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Meta-Analysis: Glycosylated Hemoglobin and Cardiovascular Disease in Diabetes Mellitus

Elizabeth Selvin, MPH; Spyridon Marinopoulos, MD, MBA; Gail Berkenblit, MD, PhD; Tejal Rami, MPH; Frederick L. Brancati, MD, MHS; Neil R. Powe, MD, MPH, MBA; and Sherita Hill Golden, MD, MHS
[+] Article and Author Information

From Johns Hopkins University Bloomberg School of Public Health and Johns Hopkins University School of Medicine, Baltimore, Maryland.


Grant Support: By the Agency for Healthcare Research and Quality (contract no. 290-97-0006). Ms. Selvin was supported by a grant from the National Heart, Lung, and Blood Institute (grant no. T32HL07024). Dr. Golden was supported by a grant from the Robert Wood Johnson Foundation Minority Medical Faculty Development Program. Dr. Brancati was supported by a Mid-Career Award for Patient-Oriented Research from the National Institutes of Health (contract no. K24-DK6222-O1). Dr. Powe was supported in part by a grant from the National Institute of Diabetes and Digestive and Kidney Diseases (grant no. K24DK02643).

Potential Financial Conflicts of Interest: None disclosed.

Requests for Single Reprints: Sherita Hill Golden, MD, MHS, Division of Endocrinology and Metabolism, Johns Hopkins University School of Medicine, 2024 East Monument Street, Suite 2-616, Baltimore, MD 21205; e-mail, sgolden1@jhem.jhmi.edu.

Current Author Addresses: Ms. Selvin, Ms. Rami, and Drs. Brancati, Powe, and Golden: Johns Hopkins University, Welch Center for Prevention, Epidemiology and Clinical Research, 2024 East Monument Street, Suite 2-600, Baltimore, MD 21205.

Dr. Marinopoulos: Johns Hopkins University, 10753 Falls Road, Suite 325, Lutherville, MD 21093.

Dr. Berkenblit: Johns Hopkins Outpatient Center, 601 North Caroline Street, Suite 7143, Baltimore, MD 21287.

Author Contributions: Conception and design: E. Selvin, S. Marinopoulos, T. Rami, F.L. Brancati, N.R. Powe, S.H. Golden.

Analysis and interpretation of the data: E. Selvin, S. Marinopoulos, G. Berkenblit, T. Rami, F.L. Brancati, N.R. Powe, S.H. Golden.

Drafting of the article: E. Selvin, S.H. Golden.

Critical revision of the article for important intellectual content: E. Selvin, S. Marinopoulos, G. Berkenblit, F.L. Brancati, N.R. Powe, S.H. Golden.

Final approval of the article: E. Selvin, S. Marinopoulos, G. Berkenblit, T. Rami, F.L. Brancati, N.R. Powe, S.H. Golden.

Statistical expertise: E. Selvin.

Obtaining of funding: F.L. Brancati, N.R. Powe, S.H. Golden.

Administrative, technical, or logistic support: T. Rami, N.R. Powe.

Collection and assembly of data: E. Selvin, S. Marinopoulos, G. Berkenblit, T. Rami, S.H. Golden.


Ann Intern Med. 2004;141(6):421-431. doi:10.7326/0003-4819-141-6-200409210-00007
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These data support a moderate increase in cardiovascular risk with increasing levels of glycosylated hemoglobin in persons with diabetes mellitus. This association seems to be similar in persons with type 1 and type 2 diabetes and is present across diverse geographic populations. In some studies, this association seems to be independent of other known risk factors for cardiovascular disease. The magnitude of the effect for total cardiovascular disease, fatal and nonfatal coronary heart disease, and stroke was similar. Compared with coronary heart disease and stroke, the pooled results of the few studies on glycosylated hemoglobin and peripheral arterial disease in persons with type 1 and type 2 diabetes suggest the possibility of a stronger association between glycosylated hemoglobin levels and this outcome (pooled risk estimates were 1.32 and 1.28 in persons with type 1 and type 2 diabetes, respectively). However, all pooled relative risk estimates reported here are based on small numbers of studies.

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Figure 1.
Relative risk (RR) estimates and 95% CIs for glycosylated hemoglobin (per 1–percentage point increase) and incident coronary heart disease and peripheral arterial disease in persons with type 1 diabetes.

Boxes are the relative risk estimates from each study; the horizontal bars are 95% CIs. The size of the box is proportional to the weight of the study in the pooled analysis. The studies are sorted by weight in the plot. Diamonds represent pooled random-effect estimates (per 1–percentage point higher glycosylated hemoglobin level). The vertical line at 1.0 indicates no effect of glycosylated hemoglobin on disease risk. The table on the right side of the graph indicates whether the study relative risk estimate was adjusted for relevant covariates. BMI = body mass index; DM = diabetes mellitus; WHR = waist-to-hip ratio. *Sample size of final multivariable analysis may differ from the sample size at baseline reported in Table 1. †Represents any measure of glycemic control, other than glycosylated hemoglobin, that was simultaneously included in the multivariable model (fasting blood glucose level, random blood glucose level, or C-peptide level).

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Figure 2.
Relative risk (RR) estimates and 95% CIs for glycosylated hemoglobin (per 1–percentage point increase) and incident cardiovascular disease in persons with type 2 diabetes.

Boxes are the relative risk estimates from each study; the horizontal bars are 95% CIs. The size of the box is proportional to the weight of the study in the pooled analysis. The studies are sorted by weight in the plot. Diamonds represent pooled random-effect estimates (per 1–percentage point higher glycosylated hemoglobin level). The vertical line at 1.0 indicates no effect of glycosylated hemoglobin on cardiovascular risk. The table on the right side of the graph indicates whether the study relative risk estimate was adjusted for relevant covariates. BMI = body mass index; DM = diabetes mellitus; WHR = waist-to-hip ratio. *Sample size of final multivariable analysis may differ from the sample size at baseline reported in Table 1. †Represents any measure of glycemic control, other than glycosylated hemoglobin, that was simultaneously included in the multivariable model (fasting blood glucose level or random blood glucose level).

Grahic Jump Location
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Figure 3.
Relative risk (RR) estimates and 95% CIs for glycosylated hemoglobin (per 1–percentage point increase) and incident peripheral arterial disease in persons with type 2 diabetes.

Boxes are the relative risk estimates from each study; the horizontal bars are 95% CIs. The size of the box is proportional to the weight of the study in the pooled analysis. The studies are sorted by weight in the plot. The diamond represents the pooled random-effect estimates (per 1–percentage point higher glycosylated hemoglobin level). The vertical line at 1.0 indicates no effect of glycosylated hemoglobin on peripheral arterial disease risk. The table on the right side of the graph indicates whether the study relative risk estimate was adjusted for relevant covariates. BMI = body mass index; DM = diabetes mellitus; WHR = waist-to-hip ratio. *Sample size of final multivariable analysis may differ from the sample size at baseline reported in Table 1. †Represents any measure of glycemic control, other than glycosylated hemoglobin, that was simultaneously included in the multivariable model (fasting blood glucose level or random blood glucose level).

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Summary for Patients

The Relationship between Blood Sugar Control and Cardiovascular Disease in Patients with Diabetes

The summary below is from the full report titled “Meta-Analysis: Glycosylated Hemoglobin and Cardiovascular Disease in Diabetes Mellitus.” It is in the 21 September 2004 issue of Annals of Internal Medicine (volume 141, pages 421-431). The authors are E. Selvin, S. Marinopoulos, G. Berkenblit, T. Rami, F.L. Brancati, N.R. Powe, and S. Hill Golden.

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