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A Rapid (Differential) Effect of Rosuvastatin and Atorvastatin on High‐Sensitivity Cardiac Troponin‐I in Subjects With Stable Cardiovascular Disease
Author(s) -
Bodde Mathijs C.,
Welsh Paul,
Bergheanu Sandrin C.,
Lijfering Willem M.,
Mertens Bart,
Liem AnHo,
Laarse Arnoud,
Sattar Naveed,
Jukema J. Wouter
Publication year - 2018
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1002/cpt.1095
Subject(s) - rosuvastatin , atorvastatin , medicine , troponin i , cardiology , statin , rosuvastatin calcium , troponin , endocrinology , myocardial infarction
Serum troponin within the normal range is an emerging predictor of cardiovascular mortality. We aimed to determine how rapidly high‐sensitivity troponin‐I (hs‐cTnI) levels are lowered by statin therapy in patients with stable cardiovascular disease. In the RADAR substudy, patients were randomized to atorvastatin 20 mg/day ( n = 39) or rosuvastatin 10 mg/day ( n = 39) and up‐titrated at 6‐week intervals to 80 mg of atorvastatin or 40 mg of rosuvastatin. Hs‐cTnI concentrations were measured at baseline and at 6 and 18 weeks of follow‐up. Statin treatment resulted in a mean change of serum hs‐cTnI of –8.2% ( P = 0.010) after 6 weeks and –12.3% ( P = 0.001) after 18 weeks. After 18 weeks, hs‐cTnI levels were lowered by 21.8% with atorvastatin and by 4.1% with rosuvastatin ( P = 0.001 and P = 0.133, respectively). During statin therapy, serum hs‐cTnI levels decreased rapidly within weeks of treatment, suggesting an effect beyond long‐term atherosclerosis regression. Mechanisms that mediate this effect require further study.