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J Am Coll Cardiol. 2014 Feb 4;63(4):345-54. doi: 10.1016/j.jacc.2013.08.1643. Epub 2013 Oct 30.

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).

Author information

1
Green Lane Cardiovascular Service, Auckland City Hospital and Auckland University, Auckland, New Zealand. Electronic address: harveyw@adhb.govt.nz.
2
Monash University, Melbourne, Australia.
3
NHMRC Clinical Trials Centre, University of Sydney, Sydney, Australia.
4
Green Lane Cardiovascular Service, Auckland City Hospital and Auckland University, Auckland, New Zealand.
5
University of Western Australia, Perth, Australia.
6
University of Queensland, Brisbane, Australia.
7
Baker IDI Heart & Diabetes Institute, Melbourne, Australia.
8
Royal Prince Alfred Hospital, Camperdown, Australia.
9
Department of Cardiology, Royal Melbourne Hospital and University of Melbourne, Melbourne, Australia.
10
University Heart Centre Hamburg, Hamburg, Germany.

Abstract

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.

KEYWORDS:

B-type natriuretic peptide; BNP; CHD; CVD; LIPID; MI; TnI; cardiovascular disease; coronary heart disease; high-sensitivity C-reactive protein; high-sensitivity troponinT; hsCRP; hsTnT; mortality; myocardial infarction; troponin I

PMID:
24140630
DOI:
10.1016/j.jacc.2013.08.1643
[Indexed for MEDLINE]
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