JaeJin An1,2, Evo Alemao3,4, Kristi Reynolds3,4, Hugh Kawabata3,4, Daniel H Solomon3,4, Katherine P Liao3,4, Fang Niu3,4, T Craig Cheetham3,4. 1. From the Department of Pharmacy Practice and Administration, Western University of Health Sciences, Pomona, California; Bristol-Myers Squibb, Princeton, New Jersey; Research and Evaluation, Kaiser Permanente Southern California, Pasadena, California; Division of Rheumatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Drug Information Services, Kaiser Permanente Southern California, Downey, California, USA. jan@westernu.edu. 2. J. An, BPharm, PhD, Department of Pharmacy Practice and Administration, Western University of Health Sciences; E. Alemao, RPh, MS, Bristol-Myers Squibb; K. Reynolds, PhD, MPH, Research and Evaluation, Kaiser Permanente Southern California; H. Kawabata, MS, Bristol-Myers Squibb; D.H. Solomon, MD, MPH, Division of Rheumatology, Brigham and Women's Hospital, Harvard Medical School; K.P. Liao, MD, MPH, Division of Rheumatology, Brigham and Women's Hospital, Harvard Medical School; F. Niu, MS, Drug Information Services, Kaiser Permanente Southern California; T.C. Cheetham, PharmD, MS, Research and Evaluation, Kaiser Permanente Southern California. jan@westernu.edu. 3. From the Department of Pharmacy Practice and Administration, Western University of Health Sciences, Pomona, California; Bristol-Myers Squibb, Princeton, New Jersey; Research and Evaluation, Kaiser Permanente Southern California, Pasadena, California; Division of Rheumatology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts; Drug Information Services, Kaiser Permanente Southern California, Downey, California, USA. 4. J. An, BPharm, PhD, Department of Pharmacy Practice and Administration, Western University of Health Sciences; E. Alemao, RPh, MS, Bristol-Myers Squibb; K. Reynolds, PhD, MPH, Research and Evaluation, Kaiser Permanente Southern California; H. Kawabata, MS, Bristol-Myers Squibb; D.H. Solomon, MD, MPH, Division of Rheumatology, Brigham and Women's Hospital, Harvard Medical School; K.P. Liao, MD, MPH, Division of Rheumatology, Brigham and Women's Hospital, Harvard Medical School; F. Niu, MS, Drug Information Services, Kaiser Permanente Southern California; T.C. Cheetham, PharmD, MS, Research and Evaluation, Kaiser Permanente Southern California.
Abstract
OBJECTIVE: To examine the associations between lowering low-density lipoprotein cholesterol (LDL-C) and cardiovascular (CV) outcomes among patients with rheumatoid arthritis (RA) and patients without it. METHODS: Adult patients with RA and 2 age- and sex-matched control cohorts [RA plus general controls (RA/GN), RA plus osteoarthritis (OA) controls (RA/OA)] were identified between January 1, 2007, and December 31, 2011. Patients with a diagnosis of hyperlipidemia who initiated statin therapy without prior CV events were included. Multivariable Cox proportional hazard analyses were used. RESULTS: The study identified 1522 patients with RA with 6511 general controls (RA/GN cohort); and 1746 patients with RA with 2554 OA controls (RA/OA cohort). During followup, mean (SD) LDL-C (mg/dl) was 96.8 (32.7) for RA, 100.1 (35.1) for general controls, and 99.1 (34.3) for OA. The relationship between lowering LDL-C and CV outcomes was similar for both RA and non-RA controls (p for interaction = 0.852 in RA/GN cohort, and p = 0.610 in RA/OA cohort). After adjusting for baseline CV risk factors, lowering LDL-C was associated with a 29%-50% lower risk of CV events (HR [95% CI] = 0.71 [0.57-0.89] in RA/GN, 0.50 [0.43-0.58] in RA/OA). Subgroup analyses showed that lowering LDL-C was associated with a similar degree of reduction of CV events in RA and non-RA controls (HR of 0.67-0.68 for RA, 0.72 for general controls, 0.76 for OA controls). CONCLUSION: Lowering LDL-C levels was associated with reduced CV events. The relationship between lowering LDL-C and CV outcomes in RA was similar to the relationship found in matched general and OA controls.
OBJECTIVE: To examine the associations between lowering low-density lipoprotein cholesterol (LDL-C) and cardiovascular (CV) outcomes among patients with rheumatoid arthritis (RA) and patients without it. METHODS: Adult patients with RA and 2 age- and sex-matched control cohorts [RA plus general controls (RA/GN), RA plus osteoarthritis (OA) controls (RA/OA)] were identified between January 1, 2007, and December 31, 2011. Patients with a diagnosis of hyperlipidemia who initiated statin therapy without prior CV events were included. Multivariable Cox proportional hazard analyses were used. RESULTS: The study identified 1522 patients with RA with 6511 general controls (RA/GN cohort); and 1746 patients with RA with 2554 OA controls (RA/OA cohort). During followup, mean (SD) LDL-C (mg/dl) was 96.8 (32.7) for RA, 100.1 (35.1) for general controls, and 99.1 (34.3) for OA. The relationship between lowering LDL-C and CV outcomes was similar for both RA and non-RA controls (p for interaction = 0.852 in RA/GN cohort, and p = 0.610 in RA/OA cohort). After adjusting for baseline CV risk factors, lowering LDL-C was associated with a 29%-50% lower risk of CV events (HR [95% CI] = 0.71 [0.57-0.89] in RA/GN, 0.50 [0.43-0.58] in RA/OA). Subgroup analyses showed that lowering LDL-C was associated with a similar degree of reduction of CV events in RA and non-RA controls (HR of 0.67-0.68 for RA, 0.72 for general controls, 0.76 for OA controls). CONCLUSION: Lowering LDL-C levels was associated with reduced CV events. The relationship between lowering LDL-C and CV outcomes in RA was similar to the relationship found in matched general and OA controls.