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Biomarkers in stable coronary heart disease, their modulation and cardiovascular risk: The LIPID biomarker study
Andrew M Tonkin1, Stefan Blankenberg2, Adrienne Kirby3
1Department of Epidemiology and Preventive Medicine, Monash University, Melbourne, Australia.
Insights
Biomarkers like sensitive troponin I and BNP at baseline and their changes over time can predict coronary heart disease (CHD) events. These markers may help guide secondary prevention therapy intensity in patients with stable CHD.
Area of Science:
- Cardiology
- Biomarker Discovery
- Clinical Trials
Background:
- Stable coronary heart disease (CHD) requires effective risk stratification and secondary prevention strategies.
- Identifying prognostic biomarkers is crucial for tailoring treatment intensity.
- Previous research has explored various biomarkers, but their dynamic changes and interaction with therapies need further investigation.
Purpose of the Study:
- To assess the prognostic power of multiple biomarkers (hemodynamics, micronecrosis, inflammation, coagulation, lipids, neurohumoral, renal function) in stable CHD.
- To determine if changes in biomarker concentrations over 12 months impact subsequent CHD risk.
- To investigate if pravastatin influences biomarker changes and subsequent cardiovascular risk.
Main Methods:
- The LIPID study randomized 9014 patients to pravastatin or placebo post-acute coronary syndrome.
- Eight key biomarkers were measured at baseline and 12 months in a subset of patients.
- Follow-up for CHD events (death, myocardial infarction) was conducted over a median of 6 years.
Main Results:
- Baseline levels of BNP, CRP, cystatin C, D-dimer, midregional pro-adrenomedullin, and sensitive troponin I predicted recurrent CHD events.
- Sensitive troponin I, BNP, and cystatin C showed the strongest associations with outcomes in multivariable analysis.
- Changes in sensitive troponin I, BNP, and Lp-PLA2 concentrations over 12 months improved CHD risk prediction.
Conclusions:
- Baseline levels and 12-month changes in sensitive troponin I and BNP are significant predictors of CHD events.
- These biomarkers hold potential for guiding the intensity of secondary prevention therapies in stable CHD patients.
- Pravastatin's effect on biomarker changes and risk requires further detailed analysis.
Aims:
In patients with stable coronary heart disease (CHD), we aimed to assess 1. the prognostic power of biomarkers reflecting haemodynamics, micronecrosis, inflammation, coagulation, lipids, neurohumoral activity, and renal function; 2. whether changes in concentrations of these biomarkers over 12 months affected subsequent CHD risk; and 3. whether pravastatin modified the change in biomarker concentrations and this influenced the risk of future events.
Methods:
In the LIPID study, 9014 patients were randomised to pravastatin 40 mg or placebo 3-36 months after an acute coronary syndrome. Eight biomarkers were measured at baseline (n=7863) and 12 months later (n=6434).
Results:
During a median of 6.0 (IQR 5.5-6.5) years follow-up, 1100 CHD-related deaths and nonfatal myocardial infarctions occurred, 694 after biomarker measurement at 12 months. Baseline BNP, CRP, cystatin C, D-dimer, midregional pro-adrenomedullin, and sensitive troponin I predicted recurrent CHD events. In a multivariable model, sensitive troponin I, BNP, and cystatin C had the strongest associations with outcome (P<0.001 for trend). The strongest improvement in risk prediction was achieved by including sensitive troponin I (net reclassification improvement (NRI) 5.5%; P=0.003), BNP (4.3%; P=0.02), history of MI (NRI 7.0%; P<0.001). In landmark analyses, among biomarkers, changes to 12 months in sensitive troponin I (HR 1.32 (1.03-1.70) for T3/T1), BNP (HR 1.37 (1.10-1.69) for Q4/Q1) and Lp-PLA2 (HR 1.52 (1.16-1.97)) improved CHD risk prediction.
Conclusions:
Baseline levels and changes in sensitive troponin I, and BNP may have the potential to guide the intensity of secondary prevention therapy.
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