BACKGROUND AND PURPOSE: Deteriorating glucose tolerance is associated with an increased cardiovascular disease (CVD) risk. The underlying mechanisms remain unclear. Arterial remodeling is the change in structural properties through time in response to atherogenic and/or hemodynamic alterations and aims to maintain circumferential wall stress constant (sigma(C)). Arterial remodeling has not been studied in relation to glucose tolerance. METHODS: The study population consisted of 278 people with normal glucose metabolism, 168 with impaired glucose metabolism, and 301 with type 2 diabetes (DM-2); their mean age was 67.8 years. We assessed carotid intima-media thickness (IMT), interadventitial diameter (IAD), lumen diameter (LD), and sigma(C). RESULTS: After adjustment for age, sex, height, body mass index, and prior CVD, DM-2 was associated with increased IAD, IMT, and sigma(C) but not LD (regression coefficients: 0.24 mm; 95% confidence interval [CI], 0.07 to 0.41; 0.050 mm; 95% CI, 0.024 to 0.077; 5.00 kPa; 95% CI, 0.92 to 9.08; and 0.13 mm; 95% CI, -0.03 to 0.29, respectively). After additional adjustment for pulse pressure, the association between DM-2 and IAD disappeared, whereas the association with IMT remained. After adjustment, impaired glucose metabolism was not significantly associated with LD (0.12 mm; 95% CI, -0.06 to 0.33), sigma(C) (0.25 kPa; 95% CI, -4.49 to 4.98), IAD (0.08 mm; 95% CI, -0.11 to 0.27), or IMT (0.029 mm; 95% CI, -0.002 to 0.060). However, the IMT regression coefficient was half that of DM-2. CONCLUSIONS: DM-2 is associated with preserved LD at increased IMT, which, however, does not normalize the increased sigma(C). In contrast, impaired glucose metabolism is not associated with changes in LD or IAD, whereas IMT is moderately increased but sigma(C) remains constant. Carotid remodeling in DM-2 thus appears maladaptive, which may explain the increased CVD risk, especially stroke, in DM-2.
BACKGROUND AND PURPOSE: Deteriorating glucose tolerance is associated with an increased cardiovascular disease (CVD) risk. The underlying mechanisms remain unclear. Arterial remodeling is the change in structural properties through time in response to atherogenic and/or hemodynamic alterations and aims to maintain circumferential wall stress constant (sigma(C)). Arterial remodeling has not been studied in relation to glucose tolerance. METHODS: The study population consisted of 278 people with normal glucose metabolism, 168 with impaired glucose metabolism, and 301 with type 2 diabetes (DM-2); their mean age was 67.8 years. We assessed carotid intima-media thickness (IMT), interadventitial diameter (IAD), lumen diameter (LD), and sigma(C). RESULTS: After adjustment for age, sex, height, body mass index, and prior CVD, DM-2 was associated with increased IAD, IMT, and sigma(C) but not LD (regression coefficients: 0.24 mm; 95% confidence interval [CI], 0.07 to 0.41; 0.050 mm; 95% CI, 0.024 to 0.077; 5.00 kPa; 95% CI, 0.92 to 9.08; and 0.13 mm; 95% CI, -0.03 to 0.29, respectively). After additional adjustment for pulse pressure, the association between DM-2 and IAD disappeared, whereas the association with IMT remained. After adjustment, impaired glucose metabolism was not significantly associated with LD (0.12 mm; 95% CI, -0.06 to 0.33), sigma(C) (0.25 kPa; 95% CI, -4.49 to 4.98), IAD (0.08 mm; 95% CI, -0.11 to 0.27), or IMT (0.029 mm; 95% CI, -0.002 to 0.060). However, the IMT regression coefficient was half that of DM-2. CONCLUSIONS:DM-2 is associated with preserved LD at increased IMT, which, however, does not normalize the increased sigma(C). In contrast, impaired glucose metabolism is not associated with changes in LD or IAD, whereas IMT is moderately increased but sigma(C) remains constant. Carotid remodeling in DM-2 thus appears maladaptive, which may explain the increased CVD risk, especially stroke, in DM-2.
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