Objectives: We compared the incidence of late increase in hs-cTnI between ACS and non-ACS patients treated with standard of care with or without darapladib. Methods: A total of 323 (161 ACS and 162 non-ACS patients) were included. High sensitivity troponin I was measured at baseline and at 4, 13, 26 and 52 weeks. Results: ACS patients had statistically higher hs-cTnI values during longer term follow-up at which these patients were no longer in the acute setting of myocardial ischemia, but were regarded to have stable CAD (mean hsTnI value in ACS patients: 1.180 versus 0.886 ng/L in non-ACS patients, p = 0.02).Multivariate logistic regression revealed three predictors of any 2-fold increase in hs-cTnI levels compared to the previous visit when interactions were not considered. Treatment with darapladib (adjusted OR 0.53; 95% CI: 0.30-0.92) and initial presentation with ACS (adjusted OR 0.42; 95% CI: 0.23-0.77) were associated with less frequent occurrence of a 2-fold increase in hs-cTnI levels. In contrast, diabetes was associated with a higher incidence of 2-fold increases in hs-cTnI levels (adjusted OR 2.20; 95% CI: 1.04-4.64). Logistic regression to predict any 2-fold increase in hs-cTnI by ACS status showed that in the ACS group, treatment with darapladib decreased the risk of elevation of hs-cTnI (OR 0.219; 95% CI: 0.087, 0.553, p = 0.0013). Conclusion: In patients with ACS, treatment with darapladib is associated with less increase in cardiac troponin I compared to standard of care alone. This beneficial effect may be associated with darapladib's capability of reducing necrotic core in coronary plaques.

Atherosclerosis, Darapladib, High sensitive troponin I
dx.doi.org/10.1016/j.atherosclerosis.2012.06.064, hdl.handle.net/1765/64694
Department of Cardiology

Garcia-Garcia, H.M, Oemrawsingh, R.M, Brugaletta, S, Vranckx, P, Shannon, J, Davies, R, … Serruys, P.W.J.C. (2012). Darapladib effect on circulating high sensitive troponin in patients with acute coronary syndromes. Atherosclerosis, 225(1), 142–147. doi:10.1016/j.atherosclerosis.2012.06.064