Alon Eisen1, Marc P Bonaca1, Petr Jarolim1, Benjamin M Scirica1, Harvey D White2, Michal Tendera3, Mikael Dellborg4, Jose C Nicolau5, Joao Morais6, Keith A A Fox7, Erin A Bohula1, Sabina A Murphy1, Eugene Braunwald1, David A Morrow8. 1. Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, MA. 2. Auckland City Hospital, Auckland, New Zealand. 3. Medical University of Silesia, Katowice, Poland. 4. University of Gothenburg and Sahlgrenska University Hospital/Östra, Gothenburg, Sweden. 5. University of São Paulo Medical School, São Paulo, Brazil. 6. Santo André's Hospital, Leiria, Portugal. 7. University of Edinburgh, Edinburgh, UK. 8. Brigham and Women's Hospital and Department of Medicine, Harvard Medical School, Boston, MA; dmorrow@partners.org.
Abstract
BACKGROUND: Cardiac troponin I, measured with a high-sensitivity assay (hs-TnI), is well-established for risk prediction in acute coronary syndromes. However, its prognostic role in stable atherosclerotic disease, particularly for future myocardial infarction (MI), is less well defined. METHODS: We measured hs-TnI (Abbott ARCHITECT) in 15833 patients with prior MI, ischemic stroke, or peripheral arterial disease from theplacebo-controlled Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2°P)-Thrombolysis in Myocardial Infarction (TIMI) 50 trial of the platelet inhibitor vorapaxar, excluding patients with recent MI (<30 days). hs-TnI was categorized into 5 groups based on the detection limit (1.9 ng/L), 99th percentile reference limit (26 ng/L), and tertiles in between (1.9-26 ng/L), as well as sex-specific reference limits. RESULTS: Higher hs-TnI concentration was associated with older age, male sex, and increased atherosclerosis burden. hs-TnI identified a graded 3-year risk of cardiovascular death, MI, or stroke from 5.0% to 18.6% (P < 0.001), driven by cardiovascular death and MI (P < 0.001). This risk was independent of established clinical risk indicators, B-type natriuretic peptide and C-reactive protein [adjusted hazard ratio 2.70 (95% CI, 1.96-3.71), P < 0.001 for hs-TnI >26 ng/L vs <1.9 ng/L]. In patients with prior MI, there was a pattern of greater absolute benefit with vorapaxar in patients with an increased hs-TnI (absolute risk difference 1.9% with hs-TnI >26 ng/L vs 0.3% with hs-TnI <1.9 ng/L; P interaction = 0.82). CONCLUSIONS: In stable patients with established atherosclerosis, hs-TnI concentrations effectively stratified the risk of new or recurrent cardiovascular (CV) events, in particular CV death and MI. High-risk patients with prior MI identified by increased hs-TnI had a substantial absolute improvement in net clinical outcome with vorapaxar.
RCT Entities:
BACKGROUND: Cardiac troponin I, measured with a high-sensitivity assay (hs-TnI), is well-established for risk prediction in acute coronary syndromes. However, its prognostic role in stable atherosclerotic disease, particularly for future myocardial infarction (MI), is less well defined. METHODS: We measured hs-TnI (Abbott ARCHITECT) in 15833 patients with prior MI, ischemic stroke, or peripheral arterial disease from the placebo-controlled Thrombin Receptor Antagonist in Secondary Prevention of Atherothrombotic Ischemic Events (TRA 2°P)-Thrombolysis in Myocardial Infarction (TIMI) 50 trial of the platelet inhibitor vorapaxar, excluding patients with recent MI (<30 days). hs-TnI was categorized into 5 groups based on the detection limit (1.9 ng/L), 99th percentile reference limit (26 ng/L), and tertiles in between (1.9-26 ng/L), as well as sex-specific reference limits. RESULTS: Higher hs-TnI concentration was associated with older age, male sex, and increased atherosclerosis burden. hs-TnI identified a graded 3-year risk of cardiovascular death, MI, or stroke from 5.0% to 18.6% (P < 0.001), driven by cardiovascular death and MI (P < 0.001). This risk was independent of established clinical risk indicators, B-type natriuretic peptide and C-reactive protein [adjusted hazard ratio 2.70 (95% CI, 1.96-3.71), P < 0.001 for hs-TnI >26 ng/L vs <1.9 ng/L]. In patients with prior MI, there was a pattern of greater absolute benefit with vorapaxar in patients with an increased hs-TnI (absolute risk difference 1.9% with hs-TnI >26 ng/L vs 0.3% with hs-TnI <1.9 ng/L; P interaction = 0.82). CONCLUSIONS: In stable patients with established atherosclerosis, hs-TnI concentrations effectively stratified the risk of new or recurrent cardiovascular (CV) events, in particular CV death and MI. High-risk patients with prior MI identified by increased hs-TnI had a substantial absolute improvement in net clinical outcome with vorapaxar.
Authors: James L Januzzi; Sunil Suchindran; Udo Hoffmann; Manesh R Patel; Maros Ferencik; Adrian Coles; Jean-Claude Tardif; Geoffrey S Ginsburg; Pamela S Douglas Journal: J Am Coll Cardiol Date: 2019-01-29 Impact factor: 24.094
Authors: Baris Gencer; Xinmin S Li; Yared Gurmu; Marc P Bonaca; David A Morrow; Marc Cohen; Deepak L Bhatt; P Gabriel Steg; Robert F Storey; Per Johanson; Zeneng Wang; Stanley L Hazen; Marc S Sabatine Journal: J Am Heart Assoc Date: 2020-05-05 Impact factor: 5.501
Authors: Evangelos Giannitsis; Moritz Biener; Hauke Hund; Matthias Mueller-Hennessen; Mehrshad Vafaie; Jochen Gandowitz; Christoph Riedle; Julia Löhr; Hugo A Katus; Kiril M Stoyanov Journal: Clin Res Cardiol Date: 2019-07-19 Impact factor: 5.460