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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| Published in: | Circulation (New York, N.Y.) Vol. 139; no. 23; p. 2642 |
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| Main Authors: | , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
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. |
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| 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 |
| Author_xml | – sequence: 1 givenname: Xiaoming surname: Jia fullname: Jia, Xiaoming organization: Baylor College of Medicine, Houston, TX (X.J., W.S., R.C.H., V.N., C.M.B.) – sequence: 2 givenname: Wensheng surname: Sun fullname: Sun, Wensheng organization: Baylor College of Medicine, Houston, TX (X.J., W.S., R.C.H., V.N., C.M.B.) – sequence: 3 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.) – sequence: 4 givenname: Vijay surname: Nambi fullname: Nambi, Vijay organization: Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX (V.N.) – sequence: 5 givenname: Kunihiro surname: Matsushita fullname: Matsushita, Kunihiro organization: Johns Hopkins University, Baltimore, MD (K.M., E.S.) – sequence: 6 givenname: Aaron R surname: Folsom fullname: Folsom, Aaron R organization: University of Minnesota, Minneapolis (A.R.F.) – sequence: 7 givenname: Gerardo surname: Heiss fullname: Heiss, Gerardo organization: University of North Carolina at Chapel Hill (G.H., D.J.C.) – sequence: 8 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.) – sequence: 10 givenname: Eric surname: Boerwinkle fullname: Boerwinkle, Eric organization: University of Texas Health Science Center at Houston (E.B.) – sequence: 11 givenname: Amil surname: Shah fullname: Shah, Amil organization: Brigham and Women's Hospital, Boston, MA (S.D.S., A.S.) – sequence: 12 givenname: Elizabeth surname: Selvin fullname: Selvin, Elizabeth organization: Johns Hopkins University, Baltimore, MD (K.M., E.S.) – sequence: 13 givenname: James A surname: de Lemos fullname: de Lemos, James A organization: University of Texas-Southwestern Medical Center, Dallas (J.A.d.L.) – sequence: 14 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.) |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31030544$$D View this record in MEDLINE/PubMed |
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| Keywords | biomarkers troponin I cardiovascular diseases |
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| PublicationTitle | Circulation (New York, N.Y.) |
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| 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. |
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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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