Abstract 18108: A Rapid Effect of Rosuvastatin and Atorvastatin on Myocardial Damage, as Measured by High Sensitivity Cardiac Troponin-I in Subjects With Stable Cardiovascular Disease, Results From the RADAR Substudy

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Introduction: Elevated troponin within the normal range is an emerging independent predictor of cardiovascular (CV) mortality. Recently, a randomized trial showed that troponin levels were lowered with 13% at 1 year in the pravastatin group as compared with placebo. However, the earliest onset of this effect, and differences between statins, are unknown. Thus, this randomized study sought to determine in what time frame troponin levels are lowered when using atorvastatin (ATOR) or rosuvastatin (ROSU) in pts with stable CV disease (CVD).

Methods: In the RADAR (Rosuvastatin and Atorvastatin in different Dosages And Reverse cholesterol transport) substudy, aged 40-80 years, with stable CVD and HDL-C <1.0 mmol/L, were randomized, after a dietary run-in phase, to ATOR 20 mg/day (n = 41) or ROSU 10 mg/day (n = 39). The doses were up-titrated in 6 week intervals to 80 mg of ATOR or 40 mg of ROSU in all pts. High sensitivity cardiac troponin-I (hscTn-I) concentrations were measured at baseline and at 6 and 18 weeks of follow up.

Results: Among 78 randomized pts, mean age was 65 yrs and 94% were male. After 6 weeks of treatment mean change of hscTn-I level was -9.1% in the total group (p=0.053) and after 18 weeks the mean change was - 14.8% (p=0.002). ATOR reduced hscTn-I with -11.8% and -25.2% after 6 and 18 weeks, respectively (p = 0.065 and p = 0.001). The reduction of hscTn-I in the ROSU group was -6.4% and -7.0% after 6 and 18 weeks, respectively (p = 0.281 and p = 0.147). Adjusted for baseline hscTn-I level, ATOR reduced hscTn-I levels more effectively than ROSU (mean difference 0.50 pg/ml; p=0.044).

Conclusions: Statin therapy reduce troponin levels in pts with stable CVD within 18 weeks of treatment. This effect is more pronounced in ATOR users than in ROSU users. This novel finding suggests a potential rapid benefit of statin treatment on ongoing subclinical myocardial damage. Further studies appear warranted to determine if statin-mediated effects on troponin levels predict long term benefits.

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