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on January 2, 2009

Arteriosclerosis, Thrombosis, and Vascular Biology. 2009
Published online before print January 2, 2009, doi: 10.1161/ATVBAHA.108.181735
A more recent version of this article appeared on March 1, 2009
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Submitted on October 7, 2008
Accepted on December 20, 2008

Prognostic Utility of ApoB/AI, Total Cholesterol/HDL, Non-HDL Cholesterol, or hs-CRP as Predictors of Clinical Risk in Patients Receiving Statin Therapy After Acute Coronary Syndromes. Results From PROVE IT–TIMI 22

Kausik K. Ray ; Christopher P. Cannon *; Richard Cairns ; David A. Morrow ; Paul M. Ridker ; and Eugene Braunwald

From the TIMI Study Group, Cardiovascular Division and the Department of Medicine (C.P.C., D.A.M., E.B.), Brigham and Women's Hospital/Harvard Medical School, Boston, Mass; the Department of Public Health and Primary Care (K.K.R.), University of Cambridge, UK; Worldwide Clinical Trials (R.C.), and the Donald W. Reynolds Center for Cardiovascular Research and the Center for Cardiovascular Disease Prevention (P.M.R.), Brigham and Women's Hospital, Boston, Mass.

* To whom correspondence should be addressed. E-mail: cpcannon{at}partners.org.

Objectives—The purpose of this study was to compare the prognostic utility of apoB/AI, total cholesterol/HDL (TC/HDL) ratio, non-HDL cholesterol (non–HDL-C), or hs-CRP as predictors of clinical risk among patients receiving statin therapy after acute coronary syndromes (ACS).

Methods and Results—Patients with ACS were randomized in the PROVE IT–TIMI 22 trial to either pravastatin 40 mg or atorvastatin 80 mg. Cox regression models adjusting for confounders were used to assess the relationship between on-treatment lipids or hs-CRP and risk of death or acute coronary events. At 4 months a 1 SD increment in apoB/AI (HR 1.10, 95% CI 1.01 to 1.20), TC/HDL (HR 1.12, 95% CI 1.01 to 1.24), and non–HDL-C (HR 1.20, 95% CI 1.07 to 1.35) predicted events to a similar extent as LDL-C (HR 1.20, 95% CI 1.07 to 1.35) with neither apoB/AI, TC/HDL, nor non–HDL-C improving risk prediction models which included LDL-C. In contrast, the addition of hs-CRP significantly improved risk prediction models irrespective of the lipid parameters included, with a 29% to 30% increased risk observed per 1 SD increment in log CRP.

Conclusion—In the present study of ACS patients receiving statin therapy, on-treatment apoB/AI, TC/HDL, and non–HDL-C offered similar prognostic information to LDL-C. However, the addition of hs-CRP to lipid-based measurements significantly improved risk prediction. On treatment CRP measurement may therefore offer additive prognostic information to lipids in ACS patients.