Protein-based risk score for cardiovascular outcomes in stable coronary heart disease

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Protein-based risk score for cardiovascular outcomes in stable coronary heart disease

JAMA, 07/12/2016 Ganz P, et al.

Researchers used large–scale analysis of circulating proteins with a goal to derive and validate a score to predict risk of cardiovascular outcomes among patients with CHD. They concluded that only modest discriminative accuracy was provided among patients with stable CHD although a risk score based on 9 proteins performed better than the refit Framingham secondary event risk score in predicting cardiovascular events. To assess whether the score is more accurate in a lower–risk population, further research is needed.

Methods

• Design of the study is prospective cohort, in participants with stable CHD.
• Outpatients from San Francisco were enrolled from 2000 through 2002 and followed up through November 2011 (<=11.1 years), for the derivation cohort (Heart and Soul study) and from 2006 through 2008 and followed up through April 2012 (5.6 years), for the validation cohort (HUNT3, a Norwegian population–based study).
• 1130 proteins were measured in plasma samples, using modified aptamers
• Derivation and validation of 9–protein risk score was done for 4–year probability of myocardial infarction, stroke, heart failure, and all–cause death.
• Researchers used tests, including the C statistic, to assess performance of the 9–protein risk score, which was compared with the Framingham secondary event model, refit to the cohorts in this study.
• From paired samples which were collected 4.8 years apart, evaluation of within–person change in the 9–protein risk score was done in the Heart and Soul study.

Results

• The results demonstrated that of the 938 samples analyzed from the derivation cohort, median age of the participants enrolled was 67.0 years and 82% were men, whereas of the 971 samples analyzed from the validation cohort, participants’ median age at enrollment was 70.2 years, and 72% were men.
• C statistics in the derivation cohort were: 0.66 for refit Framingham, 0.74 for 9–protein, and 0.75 for refit Framingham plus 9–protein models, and in the validation cohort were: 0.64 for refit Framingham, 0.70 for 9–protein, and 0.71 for refit Framingham plus 9–protein models.
• C statistics were increased by 0.09 (95% CI, 0.06–0.12) in the derivation cohort and by 0.05 (95% CI, 0.02–0.09) in the validation cohort, by adding the 9–protein risk score to the refit Framingham model .
• The integrated discrimination index for the 9–protein model was 0.12 (95% CI, 0.08–0.16) in the derivation cohort and 0.08 (95% CI, 0.05–0.10) in the validation cohort, compared with the refit Framingham model.
• Researchers analysed that in paired samples among 139 participants with cardiovascular events after the second sample, absolute within–person annualized risk increased more for the 9–protein model (median, 1.86% [95% CI, 1.15%–2.54%]) than for the refit Framingham model (median, 1.00% [95% CI, 0.87%–1.19%]) (P=.002), while among 375 participants without cardiovascular events, both scores changed less and similarly (P=.30).