Published Online
on July 12, 2004

A more recent version of this article appeared on July 27, 2004

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Submitted on November 18, 2003
Revised on April 8, 2004
Accepted on April 12, 2004

Glycated Hemoglobin Level Is Strongly Related to the Prevalence of Carotid Artery Plaques With High Echogenicity in Nondiabetic Individuals. The Tromsø Study

Lone Jørgensen PhD^*, Trond Jenssen MD, PhD, Oddmund Joakimsen MD, PhD, Ivar Heuch PhD, Ole Christian Ingebretsen MD, PhD, and Bjarne K. Jacobsen PhD

From the Institute of Community Medicine, University of Tromsø (L.J., O.J., B.K.J.); Departments of Physiotherapy (L.J.), Neurology (O.J.), and Clinical Chemistry (O.C.I.), University Hospital of Northern Norway, Tromsø; Medical Department, Division of Nephrology, Rikshospitalet, Oslo (T.J.); and Department of Mathematics, University of Bergen, Bergen (I.H.), Norway.

^* To whom correspondence should be addressed. E-mail: lone.jorgensen{at}ism.uit.no.

Background--High levels of HbA_1c have been associated with increased mortality and an increased risk of atherosclerosis assessed as carotid intima-media thickness or plaque prevalence. In the present population-based study, we examined the association between HbA_1c and plaque prevalence with emphasis on plaque echogenicity in subjects not diagnosed with diabetes.

Methods and Results--HbA_1c measurements and ultrasonography of the carotid artery were performed in 5960 subjects (3026 women, 2934 men) 25 to 84 years of age. Plaque morphology was categorized into 4 groups from low echogenicity (soft plaque) to strong echogenicity (hard plaque). HbA_1c was categorized into 5 groups: <5.0%, 5.0% to 5.4%, 5.5% to 5.9%, 6.0% to 6.4% and >6.4%. Carotid plaque prevalence increased with increasing HbA_1c level (P for linear trend=0.002). The OR for hard plaques versus no plaques was 5.8 in the highest HbA_1c group (>6.4%) compared with subjects in the lowest group (<5.0%) after adjustment for several possible confounders. The risk of predominantly hard plaques was also significantly associated with HbA_1c levels, although the ORs at each level were somewhat lower than for hard plaques. With respect to the risk of soft plaques versus no plaques, no statistically significant relationship with HbA_1c levels was found.

Conclusions--Metabolic changes reflected by HbA_1c levels may contribute to the development of hard carotid artery plaques, even at modestly elevated levels.

Key words: carotid arteries • plaque • hemoglobin A, glycosylated • ultrasonics

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