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 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.

Office and ambulatory pulse pressure—association with clinical characteristics and cardiovascular risk factors in normoalbuminuric patients with type 2 diabetes (ROADMAP study)

“…22 In a recent report, based on a small number of patients with type 2 diabetes, PP was related to albumin excretion. 23 The present study showed that office PP correlated with albumin excretion within the normoalbuminuric range. In this study we also found that patients in the higher office PP quartiles were characterized by the more pronounced albumin/ creatinine ratio.…”

Increased Central Artery Stiffness in Impaired Glucose Metabolism and Type 2 Diabetes

“…3 We then determined the average time delay (mean of 3 recordings of 4 seconds per artery) from the electrocardiograph trigger to 10% of the ascending slope of the distension curve of both arteries and subtracted the carotid value from the femoral value to obtain the carotid-femoral transit time. 14 Reproducibilities of the time-decay method, carotid pulse pressure, augmentation index, and carotid-femoral transit time have been reported. 3,14 …”

“…14 Reproducibilities of the time-decay method, carotid pulse pressure, augmentation index, and carotid-femoral transit time have been reported. 3,14 …”

“…Total systemic arterial compliance (mL/mm Hg) was determined according to 2 methods: the exponential-decay method based on the Windkessel model 13,14 and the ratio of stroke volume to aortic pulse pressure. 15 The first method used data obtained by applanation tonometry (vide infra).…”

Aggressive antihypertensive strategies based on hydrochlorothiazide, candesartan or lisinopril decrease left ventricular mass and improve arterial compliance in patients with type II diabetes mellitus and hypertension

“…[22][23][24] Briefly, we measured distensibility and compliance of the carotid, the femoral and the brachial arteries, Young's elastic modulus of the carotid artery and total systemic arterial compliance. These measurements were performed by use of an ultrasound scanner (Pie350 scanner, (linear array, 7.5 MHz transducer), Pie Medical BV, Maastricht, The Netherlands) that was connected to a PC equipped with vessel wall movement detection software and an acquisition system (Wall Track System, Pie Medical).…”