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Hypertension. 2008;52:e24-e25
Published online before print July 28, 2008, doi: 10.1161/HYPERTENSIONAHA.108.118513
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(Hypertension. 2008;52:e24.)
© 2008 American Heart Association, Inc.


Letters to the Editor

Impact of Radial Artery Pressure Waveform Calibration on Estimated Central Pressure Using a Transfer Function Approach

Patrick Segers

Cardiovascular Mechanics and Biofluid Dynamics, IBiTech, Ghent University, Ghent, Belgium

Dries Mahieu

Department of Pharmacology, Ghent University Hospital, Ghent, Belgium

Ernst R. Rietzschel; Marc L. De Buyzere

Department of Cardiovascular Diseases, Ghent University Hospital, Ghent, Belgium

Luc M. Van Bortel

Department of Pharmacology, Ghent University Hospital, Ghent, Belgium

To the Editor:

It is with great interest that we have read the excellent work of McEniery et al1 on the variability of the relation between central and brachial pulse pressure (pressure amplification), assessed in >10 000 subjects. We were, however, a little surprised about the magnitude of the central-to-brachial pressure amplification, which is in the order of 1.38 for the entire population (estimated from their Table 1). We hypothesize that these high values arise from the use of central aortic pressure curves synthesized from radial pressure tracings, with the most important factor not being the generalized pressure transfer function but the calibration of the radial pressure waveforms. To illustrate this, we applied 4 calibration strategies to radial artery pressure waveforms measured within the framework of the Asklepios Study.2


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Table. Pulse Pressure (SD) at Radial, Brachial, and Ascending Aorta Obtained With Radial-to-Aorta Transfer Function in Millimeters of Mercury

All of the strategies assume equal radial and brachial diastolic blood pressure (DBP). Method 1 further assumes similar radial and brachial systolic blood pressure (SBPBA and SBPRA, SBPBA=SBPRA; ignoring brachial-to-radial amplification). Methods 2 to 4 assume similar radial and brachial mean blood pressure (MAP), but MAP is calculated differently, as follows:

Method 2: one-third rule: MAP=DBP+(SBP–DBP)/3.

Method 3: 40% rule: MAP=DBP+0.4(SBP–DBP), following Bos et al.3

Method 4: pressure curve: MAP is the average of a calibrated brachial pressure curve.4

Central pressure waveforms were calculated using the transfer function as published by Karamanoglu et al,5 and the ratio of brachial:aortic pulse pressure was calculated (Table).

Data clearly demonstrate the impact of the calibration procedure on the brachial-to-aortic amplification factor. Strategies 1 and 2 explicitly ignore or do not lead to brachial-to-radial amplification; application of the transfer function to a nonamplified wave will yield a central pulse pressure, which is lower than the value obtained after transferring a radial pressure wave where some brachial-to-radial amplification has been accounted for (methods 3 and 4).

Definite proof of the importance of brachial-to-radial amplification can only be provided by invasive data, but it seems unlikely that central-to-peripheral amplification would not continue in the radial artery. Invasive data have demonstrated that the one-third rule underestimates MAP3 and, as illustrated in the Table, causes subsequent low estimates of radial SBP on radial artery waveform calibration.

Tonometer (radial and carotid) waveform calibration is a key factor in noninvasive central pressure estimation, often based on MAP estimated with the one-third rule. We might need to reconsider this widely adopted rule-of-thumb, especially in times where the debate is held on pressure differences in the order of a few millimeters of mercury. Moreover, given the fact that central-to-brachial amplification is susceptible to hemodynamic factors, such as heart rate, and to cardiovascular risk factors,1 it is per definition that a simple estimate of MAP based on only SBP and DBP must be susceptible to these very same factors.


*    Acknowledgments
 
Source of Funding

This research was partly funded by FWO research grant G.0427.03 (the Asklepios Study).

Disclosures

None.


*    References
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*References
 
1. McEniery CM, McDonnell B, Munnery M, Wallace SM, Rowe CV, Cockcroft JR, Wilkinson IB. Central pressure: variability and impact of cardiovascular risk factors–the Anglo-Cardiff Collaborative Trial II. Hypertension. 2008; 51: 1476–1482.[Abstract/Free Full Text]

2. Rietzschel ER, De Buyzere ML, Bekaert S, Segers P, De Bacquer D, Cooman L, Van Damme P, Cassiman P, Langlois M, Van Oostveldt P, Verdonck P, De Backer G, Gillebert TC. Rationale, design, methods and baseline characteristics of the Asklepios Study. Eur J Cardiovasc Prev Rehabil. 2007; 14: 179–191.[CrossRef][Medline] [Order article via Infotrieve]

3. Bos WJW, Verrij E, Vincent HH, Westerhof BE, Parati G, van Montfrans GA. How to assess mean blood pressure properly at the brachial artery level. J Hypertens. 2007; 25: 751–755.[Medline] [Order article via Infotrieve]

4. Van Bortel LM, Balkestein EJ, van der Heijden-Spek JJ, Vanmolkot FH, Staessen JA, Kragten JA, Vredeveld JW, Safar ME, Struijker Boudier HA, Hoeks AP. Non-invasive assessment of local arterial pulse pressure: comparison of applanation tonometry and echo-tracking. J Hypertens. 2001; 19: 1037–1044.[CrossRef][Medline] [Order article via Infotrieve]

5. Karamanoglu M, O'Rourke MF, Avolio AP, Kelly RP. An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man. Eur Heart J. 1993; 14: 160–167.[Abstract/Free Full Text]




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C. M. McEniery, J. R. Cockcroft, and I. B. Wilkinson
Response to Impact of Radial Artery Pressure Waveform Calibration on Estimated Central Pressure Using a Transfer Function Approach
Hypertension, September 1, 2008; 52(3): e26 - e26.
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This Article
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