ß-blocker Treatment is Associated with High Augmentation Index and with High Aortic, but not Brachial, Pulse Pressure in Type 2 Diabetes
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In patients with type 2 diabetes, the risk of premature mortality is predicted by brachial pulse pressure (PP) as measured either in the clinic [] or during ambulatory blood pressure (BP) measurement []. Brachial PP is considered to be an indirect marker of arterial stiffness []. However, due to pressure wave amplification caused by pulse wave reflections from peripheral reflection sites of the arterial tree, PP is amplified throughout the vascular bed, and accordingly, brachial PP is not the same as central (aortic) PP []. The proportion of the central PP that is accounted for by such augmentation caused by reflected pulse waves is referred to as the central augmentation index (AIx) []. By recording the contour of the radial pulse wave form with an applanation tonometer, and by applying a validated transfer function [, ], the shape of the corresponding aortic wave form can be generated and central hemodynamic indices, such as the central PP and the central AIx can be determined. Given the proximity of the aorta to target organs, such as the heart, the carotid arteries, and the brain, it is plausible to believe that such central hemodynamic parameters are more appropriate markers of risk than brachial PP. Previous investigations have shown that central AIx is related to markers of cardiovascular risk [] and with the risk of coronary artery disease [], and that treatment-induced changes of central AIx are superior to treatment-induced changes of brachial BP for the prediction of left ventricular hypertrophy (LVH) regression []. As for central PP, it predicts cardiovascular events better than brachial PP []. In patients with type 2 diabetes, central but not brachial PP has been shown to be independently associated with left ventricular mass [], and in treated hypertensives, LVH regression is influenced more by treatment-induced changes in central PP than by brachial PP [, ]. Interestingly, -blockers have been shown to lower the central systolic BP, a main determinant of central PP, less effectively than other antihypertensive drugs [–]. Furthermore, patients who were randomly assigned to atenolol-based antihypertensive treatment had higher central PP compared with patients assigned to amlodipine-based treatment, but no difference in clinic PP was observed between the two groups []. This difference in central PP would not have been discovered in clinical practice, and may account for the less favorable outcome that has been associated with -blockers in patients with diabetes and hypertension [, ]. However, there are no data regarding the associations between -blockade, central PP levels, and central AIx in unselected patients with type 2 diabetes treated in primary care. Therefore, our aim was to investigate whether the clinic, ambulatory, and central PP and central AIx, respectively, differed in patients treated with or not treated with -blockers in a population-based cohort of middle-aged patients with type 2 diabetes and treated hypertension. To evaluate other markers of hypertensive target organ damage, we also performed echocardiography, carotid artery ultrasonography, and measurements of aortic pulse wave velocity (PWV).
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Keywords
β, cardiac mass, diabetes, hypertension, pulse pressure,
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