Published online before print November 29, 2004, doi: 10.1161/01.CIR.0000149806.01354.BF
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(Circulation. 2004;110:3667-3673.)
© 2004 American Heart Association, Inc.
Heart Failure |
Chronic Kidney Disease, Cardiovascular Risk, and Response to Angiotensin-Converting Enzyme Inhibition After Myocardial Infarction
The Survival And Ventricular Enlargement (SAVE) Study
From the Department of Cardiology, St. George Hospital, Medical University Plovdiv (M.P.T.), Plovdiv, Bulgaria; Division of Cardiology, Brigham and Women’s Hospital (H.S., S.K., E.B., M.A.P., S.D.S.), Boston, Mass; Office of the Dean, University of Montreal (J.L.R.), Quebec, Canada; Center for Biostatistics and Clinical Science, University of Texas Southwestern Medical Center (M.P.), Dallas, Tex; Division of Nephrology, University of California (G.M.C.), San Francisco, Calif; and School of Public Health, University of Texas (L.A.M.), Houston, Tex.
Reprint requests to Scott D. Solomon MD, Director, Noninvasive Cardiac Lab, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis St, Boston, MA. E-mail ssolomon{at}rics.bwh.harvard.edu
Received July 16, 2004; accepted September 14, 2004.
Background— Persons with end-stage renal disease and those with lesser degrees of chronic kidney disease (CKD) have an increased risk of death after myocardial infarction (MI) that is not fully explained by associated comorbidities. Future cardiovascular event rates and the relative response to therapy in persons with mild to moderate CKD are not well characterized.
Methods and Results— We calculated the estimated glomerular filtration rate (eGFR) using the 4-variable Modification of Diet in Renal Disease method in 2183 Survival And Ventricular Enlargement (SAVE) trial subjects. SAVE randomized post-MI subjects (3 to 16 days after MI) with left ventricular ejection fraction 
40% and serum creatinine <2.5 mg/dL to captopril or placebo. Cox proportional hazards models were used to evaluate the relative hazard rates for death and cardiovascular events associated with reduced eGFR. Subjects with reduced eGFR were older and had more extensive comorbidities. The multivariable adjusted risk ratio for total mortality associated with reduced eGFR from 60 to 74, 45 to 59, and <45 mL · min–1 · 1.73 m–2 (compared with eGFR 
75 mL · min–1 · 1.73 m–2) was 1.11 (0.86 to 1.42), 1.24 (0.96 to 1.60) and 1.81 (1.32 to 2.48), respectively (P for trend =0.001). Similar adjusted trends were present for CV mortality (P=0.001), recurrent MI (P=0.017), and the combined CV mortality and morbidity outcome (P=0.002). The absolute benefit of captopril tended to be greater in subjects with CKD: 12.4 versus 5.5 CV events prevented per 100 subjects with (n=719) and without (n=1464) CKD, respectively.
Conclusions— CKD was associated with a heightened risk for all major CV events after MI, particularly among subjects with an estimated glomerular filtration rate <45 mL · min–1 · 1.73 m–2. Randomization to captopril resulted in a reduction of CV events irrespective of baseline kidney function.
Key Words: kidney • myocardial infarction • mortality
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