Alka M. Kanaya, MD; David Herrington, MD, MHS; Eric Vittinghoff, PhD; Feng Lin, MS; Vera Bittner, MD, MSPH; Jane A. Cauley, DrPH; Stephen Hulley, MD; Elizabeth Barrett-Connor, MD
Acknowledgments: The authors thank members of the HERS Coordinating Center and the Executive Committee for their review and recommended revisions.
Grant Support: By National Institutes of Health grants 5 K12 AR47659 and P30–AG15272 (Dr. Kanaya). Wyeth-Ayerst Research funded the Heart and Estrogen/progestin Replacement Study.
Potential Financial Conflicts of Interest: Honoraria: J.A. Cauley (Eli Lilly Inc., Merck & Co. Inc., Novartis); Grants received: E. Vittinghoff (Wyeth), V. Bittner (Wyeth), J.A. Cauley (Eli Lilly Inc., Merck & Co. Inc., Pfizer Inc., Novartis), E. Barrett-Connor (National Institutes of Health); Other: J.A. Cauley (Eli Lilly Inc., Merck & Co. Inc.).
Requests for Single Reprints: Alka M. Kanaya, MD, Women's Health Clinical Research Center, 1635 Divisadero Street, Suite 600, San Francisco, CA 94115; e-mail, email@example.com.
Current Author Addresses: Drs. Kanaya and Vittinghoff: Women's Health Clinical Research Center, University of California, San Francisco, 1635 Divisadero Street, Suite 600, San Francisco, CA 94115.
Dr. Herrington: Wake Forest University School of Medicine, One Medical Center Boulevard, Winston-Salem, NC 27157-1066.
Dr. Hulley and Ms. Lin: Prevention Sciences Group, 74 New Montgomery Street, Suite 600, San Francisco, CA 94105.
Dr. Bittner: University of Alabama at Birmingham, Division of Cardiovascular Disease, 701 19th Street South, LHRB 310, Birmingham, AL 35294.
Dr. Cauley: University of Pittsburgh, 130 DeSoto Street, A524, Pittsburgh, PA 15261.
Dr. Barrett-Connor: Department of Family and Preventive Medicine, University of California, San Diego, 9500 Gilman Drive, Stein Clinical Research Building, La Jolla, CA 92093-0607.
Author Contributions: Conception and design: A.M. Kanaya, D. Herrington, S. Hulley.
Analysis and interpretation of the data: A.M. Kanaya, D. Herrington, E. Vittinghoff, F. Lin, V. Bittner, J.A. Cauley, S. Hulley, E. Barrett-Connor.
Drafting of the article: A.M. Kanaya, D. Herrington, S. Hulley.
Critical revision of the article for important intellectual content: A.M. Kanaya, D. Herrington, E. Vittinghoff, V. Bittner, J.A. Cauley, S. Hulley, E. Barrett-Connor.
Final approval of the article: A.M. Kanaya, D. Herrington, E. Vittinghoff, F. Lin, V. Bittner, J.A. Cauley, S. Hulley, E. Barrett-Connor.
Provision of study materials or patients: D. Herrington, V. Bittner, S. Hulley.
Statistical expertise: E. Vittinghoff, F. Lin, S. Hulley.
Obtaining of funding: A.M. Kanaya, S. Hulley.
Administrative, technical, or logistic support: A.M. Kanaya, S. Hulley.
Collection and assembly of data: A.M. Kanaya, V. Bittner, E. Barrett-Connor.
Type 2 diabetes increases risk for cardiovascular disease. Persons with impaired fasting glucose levels may also have increased risk.
To evaluate the association between glucose status and cardiovascular outcomes and the effect of lowering the fasting glucose level criterion for impaired fasting glucose from a lower limit of 6.1 mmol/L (110 mg/dL) to 5.6 mmol/L (100 mg/dL).
Prospective cohort study.
20 U.S. clinical centers.
2763 postmenopausal women with established coronary heart disease (CHD) who were followed for 6.8 years.
Any CHD event (nonfatal myocardial infarction or CHD death), stroke or transient ischemic attack (TIA), congestive heart failure (CHF) hospitalization, and any cardiovascular event.
During follow-up, 583 women had a CHD event, 329 women had a stroke or TIA, and 348 women were hospitalized for CHF. Women with diabetes were at an approximately 75% increased risk for each outcome compared with normoglycemic women. The 218 women with impaired fasting glucose according to the 1997 definition (fasting glucose level, 6.1 to 6.9 mmol/L [110 to 125 mg/dL]) had increased risk for any CHD event (hazard ratio, 1.37 [95% CI, 1.08 to 1.74]), while the 698 women with impaired fasting glucose according to the 2003 definition (fasting glucose level, 5.6 to 6.9 mmol/L [100 to 125 mg/dL]) were not at increased risk (hazard ratio, 1.09 [CI, 0.90 to 1.34]). Most of the women (n = 480) with fasting glucose levels between 5.6 mmol/L (100 mg/dL) and 6.0 mmol/L (109 mg/dL) had no increased risk for CHD (hazard ratio, 0.90 [CI, 0.73 to 1.12]). Women with impaired fasting glucose according to either definition were not at increased risk for stroke or TIA or CHF.
These findings may not be generalizable to men or women without existing heart disease.
Among postmenopausal women with coronary artery disease, the 2003 definition for impaired fasting glucose was not associated with increased risk for new CHD, stroke or TIA, or CHF.
Kanaya AM, Herrington D, Vittinghoff E, et al. Impaired Fasting Glucose and Cardiovascular Outcomes in Postmenopausal Women with Coronary Artery Disease. Ann Intern Med. 2005;142:813–820. doi: https://doi.org/10.7326/0003-4819-142-10-200505170-00006
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Published: Ann Intern Med. 2005;142(10):813-820.
Cardiology, Coronary Heart Disease, Coronary Risk Factors, Diabetes, Endocrine and Metabolism.
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