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From Kaiser Permanente of Northern California, Oakland, California; University of California, San Francisco, San Francisco, California; and Stanford University School of Medicine, Stanford, California.
Grant Support: By the Donald W. Reynolds Foundation, Las Vegas, Nevada.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Alan S. Go, MD, Division of Research, Kaiser Permanente of Northern California, 2000 Broadway Street, 3rd Floor, Oakland, CA 94612-2304; e-mail, Alan.S.Go@kp.org.
Current Author Addresses: Drs. Go and Iribarren, Ms. Chandra, and Mr. Lathon: Division of Research, Kaiser Permanente of Northern California, 2000 Broadway Street, 3rd Floor, Oakland, CA 94612-2304.
Dr. Fortmann: Stanford Medical School, Hoover Pavillion, MD 5705, Stanford, CA 94305-5705.
Dr. Quertermous: Stanford University, Falk Building, 300 Pasteur Drive, Stanford, CA 94305.
Dr. Hlatky: Stanford University, HRP Redwood Building, Room 150, Stanford, CA 94305.
Author Contributions: Conception and design: A.S. Go, C. Iribarren, M. Chandra, S.P. Fortmann, T. Quertermous, M.A. Hlatky.
Analysis and interpretation of the data: A.S. Go, C. Iribarren, M. Chandra, P.V. Lathon, S.P. Fortmann, M.A. Hlatky.
Drafting of the article: A.S. Go, M. Chandra, M.A. Hlatky.
Critical revision of the article for important intellectual content: A.S. Go, C. Iribarren, M. Chandra, P.V. Lathon, S.P. Fortmann, T. Quertermous, M.A. Hlatky.
Final approval of the article: A.S. Go, C. Iribarren, M. Chandra, P.V. Lathon, S.P. Fortmann, T. Quertermous, M.A. Hlatky.
Provision of study materials or patients: A.S. Go.
Statistical expertise: A.S. Go, M. Chandra, M.A. Hlatky.
Obtaining of funding: A.S. Go, C. Iribarren, S.P. Fortmann, T. Quertermous, M.A. Hlatky.
Administrative, technical, or logistic support: A.S. Go, M. Chandra, P.V. Lathon, T. Quertermous, M.A. Hlatky.
Collection and assembly of data: A.S. Go, C. Iribarren, M. Chandra, P.V. Lathon, M.A. Hlatky.
The natural history of coronary atherosclerosis is characterized by long periods of clinical stability punctuated by episodes of unstable, acute ischemic symptoms that are associated with atherosclerotic plaque rupture and thrombosis. Much of the risk for coronary disease is the consequence of these episodes of clinical instability, particularly at the point when the first symptoms of the disease develop. Systematic differences among patients may affect patients' vulnerability to acute ischemic episodes and may allow identification of higher-risk patients who may benefit from more aggressive primary prevention measures. Treatments that reduce the risk for unstable episodes of acute ischemia in patients with underlying coronary atherosclerosis might prevent the most serious complications of the disease.
Variables in the final model included all listed medication classes, age, sex, race or ethnicity, parental history of coronary heart disease, smoking status, previous alcohol use, physical activity, previous stroke, previous peripheral arterial disease, previous hospitalization for heart failure, diabetes mellitus, previous hypertension, systemic malignant condition, diagnosed dementia, diagnosed depression, cirrhosis, chronic lung disease, body mass index, number of outpatient medical visits in the previous 12 months, and number of prescription medications within the 160 days before the index date. Error bars represent 95% CIs. ACE = angiotensin-converting enzyme; ARB = angiotensin-II–receptor blocker.
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The Effects of Cholesterol and Blood Pressure Treatments on Severity of Coronary Artery Disease
The summary below is from the full report titled “Statin and β-Blocker Therapy and the Initial Presentation of Coronary Heart Disease.” It is in the 21 February 2006 issue of Annals of Internal Medicine (volume 144, pages 229-238). The authors are A.S. Go, C. Iribarren, M. Chandra, P.V. Lathon, S.P. Fortmann, T. Quertermous, and M.A. Hlatky, for the Atherosclerotic Disease, Vascular Function and Genetic Epidemiology (ADVANCE) Study.
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