Central Blood Pressure Under Angiotensin and Calcium Channel Blockade

Abstract

Hemodynamic studies have shown that, in healthy subjects, there is a gradual widening of the height of the pressure waveform as it travels from the central (aortic) elastic arteries to the peripheral muscular arteries (brachial artery)1 (Figure). This disparity, which tends to disappear in the presence of vascular disease/aging, does not require any additional energy input within the arterial system, because the mean arterial pressure (MAP) and even the diastolic blood pressure (BP) remain almost unchanged between the 2 arterial sites. This finding is mainly attributed to the gradual increase (ie, amplification) of systolic BP (SBP) or pulse pressure (PP) along the arterial tree and is conventionally quantified as the ratio of the SBP or PP between the 2 sites (eg, SBP arm:SBP aorta)1 (Figure). Figure. Schematic personal representation of the forward and reflected pressure waves in the aorta and the influence of their timing on local PP. The definition of SBP amplification is indicated. In the present issue of Hypertension , Matsui et al2 have shown the superiority of calcium channel blockers (CCBs) over diuretics using the following protocol: the angiotensin receptor blocker olmesartan was combined with the CCB azelnidipine and compared with the same olmesartan associated with the diuretic hydrochlorothiazide. Central SBP was reduced to a greater degree with the CCB than with the hydrochlorothiazide. This resulted in an increase of SBP and PP amplification with the CCB, despite the lack of a significant difference in the brachial SBP reduction between the 2 …