DOI: 10.1097/HJH.0b013e3281c4a046

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PMID: 17563552

Issn Print: 0263-6352

Publication Date: 2007/07/01


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How to estimate central pressure augmentation?

Stéphane Laurent

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The CAFE study [1], an ancillary study of the ASCOT study [2], showed in 2073 hypertensive patients that the reduction in central systolic blood pressure (SBP), pulse pressure (PP) and augmentation index (AIx) was higher in patients receiving vasodilating drugs [calcium channel blocker (CCB) + angiotensin-converting enzyme inhibitor (CEI)] than in patients receiving a nonvasodilating beta-blocker and a diuretic, despite similar reduction in SBP and PP at the brachial level. Because, in the ASCOT study [2], amlodipine-based treatment proved to be more effective than atenolol-based treatment for reducing cardiovascular (CV) events, the question arises whether the reduction in CV events is better predicted by central blood pressure (BP) (SBP, PP and AIx) than brachial BP. Unfortunately, because central PP and AIx were not measured at baseline in the CAFÉ study [1] but only after 1 year of treatment, it was not possible to determine the amplitude of central PP and AIx reduction, and thus its influence on CV events.
Central SBP and PP may better estimate the true load imposed on the left ventricle and arterial walls than brachial SBP and PP, because they take into account the ‘amplification phenomenon’ [3]. Briefly, the arterial pressure waveform is a composite of the forward pressure wave created by ventricular contraction and a reflected wave. Waves are reflected from the periphery, mainly at branch points or sites of impedance mismatch. In elastic vessels, because velocity of the pressure wave along the arterial tree (pulse wave velocity, PWV) is low, the reflected wave tends to arrive back at the aortic root during diastole. In the case of stiff arteries, PWV rises and the reflected wave arrives back at the central arteries earlier, adding to the forward wave, and augmenting the systolic pressure. This can be quantified through the AIx, defined as the difference between the second and first systolic peaks expressed as a percentage of the pulse pressure [3]. In peripheral arteries, wave reflections can amplify the pressure wave because reflection sites are closer to peripheral sites than to central arteries, and PWV is higher in a peripheral stiffer artery. The net result is that the amplitude of the pressure wave is higher in peripheral arteries than in central arteries, the so-called ‘amplification phenomenon’. These data strongly suggest that therapy based on brachial artery recordings may overestimate the lowering effect of nonvasodilating beta-blockers on central aortic SBP and PP and underestimate the effectiveness of vasodilators, including CCBs and ACEIs [4].
It is thus mandatory to estimate central PP and AIx during large clinical trials to determine whether the reduction in central PP and AIx is associated with a concomitant reduction in CV events, independently of the lowering of brachial BP and normalization of classical CV risk factors [4].
How to determine central PP and AIx? This issue has been a matter of debate for several years. Direct measurements of carotid (i.e. central) pressure waveforms by applanation tonometry are technically challenging, with moderate-to-large between-observer variability [4]. The most widely-used approach is to perform radial artery tonometry and then apply an inverse transfer function to reconstruct the aortic pressure waveform from the radial waveform [5–7]. Indeed, by contrast to the carotid artery, the radial artery is well supported by bony tissue, making optimal applanation easier to achieve.
Although the use of a general transfer function has been well established and has demonstrated its reliability for calculating central PP in the CAFE study [1], the accuracy of this approach for the determination of aortic AIx has been disputed [8–10].

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