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Diabetes Care, Vol 22, Issue 10 1722-1727, Copyright © 1999 by American Diabetes Association


ARTICLES

Augmentation of central arterial pressure in type 1 diabetes

B Brooks, L Molyneaux and DK Yue
Diabetes Center, Royal Prince Alfred Hospital, Camperdown, NSW, Australia. belinda@diab.rpa.cs.nsw.gov.au

OBJECTIVE: Atherosclerosis is more severe in individuals with diabetes. Whether diabetic subjects have accelerated arterial hardening (i.e., arteriosclerosis) is less clear. Arteriosclerosis increases pulse-wave velocity and can augment central arterial pressure due to early wave reflection. The aim of this study was to determine whether subjects with type 1 diabetes had evidence of increased arterial stiffness by using pulse-wave analysis. RESEARCH DESIGN AND METHODS: Radial artery pressure waveforms were obtained noninvasively by applanation tonometry (PWV Medical Blood Pressure Analysis System, Sydney). A central aortic waveform can be derived by using a transfer function used in previous studies during cardiac catheterization. A total of 89 subjects with type 1 diabetes (46 men and 43 women, aged 34.0 +/- 11.0 years, duration of diabetes 13.1 years [interquartile range 5.8-24.3], HbA1c 8.2 +/- 1.7%) and 95 control subjects (44 men and 51 women, aged 36.1 +/- 12.0 years) were studied. The central aortic waveform allowed the determination of 1) the aortic augmentation index (AAI), a parameter that reflects the degree to which central arterial pressure is augmented by wave reflection, and 2) the subendocardial viability ratio (SEVR), which is a measure of myocardial perfusion relative to cardiac workload. RESULTS: In multivariate analysis, diabetes was an important determinant of AAI (P = 0.001). The higher AAI was mainly evident in the men, for whom diabetes was a highly significant covariate (P = 0.006); this was not the case for diabetic women (P = 0.2). Nondiabetic men had a lower AAI than nondiabetic women (103.7 +/- 18.6 vs. 117.0 +/- 22.3%, respectively, P = 0.002), but this difference was abolished by diabetes (110.7 +/- 18.5 vs. 116.1 +/- 18.7%, respectively, P = 0.2). Subjects with type 1 diabetes had a significantly lower mean SEVR compared with control subjects (139.2 +/- 28.3 vs. 163.6 +/- 27.4%, respectively, P < 0.0001). In multivariate analysis, diabetes was an important determinant of SEVR (P = 0.001). A significant interaction between diabetes and age was evident (P = 0.0001), which suggests that the effect of age is modified by diabetes. CONCLUSIONS: These findings suggest that central systolic blood pressure is increased in relatively young individuals with type 1 diabetes, although myocardial perfusion related to cardiac workload is decreased. These changes can be explained by more rapid pulse-wave velocity resulting from arterial stiffening.
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