David H Smith1, Eric S Johnson2, Denise M Boudreau3, Andrea E Cassidy-Bushrow4, Stephen P Fortmann2, Robert T Greenlee5, Jerry H Gurwitz6, David J Magid7, Catherine J McNeal8, Kristi Reynolds9, Steven R Steinhubl10, Micah Thorp2, Jeffrey O Tom11, Suma Vupputuri12, Jeffrey J VanWormer5, Jessica Weinstein2, Xiuhai Yang2, Alan S Go13, Stephen Sidney14. 1. Kaiser Permanente Center for Health Research - Northwest, Portland, Ore. Electronic address: David.H.Smith@kpchr.org. 2. Kaiser Permanente Center for Health Research - Northwest, Portland, Ore. 3. Group Health Research Institute, Seattle, Wash. 4. Henry Ford Hospital, Detroit, Mich. 5. Marshfield Clinic Research Foundation, Marshfield, Wis. 6. Meyers Primary Care Institute, Worcester, Mass; Fallon Community Health Plan, Worcester, Mass; University of Massachusetts, Worcester. 7. Kaiser Permanente Institute for Health Research, Denver, Colo; University of Colorado Health Sciences Center, Denver. 8. Baylor Scott & White Center for Applied Health Research, Temple, Tex; Texas A&M Health Science Center, Round Rock. 9. Kaiser Permanente Department of Research & Evaluation, Pasadena, Calif. 10. Geisinger Clinic, Danville, Pa. 11. Kaiser Permanente Center for Health Research - Hawaii, Honolulu. 12. Mid-Atlantic Permanente Research Institute, Rockville, Md. 13. Kaiser Permanente Division of Research, Oakland, Calif; University of California, San Francisco. 14. Kaiser Permanente Division of Research, Oakland, Calif.
Abstract
BACKGROUND: Whether there is a kidney function threshold to statin effectiveness in patients with acute myocardial infarction is poorly understood. Our study sought to help fill this gap in clinical knowledge. METHODS: We undertook a new-user cohort study of the effectiveness of statin therapy by level of estimated glomerular filtration rate (eGFR) in adults who were hospitalized for myocardial infarction between 2000 and 2008. Data came from the Cardiovascular Research Network. The primary clinical outcomes were 1-year all-cause mortality and cardiovascular hospitalizations, with adverse outcomes of myopathy and development of diabetes mellitus. We calculated incidence rates, the number needed to treat, and used Cox proportional hazards regression with propensity score matching and adjustment to control for confounding, with testing for variation of effect by level of kidney function. RESULTS: Compared with statin non-initiators (n = 5583), statin initiators (n = 5597) had a lower propensity score-adjusted risk for death (hazard ratio 0.79; 95% confidence interval [CI], 0.71-0.88) and cardiovascular hospitalizations (hazard ratio 0.90; 95% CI, 0.82-1.00). We found little evidence of variation in effect by level of eGFR (P = .86 for death; P = .77 for cardiovascular hospitalization). Adverse outcomes were similar for statin initiators and statin non-initiators. The number needed to treat to prevent 1 additional death over 1 year of follow-up ranged from 15 (95% CI, 11-28) for eGFR <30 mL/min/1.73 m(2) requiring statin treatment over 2 years to prevent 1 additional death, to 67 (95% CI, 49-118) for patients with eGFR >90 mL/min/1.73 m(2). CONCLUSIONS: Our findings suggest that there is potential for important public health gains by increasing the routine use of statin therapy for patients with lower levels of kidney function.
BACKGROUND: Whether there is a kidney function threshold to statin effectiveness in patients with acute myocardial infarction is poorly understood. Our study sought to help fill this gap in clinical knowledge. METHODS: We undertook a new-user cohort study of the effectiveness of statin therapy by level of estimated glomerular filtration rate (eGFR) in adults who were hospitalized for myocardial infarction between 2000 and 2008. Data came from the Cardiovascular Research Network. The primary clinical outcomes were 1-year all-cause mortality and cardiovascular hospitalizations, with adverse outcomes of myopathy and development of diabetes mellitus. We calculated incidence rates, the number needed to treat, and used Cox proportional hazards regression with propensity score matching and adjustment to control for confounding, with testing for variation of effect by level of kidney function. RESULTS: Compared with statin non-initiators (n = 5583), statin initiators (n = 5597) had a lower propensity score-adjusted risk for death (hazard ratio 0.79; 95% confidence interval [CI], 0.71-0.88) and cardiovascular hospitalizations (hazard ratio 0.90; 95% CI, 0.82-1.00). We found little evidence of variation in effect by level of eGFR (P = .86 for death; P = .77 for cardiovascular hospitalization). Adverse outcomes were similar for statin initiators and statin non-initiators. The number needed to treat to prevent 1 additional death over 1 year of follow-up ranged from 15 (95% CI, 11-28) for eGFR <30 mL/min/1.73 m(2) requiring statin treatment over 2 years to prevent 1 additional death, to 67 (95% CI, 49-118) for patients with eGFR >90 mL/min/1.73 m(2). CONCLUSIONS: Our findings suggest that there is potential for important public health gains by increasing the routine use of statin therapy for patients with lower levels of kidney function.
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