Association of contemporary sensitive troponin i levels at baseline and change at 1 year with long-term coronary events following myocardial infarction or unstable angina: Results from the LIPID study (Long-Term Intervention with Pravastatin in Ischaemic Disease)

TY - JOUR

T1 - Association of contemporary sensitive troponin i levels at baseline and change at 1 year with long-term coronary events following myocardial infarction or unstable angina: Results from the LIPID study (Long-Term Intervention with Pravastatin in Ischaemic Disease)

AU - White, Harvey D.

AU - Tonkin, Andrew

AU - Simes, John

AU - Stewart, Ralph

AU - Mann, Kristy

AU - Thompson, Peter

AU - Colquhoun, David

AU - West, Malcolm

AU - Nestel, Paul

AU - Sullivan, David

AU - Keech, Anthony C.

AU - Hunt, David

AU - Blankenberg, Stefan

N1 - Funding Information: This study was supported by research grants from the National Health and Medical Research Council Australia ( NHMRC 512657 and 490968 ). The LIPID study was supported by Bristol-Myers Squibb and conducted under the auspices of the National Heart Foundation of Australia. Dr. White has received research grants from sanofi-aventis, Eli Lilly, The Medicines Company, National Institutes of Health (NIH), Pfizer, Roche, Johnson & Johnson, Schering-Plough, Merck Sharpe & Dohme, AstraZeneca, GlaxoSmithKline, Daiichi-Sankyo Pharma Development, and Bristol-Myers Squibb ; and has served on advisory boards for Merck Sharpe & Dohme, Roche, and Regado Biosciences. Dr. Tonkin has received research grants from AstraZeneca, Bristol-Myers Squibb, Merck Sharpe & Dohme, and the NIH; and has served on advisory boards for AstraZeneca, Merck Sharpe & Dohme, and Pfizer. Dr. West has received research grants from Merck Sharpe & Dohme, AstraZeneca, GlaxoSmithKline, and Bristol-Myers Squibb . Dr. Nestel has served on advisory boards for and has received consulting fees from AstraZeneca and Merck Sharpe & Dohme. Dr. Keech has received research support from and has served on speakers bureaus for Abbott, AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Merck, Novartis, Pfizer, Roche Diagnostics, and Solvay . Dr. Blankenberg has received research grants from Boehringer Ingelheim, Bayer, Abbott Diagnostics, Siemens, and Thermo Fisher ; has received lecture fees from AstraZeneca, Bayer, Boehringer Ingelheim, Siemens, and Abbott Diagnostics; and has served on advisory boards for Boehringer Ingelheim, Bayer, and Thermo Fisher. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

PY - 2014/2/4

Y1 - 2014/2/4

N2 - Objectives This study sought to assess whether baseline and change in contemporary sensitive troponin I (TnI) levels predicts coronary heart disease (CHD) death and myocardial infarction (MI), and to determine the effects of pravastatin on TnI levels. Background The role of troponins in predicting long-term outcomes in patients with stable CHD is not clearly defined. Methods The LIPID (Long-Term Intervention With Pravastatin in Ischaemic Disease) study randomized patients with cholesterol levels of 155 to 271 mg/dl 3 to 36 months after MI or unstable angina to placebo or pravastatin 40 mg per day. TnI levels were measured at baseline and after 1 year in 7,863 patients. Median follow-up was 6 years. Change in TnI was defined as moving up or down 1 tertile or ≥50% change. Results Baseline TnI tertiles were <0.006 ng/ml, 0.006 to <0.018 ng/ml, and ≥0.018 ng/ml. TnI levels were related to CHD death and MI after adjustment for 23 risk factors and treatment (≥0.018 ng/ml vs. <0.006 ng/ml hazard ratio [HR]: 1.64; 95% CI: 1.41 to 1.90; p < 0.001). TnI levels increased in 23.0%, were unchanged in 51.3%, and decreased in 25.7% of patients. Pravastatin decreased TnI levels by 0.003 ng/ml versus placebo (p = 0.002). In landmark analyses, increases in TnI levels were associated with increased numbers of CHD death and MI (HR: 1.31; 95% CI: 1.06 to 1.62) and decreases with decreased risk (HR: 0.90; 95% CI: 0.74 to 1.09; overall p = 0.01). Data were similar with 50% change criteria. Net reclassification improvement by adding TnI to the baseline model for CHD death and MI was 4.8% (p = 0.01). Conclusions Baseline TnI levels and change at 1 year are independent predictors of CHD death and MI. TnI levels are strong predictors of risk, and change modifies risk.

AB - Objectives This study sought to assess whether baseline and change in contemporary sensitive troponin I (TnI) levels predicts coronary heart disease (CHD) death and myocardial infarction (MI), and to determine the effects of pravastatin on TnI levels. Background The role of troponins in predicting long-term outcomes in patients with stable CHD is not clearly defined. Methods The LIPID (Long-Term Intervention With Pravastatin in Ischaemic Disease) study randomized patients with cholesterol levels of 155 to 271 mg/dl 3 to 36 months after MI or unstable angina to placebo or pravastatin 40 mg per day. TnI levels were measured at baseline and after 1 year in 7,863 patients. Median follow-up was 6 years. Change in TnI was defined as moving up or down 1 tertile or ≥50% change. Results Baseline TnI tertiles were <0.006 ng/ml, 0.006 to <0.018 ng/ml, and ≥0.018 ng/ml. TnI levels were related to CHD death and MI after adjustment for 23 risk factors and treatment (≥0.018 ng/ml vs. <0.006 ng/ml hazard ratio [HR]: 1.64; 95% CI: 1.41 to 1.90; p < 0.001). TnI levels increased in 23.0%, were unchanged in 51.3%, and decreased in 25.7% of patients. Pravastatin decreased TnI levels by 0.003 ng/ml versus placebo (p = 0.002). In landmark analyses, increases in TnI levels were associated with increased numbers of CHD death and MI (HR: 1.31; 95% CI: 1.06 to 1.62) and decreases with decreased risk (HR: 0.90; 95% CI: 0.74 to 1.09; overall p = 0.01). Data were similar with 50% change criteria. Net reclassification improvement by adding TnI to the baseline model for CHD death and MI was 4.8% (p = 0.01). Conclusions Baseline TnI levels and change at 1 year are independent predictors of CHD death and MI. TnI levels are strong predictors of risk, and change modifies risk.

KW - coronary heart disease

KW - LIPID

KW - mortality

KW - troponin I

UR - http://www.scopus.com/inward/record.url?scp=84893167287&partnerID=8YFLogxK

U2 - 10.1016/j.jacc.2013.08.1643

DO - 10.1016/j.jacc.2013.08.1643

M3 - SCORING: Journal article

C2 - 24140630

AN - SCOPUS:84893167287

VL - 63

SP - 345

EP - 354

JO - J AM COLL CARDIOL

JF - J AM COLL CARDIOL

SN - 0735-1097

IS - 4

ER -