-TnI) is associated with incident cardiovascular disease (CVD) and mortality in a community-based sample without prior CVD. ARIC study (Atherosclerosis Risk in Communities) participants aged 54 to 74 years without baseline CVD were included in this study (n=8121). Cox proportional hazards models were constructed to determine associations between hs-TnI and incident coronary heart disease (CHD; myocardial infarction and fatal CHD), ischemic stroke, atherosclerotic CVD (CHD and stroke), heart failure hospitalization, global CVD (atherosclerotic CVD and heart failure), and all-cause mortality. The comparative association of hs-TnI and high-sensitivity troponin T with incident CVD events was also evaluated. Risk prediction models were constructed to assess prediction improvement when hs-TnI was added to traditional risk factors used in the Pooled Cohort Equation. The median follow-up period was ≈15 years. Detectable hs-TnI levels were observed in 85% of the study population. In adjusted models, in comparison to low hs-TnI (lowest quintile, hs-TnI ≤1.3 ng/L), elevated hs-TnI (highest quintile, hs-TnI ≥3.8 ng/L) was associated with greater incident CHD (hazard ratio [HR], 2.20; 95% CI, 1.64-2.95), ischemic stroke (HR, 2.99; 95% CI, 2.01-4.46), atherosclerotic CVD (HR, 2.36; 95% CI, 1.86-3.00), heart failure hospitalization (HR, 4.20; 95% CI, 3.28-5.37), global CVD (HR, 3.01; 95% CI, 2.50-3.63), and all-cause mortality (HR, 1.83; 95% CI, 1.56-2.14). hs-TnI was observed to have a stronger association with incident global CVD events in white than in black individuals and a stronger association with incident CHD in women than in men. hs-TnI and high-sensitivity troponin T were only modestly correlated ( r=0.47) and were complementary in prediction of incident CVD events, with elevation of both troponins conferring the highest risk in comparison with elevation in either one alone. The addition of hs-TnI to the Pooled Cohort Equation model improved risk prediction for atherosclerotic CVD, heart failure, and global CVD. Elevated hs-TnI is strongly associated with increased global CVD incidence in the general population independent of traditional risk factors. hs-TnI and high-sensitivity troponin T provide complementary rather than redundant information.
We assessed whether plasma troponin I measured by a high-sensitivity assay (hs-TnI) is associated with incident cardiovascular disease (CVD) and mortality in a community-based sample without prior CVD.BACKGROUNDWe assessed whether plasma troponin I measured by a high-sensitivity assay (hs-TnI) is associated with incident cardiovascular disease (CVD) and mortality in a community-based sample without prior CVD.ARIC study (Atherosclerosis Risk in Communities) participants aged 54 to 74 years without baseline CVD were included in this study (n=8121). Cox proportional hazards models were constructed to determine associations between hs-TnI and incident coronary heart disease (CHD; myocardial infarction and fatal CHD), ischemic stroke, atherosclerotic CVD (CHD and stroke), heart failure hospitalization, global CVD (atherosclerotic CVD and heart failure), and all-cause mortality. The comparative association of hs-TnI and high-sensitivity troponin T with incident CVD events was also evaluated. Risk prediction models were constructed to assess prediction improvement when hs-TnI was added to traditional risk factors used in the Pooled Cohort Equation.METHODSARIC study (Atherosclerosis Risk in Communities) participants aged 54 to 74 years without baseline CVD were included in this study (n=8121). Cox proportional hazards models were constructed to determine associations between hs-TnI and incident coronary heart disease (CHD; myocardial infarction and fatal CHD), ischemic stroke, atherosclerotic CVD (CHD and stroke), heart failure hospitalization, global CVD (atherosclerotic CVD and heart failure), and all-cause mortality. The comparative association of hs-TnI and high-sensitivity troponin T with incident CVD events was also evaluated. Risk prediction models were constructed to assess prediction improvement when hs-TnI was added to traditional risk factors used in the Pooled Cohort Equation.The median follow-up period was ≈15 years. Detectable hs-TnI levels were observed in 85% of the study population. In adjusted models, in comparison to low hs-TnI (lowest quintile, hs-TnI ≤1.3 ng/L), elevated hs-TnI (highest quintile, hs-TnI ≥3.8 ng/L) was associated with greater incident CHD (hazard ratio [HR], 2.20; 95% CI, 1.64-2.95), ischemic stroke (HR, 2.99; 95% CI, 2.01-4.46), atherosclerotic CVD (HR, 2.36; 95% CI, 1.86-3.00), heart failure hospitalization (HR, 4.20; 95% CI, 3.28-5.37), global CVD (HR, 3.01; 95% CI, 2.50-3.63), and all-cause mortality (HR, 1.83; 95% CI, 1.56-2.14). hs-TnI was observed to have a stronger association with incident global CVD events in white than in black individuals and a stronger association with incident CHD in women than in men. hs-TnI and high-sensitivity troponin T were only modestly correlated ( r=0.47) and were complementary in prediction of incident CVD events, with elevation of both troponins conferring the highest risk in comparison with elevation in either one alone. The addition of hs-TnI to the Pooled Cohort Equation model improved risk prediction for atherosclerotic CVD, heart failure, and global CVD.RESULTSThe median follow-up period was ≈15 years. Detectable hs-TnI levels were observed in 85% of the study population. In adjusted models, in comparison to low hs-TnI (lowest quintile, hs-TnI ≤1.3 ng/L), elevated hs-TnI (highest quintile, hs-TnI ≥3.8 ng/L) was associated with greater incident CHD (hazard ratio [HR], 2.20; 95% CI, 1.64-2.95), ischemic stroke (HR, 2.99; 95% CI, 2.01-4.46), atherosclerotic CVD (HR, 2.36; 95% CI, 1.86-3.00), heart failure hospitalization (HR, 4.20; 95% CI, 3.28-5.37), global CVD (HR, 3.01; 95% CI, 2.50-3.63), and all-cause mortality (HR, 1.83; 95% CI, 1.56-2.14). hs-TnI was observed to have a stronger association with incident global CVD events in white than in black individuals and a stronger association with incident CHD in women than in men. hs-TnI and high-sensitivity troponin T were only modestly correlated ( r=0.47) and were complementary in prediction of incident CVD events, with elevation of both troponins conferring the highest risk in comparison with elevation in either one alone. The addition of hs-TnI to the Pooled Cohort Equation model improved risk prediction for atherosclerotic CVD, heart failure, and global CVD.Elevated hs-TnI is strongly associated with increased global CVD incidence in the general population independent of traditional risk factors. hs-TnI and high-sensitivity troponin T provide complementary rather than redundant information.CONCLUSIONSElevated hs-TnI is strongly associated with increased global CVD incidence in the general population independent of traditional risk factors. hs-TnI and high-sensitivity troponin T provide complementary rather than redundant information.
Author Selvin, Elizabeth
Hoogeveen, Ron C
Heiss, Gerardo
Folsom, Aaron R
de Lemos, James A
Nambi, Vijay
Couper, David J
Shah, Amil
Boerwinkle, Eric
Ballantyne, Christie M
Jia, Xiaoming
Solomon, Scott D
Sun, Wensheng
Matsushita, Kunihiro
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  organization: Baylor College of Medicine, Houston, TX (X.J., W.S., R.C.H., V.N., C.M.B.)
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  givenname: Ron C
  surname: Hoogeveen
  fullname: Hoogeveen, Ron C
  organization: Baylor College of Medicine, Houston, TX (X.J., W.S., R.C.H., V.N., C.M.B.)
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  fullname: Matsushita, Kunihiro
  organization: Johns Hopkins University, Baltimore, MD (K.M., E.S.)
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  surname: Folsom
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  organization: University of Minnesota, Minneapolis (A.R.F.)
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  organization: University of North Carolina at Chapel Hill (G.H., D.J.C.)
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  givenname: David J
  surname: Couper
  fullname: Couper, David J
  organization: University of North Carolina at Chapel Hill (G.H., D.J.C.)
– sequence: 9
  givenname: Scott D
  surname: Solomon
  fullname: Solomon, Scott D
  organization: Brigham and Women's Hospital, Boston, MA (S.D.S., A.S.)
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  surname: Boerwinkle
  fullname: Boerwinkle, Eric
  organization: University of Texas Health Science Center at Houston (E.B.)
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  organization: Brigham and Women's Hospital, Boston, MA (S.D.S., A.S.)
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  surname: Selvin
  fullname: Selvin, Elizabeth
  organization: Johns Hopkins University, Baltimore, MD (K.M., E.S.)
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  surname: de Lemos
  fullname: de Lemos, James A
  organization: University of Texas-Southwestern Medical Center, Dallas (J.A.d.L.)
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  givenname: Christie M
  surname: Ballantyne
  fullname: Ballantyne, Christie M
  organization: Baylor College of Medicine, Houston, TX (X.J., W.S., R.C.H., V.N., C.M.B.)
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troponin I
cardiovascular diseases
Language English
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PublicationTitle Circulation (New York, N.Y.)
PublicationTitleAlternate Circulation
PublicationYear 2019
References 31710524 - Circulation. 2019 Nov 12;140(20):e770-e771. doi: 10.1161/CIRCULATIONAHA.119.042124.
31092916 - Nat Rev Cardiol. 2019 Jul;16(7):386. doi: 10.1038/s41569-019-0212-3.
31710526 - Circulation. 2019 Nov 12;140(20):e772-e773. doi: 10.1161/CIRCULATIONAHA.119.043149.
References_xml – reference: 31092916 - Nat Rev Cardiol. 2019 Jul;16(7):386. doi: 10.1038/s41569-019-0212-3.
– reference: 31710526 - Circulation. 2019 Nov 12;140(20):e772-e773. doi: 10.1161/CIRCULATIONAHA.119.043149.
– reference: 31710524 - Circulation. 2019 Nov 12;140(20):e770-e771. doi: 10.1161/CIRCULATIONAHA.119.042124.
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Snippet We assessed whether plasma troponin I measured by a high-sensitivity assay (hs-TnI) is associated with incident cardiovascular disease (CVD) and mortality in a...
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SubjectTerms Aged
Biomarkers - blood
Cause of Death
Coronary Disease - blood
Coronary Disease - diagnosis
Coronary Disease - mortality
Coronary Disease - therapy
Female
Heart Failure - blood
Heart Failure - diagnosis
Heart Failure - mortality
Heart Failure - therapy
Hospitalization
Humans
Incidence
Male
Middle Aged
Predictive Value of Tests
Prognosis
Prospective Studies
Risk Assessment
Risk Factors
Stroke - blood
Stroke - diagnosis
Stroke - mortality
Stroke - therapy
Time Factors
Troponin I - blood
Troponin T - blood
United States - epidemiology
Up-Regulation
Title High-Sensitivity Troponin I and Incident Coronary Events, Stroke, Heart Failure Hospitalization, and Mortality in the ARIC Study
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