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Clinical usefulness of noninvasively estimated central blood pressure

Chen, Yi; Wang, Ji-Guang

doi: 10.1097/HJH.0000000000001744

Department of Hypertension, Centre for Epidemiological Studies and Clinical Trials, Shanghai Key Laboratory of Hypertension, The Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

Correspondence to Ji-Guang Wang, MD, PhD, Department of Hypertension, Centre for Epidemiological Studies and Clinical Trials, Shanghai Key Laboratory of Hypertension, The Shanghai Institute of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Ruijin 2nd Road 197, Shanghai 200025, China. Tel: +86 21 64370045x610911; fax: +86 21 64662193; e-mail:

Blood pressure (BP) measured at the brachial artery is a documented predictor of cardiovascular risk and events. However, it is also appreciated that peripheral arterial pressure may be an inaccurate substitute for the BP in the central aorta [1]. SBP is usually lower in the central aorta than in the brachial artery, as pulse pressure (PP) is amplified from central to peripheral arteries, the pressure amplification varying between individuals. The heart and large arteries are directly exposed to the central rather than the peripheral BP. Thus, central BP may potentially have a superior value for prediction of cardiovascular events [2].

There is indeed growing evidence that central BP is better related to the risk of future cardiovascular events than brachial BP [3,4]. Antihypertensive drugs have differential effects on brachial and central BPs [5]. In general, β-blockers are less efficacious in lowering central BP than other classes of antihypertensive drugs, such as angiotensin-converting enzyme inhibitors, AT1 blockers and calcium channel blockers [5]. Some [6], though not all [7], current hypertension guidelines recommend central BP for risk assessment in the management of hypertension.

Central BP can be accurately measured with intra-arterial catheters [3]. Invasive techniques, however, cannot be used in clinical practice, which has led to the development, in the last decades, of a variety of noninvasive methods to calculate central BP-based cardiovascular risk in hypertension and other chronic diseases [8–20]. The general principle of these noninvasive methods is to record the pressure waveforms from peripheral arterial sites (e.g. radial, brachial and carotid arteries), calibrate them against peripheral BP and then derive central BP by use of a transfer function or identification of pressure waveform components reflecting central BP values (Table 1).



Applanation tonometry is the currently recommended noninvasive method to obtain central BP. This method requires the acquisition of a carotid pressure waveform that is considered as a surrogate for central aortic pressure waveform [8–9,11] or a peripheral arterial pressure waveform that is subsequently transformed into a central aortic pressure waveform by a generalized transfer function [10] or the identification of its late systolic shoulder which is taken as an approximation for central SBP [12,13]. The applanation tonometry method requires training and is operator-dependent. Although it may be clinically useful, it is time consuming and costly, which limits its use in medical practice. The pulse volume plethysmography method has been recently developed, based on oscillometric BP monitors that use either the subdiastolic or suprasystolic waveform analysis method with a generalized transfer function [16–18,20] or a ‘multivariate regression equation’ for the derivation of the central haemodynamic parameters from the oscillometrically collected brachial pressure waveforms calibrated against brachial BP [19].

The ‘regression equation’ method was applied to the device for the measurement of central BP in the article by Lindroos et al. [21] published in this issue of the Journal. This device has been previously validated against invasive central BP measurement in patients undergoing cardiac catheterization [18]. This has limitations as the ‘regression equation’ may not have a general value. That is, the intercept and coefficient of a regression equation may be population specific, and the method may not be generalizable to populations other than the one in which the equation was developed and validated. At present, there is no standardized protocol for the validation of such devices and algorithms [22]. Indeed, the correlating of the central BP obtained by this device with clinical outcomes, such as the current study [21], may represent as a device validation.

The basic finding of the current study was that the central SBP and PP obtained with the noninvasive BP monitor had similar associations with hypertensive end-organ damage as their brachial counterparts [21]. In other words, central and brachial measurements of SBP and PP had a similar discriminatory power to detect left ventricular hypertrophy or carotid intima–media thickening. Thus, the study did not show any incremental value of central BP in assessing hypertensive end-organ damage over and above brachial BP measurements.

Which can be the explanation for this negative finding, the inadequacy of the notion that central BP is prognostically superior, the inadequacy of the device or the limitations of the data obtained in the study? Although very unlikely, the inadequacy that central BP is prognostically superior to peripheral BP can be in theory an explanation. Even when measured at the brachial artery, BP is highly predictive of cardiovascular events. The central and brachial BPs are closely correlated. The predictive value of central BP over and beyond brachial BP may be too tiny to unveil, especially when brachial BP measurements are accurate, well standardized or obtained in ambulatory conditions, that is when association of peripheral BP with events is closer [23].

The device is a more likely explanation, as its ability to derive central BP may not be sufficiently accurate to show its superiority over brachial BP for the association with target organ damage. As mentioned above and acknowledged in the article [21], a multivariate regression equation was used for the estimation of central BP, but a regression equation validated in other populations may not be applicable to the current study population. This technical issue might also explain why in the current study, central SBP was higher than its brachial counterpart, which is in contrast to the widespread notion that the reverse is indeed the case of central haemodynamics. In addition, previous studies using the carotid or radial applanation tonometry method consistently showed that central BP was more closely associated with left ventricular hypertrophy and carotid intima–media thickening than brachial BP [2]. In devices implemented with the pulse volume recording technique, the accuracy of measurement should be compared between the two algorithm approaches of regression equation and generalized transfer function.

Several design and technical issues might also weaken the conclusion of the current study that there is no difference between central and brachial BPs in their relationship with target organ damage. Both left ventricular mass and intima–media thickness are structural. Structural measures are often the consequence of long-term influence. A cross-sectional study usually has limited power to show any difference in structural measures. The negative finding of the current study does not exclude the possibility that the central and brachial BPs still have different clinical significance for functional measures and in longitudinal studies for structural measures, such as cardiac and vascular hypertrophy.

In the field of central haemodynamics, technology and apparatus for measurement are still the main topics of research. Accurate devices are essential for clinical research as well as practice. There is an urgent need for standardized protocol for validation of central BP measuring devices [22]. In addition, as we have achieved with research on brachial BP, prospective observational and intervention studies are required to determine the clinical significance of central haemodynamics for cardiovascular prediction and disease prevention by treatment.

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Conflicts of interest

There are no conflicts of interest.

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