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Determinants of brachial artery mean 24 h pulse pressure in individuals with Type II diabetes mellitus and untreated mild hypertension.

Brachial artery pulse pressure is a predictor of (cardiovascular) morbidity, but its determinants in individuals with Type II diabetes and untreated mild hypertension have not been elucidated. We therefore cross-sectionally investigated determinants of brachial artery mean 24 h pulse pressure in 60 individuals (40 males; age, mean +/- S.D., 57.8 +/- 7.5 years) with Type II diabetes [median diabetes duration (interquartile range), 6.3 (3.6-10.1) years] and untreated mild hypertension [sitting blood pressure >140/90 mmHg and <190/120 mmHg (mean of two consecutive auscultatory office measurements after 5 min of rest)]. We measured (1) three potential determinants reflecting different aspects of central artery stiffness [the overall systemic arterial compliance, the aortic augmentation index and 1/(regional carotido-femoral transit time)], (2) structural and functional changes of the circulatory system often observed in Type II diabetes, and (3) diabetes-associated metabolic variables. After adjustment for age, gender and mean arterial pressure, brachial artery pulse pressure was associated with autonomic function [standardized regression coefficient (beta), -0.27 (P=0.01)], blood pressure decline during sleep [standardized beta, -0.32 (P=0.002)], fasting glucose concentration [standardized beta, 0.26 (P=0.01)], HbA(1c) concentration [standardized beta, 0.27 (P=0.003)] and diabetes duration [standardized beta, 0.28 (P=0.002)] in linear regression analyses. In a combined multivariate model, brachial artery pulse pressure was independently determined by gender [1=male, 2=female; standardized beta, 0.24 (P=0.01)], diabetes duration [standardized beta, 0.18 (P=0.03)], mean arterial pressure [standardized beta, 0.32 (P=0.002)], systemic arterial compliance [standardized beta, -0.23 (P=0.02)] and fasting glucose concentration [standardized beta, 0.20 (P=0.02)]. Aortic augmentation index and 1/(carotido-femoral transit time) were not independently associated with pulse pressure. In conclusion, in individuals with Type II diabetes and untreated mild hypertension, brachial artery pulse pressure is determined mainly by proximal aortic stiffness in a way which is not strongly influenced by peripheral pulse wave reflection. Approx. 60% of the variance in brachial artery pulse pressure could be explained by potentially modifiable determinants.