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

Abstract

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 24h 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 >140/90mmHg and <190/120mmHg (mean of two consecutive auscultatory office measurements after 5min 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 (β), -0.27 (P = 0.01)], blood pressure decline during sleep [standardized β, -0.32 (P = 0.002)], fasting glucose concentration [standardized β, 0.26 (P = 0.01)], HbA1c concentration [standardized β, 0.27 (P = 0.003)] and diabetes duration [standardized β, 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 β, 0.24 (P = 0.01)], diabetes duration [standardized β, 0.18 (P = 0.03)], mean arterial pressure [standardized β, 0.32 (P = 0.002)], systemic arterial compliance [standardized β, -0.23 (P = 0.02)] and fasting glucose concentration [standardized β, 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.