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Troponin I levels predicted CHD death, nonfatal MI
Baseline levels of troponin I as measured by a contemporary assay were independent predictors of CHD death and nonfatal MI, among other outcomes, according to new data from the LIPID study.
Increases in troponin I at 1 year were linked to higher rates of total mortality, and decreases at 1 year were linked to lower rates of all-cause mortality, researchers found.
Harvey D. White, DSc, of Auckland City Hospital, New Zealand, and colleagues analyzed measurements of troponin I in 7,863 participants of the LIPID study. Levels were measured using a contemporary sensitive assay (TnI-Ultra, Siemens) at baseline and 1 year.
Participants had cholesterol levels between 155 mg/dL and 271 mg/dL and had MI or unstable angina in the previous 36 months. Each was randomly assigned to pravastatin (Pravachol, Bristol-Myers Squibb) 40 mg/day or placebo. Median follow-up was 6 years.
The researchers defined a change in troponin I as 50% or movement into another tertile. At baseline, troponin I tertiles were <0.006 ng/mL, ≥0.006 ng/mL to 0.018 ng/mL and ≥0.018 ng/mL. At 1 year, troponin I levels increased in 23% of participants, were unchanged in 51.3% and decreased in 25.7%.
After adjustment for 23 risk factors and treatments, the researchers found that high troponin I levels at baseline were associated with higher rates of CHD death (P<.001), nonfatal MI (P=.04), stroke (P=.02) and HF (P<.001). Participants in the highest tertile of troponin I levels had an elevated risk for CHD death or MI compared with those in the lowest tertile (HR=1.64; 95% CI, 1.41-1.9).
An increase in troponin I levels was associated with higher rates of CHD death and MI (HR=1.31; 95% CI, 1.06-1.62) and a decrease was associated with lower rates of CHD death and MI (HR=0.9; 95% CI, 0.74-1.09).
Compared with undetectable levels, troponin I levels in the 99th percentile (>0.04 ng/mL) were associated with elevated risk for CHD death or MI (adjusted HR=2.02; 95% CI, 1.66-2.45) and for all-cause mortality (adjusted HR=2.22; 95% CI, 1.81-2.72).
Although those assigned pravastatin had median decreased troponin I levels of 0.003 ng/mL at 1 year compared with those assigned placebo (P=.002), the treatment effect “did not result in important differences in the proportion of patients changing category,” White and colleagues wrote. “The effect of pravastatin on CVD event reduction remained essentially unchanged after adjustment for change in [troponin I levels].”
Disclosure: The study was funded by the National Health and Medical Research Council Australia; the original LIPID study was funded by Bristol-Myers Squibb. See the full study for a list of the researchers’ relevant financial disclosures.