Share this article on:

Clinical usefulness of noninvasively estimated central blood pressure

Chen, Yi; Wang, Ji-Guang

doi: 10.1097/HJH.0000000000001744
Editorial Commentaries

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.

Back to Top | Article Outline


Conflicts of interest

There are no conflicts of interest.

Back to Top | Article Outline


1. Avolio AP, Van Bortel LM, Boutouyrie P, Cockcroft JR, McEniery CM, Protogerou AD, et al. Role of pulse pressure amplification in arterial hypertension: experts’ opinion and review of the data. Hypertension 2009; 54:375–383.
2. Kollias A, Lagou S, Zeniodi ME, Boubouchairopoulou N, Stergiou GS. Association of central versus brachial blood pressure with target-organ damage: systematic review and meta-analysis. Hypertension 2016; 67:183–190.
3. Jankowski P, Kawecka-Jaszcz K, Czarnecka D, Brzozowska-Kiszka M, Styczkiewicz K, Loster M, et al. Pulsatile but not steady component of blood pressure predicts cardiovascular events in coronary patients. Hypertension 2008; 51:848–855.
4. Vlachopoulos C, Aznaouridis K, O’Rourke MF, Safar ME, Baou K, Stefanadis C. Prediction of cardiovascular events and all-cause mortality with central haemodynamics: a systematic review and meta-analysis. Eur Heart J 2010; 31:1865–1871.
5. Ding FH, Li Y, Li LH, Wang JG. Impact of heart rate on central hemodynamics and stroke: a meta-analysis of β-blocker trials. Am J Hypertens 2013; 26:118–125.
6. Shimamoto K, Ando K, Fujita T, Hasebe N, Higaki J, Horiuchi M, et al. The Japanese Society of Hypertension guidelines for the management of hypertension (JSH 2014). Hypertens Res 2014; 37:253–390.
7. Mancia G, Fagard R, Narkiewicz K, Redon J, Zanchetti A, Böhm M, et al. 2013 ESH/ESC Guidelines for the management of arterial hypertension: the Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). J Hypertens 2013; 31:1281–1357.
8. Kelly R, Karamanoglu M, Gibbs H, Avolio A, O’Rourke M. Noninvasive carotid pressure wave registration as an indicator of ascending aortic pressure. J Vasc Med Biol 1989; 1:241–247.
9. Wang KL, Cheng HM, Sung SH, Chuang SY, Li CH, Spurgeon HA, et al. Wave reflection and arterial stiffness in the prediction of 15-year all-cause and cardiovascular mortalities: a community-based study. Hypertension 2010; 55:799–805.
10. Roman MJ, Okin PM, Kizer JR, Lee ET, Howard BV, Devereux RB. Relations of central and brachial blood pressure to left ventricular hypertrophy and geometry: the Strong Heart Study. J Hypertens 2010; 28:384–388.
11. Salvi P, Lio G, Labat C, Ricci E, Pannier B, Benetos A. Validation of a new noninvasive portable tonometer for determining arterial pressure wave and pulse wave velocity: the PulsePen device. J Hypertens 2004; 22:2285–2293.
12. Takazawa K, Kobayashi H, Shindo N, Tanaka N, Yamashina A. Relationship between radial and central arterial pulse wave and evaluation of central aortic pressure using the radial arterial pulse wave. Hypertens Res 2007; 30:219–228.
13. Odaira M, Tomiyama H, Hashimoto H, Kojima I, Matsumoto C, Yamashina A, et al. Increased arterial stiffness weakens the relationship between wave reflection and the central pressure indexes in men younger than 60 years of age. Am J Hypertens 2011; 24:881–886.
14. Horváth IG, Németh Á, Lenkey Z, Alessandri N, Tufano F, Kis P, et al. Invasive validation of a new oscillometric device (Arteriograph) for measuring augmentation index, central blood pressure and aortic pulse wave velocity. J Hypertens 2010; 28:2068–2075.
15. Williams B, Lacy PS, Yan P, Hwee CN, Liang C, Ting CM. Development and validation of a novel method to derive central aortic systolic pressure from the radial pressure waveform using an N-point moving average method. J Am Coll Cardiol 2011; 57:951–961.
16. Weber T, Wassertheurer S, Rammer M, Maurer E, Hametner B, Mayer CC, et al. Validation of a brachial cuff-based method for estimating central systolic blood pressure. Hypertension 2011; 58:825–832.
17. Climie RE, Schultz MG, Nikolic SB, Ahuja KD, Fell JW, Sharman JE. Validity and reliability of central blood pressure estimated by upper arm oscillometric cuff pressure. Am J Hypertens 2012; 25:414–420.
18. Pucci G, Cheriyan J, Hubsch A, Hickson SS, Gajendragadkar PR, Watson T, et al. Evaluation of the Vicorder, a novel cuff-based device for the noninvasive estimation of central blood pressure. J Hypertens 2013; 31:77–85.
19. Cheng HM, Sung SH, Shih YT, Chuang SY, Yu WC, Chen CH. Measurement accuracy of a stand-alone oscillometriccentral blood pressure monitor: avalidation report for Microlife WatchBP Office Central. Am J Hypertens 2013; 26:42–50.
20. Peng X, Schultz MG, Abhayaratna WP, Stowasser M, Sharman JE. Comparison of central blood pressure estimated by a cuff-based device with radial tonometry. Am J Hypertens 2016; 29:1173–1178.
21. Lindroos AS, Langén VL, Kantola I, Salomaa V, Juhanoja EP, Sivén SS, et al. Relation of blood pressure and organ damage: comparison between feasible, noninvasive central hemodynamic measures and conventional brachial measures. J Hypertens 2018; 36:1276–1283.
22. Sharman JE, Avolio AP, Baulmann J, Benetos A, Blacher J, Blizzard CL, et al. Validation of noninvasive central blood pressure devices: ARTERY Society task force consensus statement on protocol standardization. Eur Heart J 2017; 38:2805–2812.
23. Huang CM, Wang KL, Cheng HM, Chuang SY, Sung SH, Yu WC, et al. Central versus ambulatory blood pressure in the prediction of all-cause and cardiovascular mortalities. J Hypertens 2011; 29:454–459.
Copyright © 2018 Wolters Kluwer Health, Inc. All rights reserved.