Glucose-related arterial stiffness and carotid artery remodeling: a study in normal subjects and type 2 diabetes patients.

Kozakova, Michaela; Morizzo, Carmela; Bianchi, Cristina; Di Filippi, Marianna; Miccoli, Roberto; Paterni, Marco; Di Bello, Vitantonio; Palombo, Carlo · J Clin Endocrinol Metab · 2014

case_control · Level III

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Abstract

Hyperglycemia is associated with a higher carotid intima-media thickness (IMT); however, it is not established whether this increase reflects early atherosclerotic changes or adaptive remodeling responding to hyperglycemia-induced alteration in mechanical properties of the arterial wall. The aims of this study were to compare carotid geometry and circumferential wall stress between patients with type 2 diabetes mellitus (T2DM) and healthy controls and to evaluate the associations between chronic glucose exposure and measures of arterial structure and function. This was a case-control and cross-sectional study within institutional practice. PARTICIPANTS included 133 T2DM patients free of cardiovascular complications and 133 healthy controls with normal glucose metabolism, matched for sex, age, and body mass index. Common carotid artery (CCA) IMT, luminal diameter, wave speed, and local pulse pressure (PP) were evaluated. As compared with controls, T2DM patients had higher (P < .0001) CCA IMT (640 ± 81 vs 709 ± 118 μm), luminal diameter (6.12 ± 0.67 vs 6.69 ± 0.56 mm), and brachial PP (47 ± 7 vs 57 ± 12 mm Hg), whereas luminal radius to IMT ratio (4.8 ± 0.7 vs 4.8 ± 0.8, P = .57) and circumferential wall stress (49.0 ± 8.3 vs 50.6 ± 10.3 kPa, P = .26) were comparable between the 2 groups. In T2DM patients, glycosylated hemoglobin was independently related to CCA wave speed and local PP, but not to IMT that was determined by age, local PP, and luminal diameter. This study suggests that the increase in IMT associated with a higher glucose exposure might reflect adaptive remodeling counteracting an increase in pulsatile strain and preventing increase in circumferential wall stress caused by luminal enlargement of stiff arteries.

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