Response to Flawed Measurement of Brachial Tonometry for Calculating Aortic Pressure?
We share O’Rourke and Takazawa’s1 interest in and pursuit of reliable, accurate noninvasive central blood pressure assessment. To that end, we use carotid applanation tonometry, calibrated with diastolic and mean blood pressures, for which we rely on brachial tonometry.
In the Asklepios Study, all of the radial, brachial, and carotid artery data were measured by a single skilled, trained operator (a prerequisite for applanation tonometry in general) with a high-fidelity Millar pen-type tonometer, and 20-second sequences were processed automatically to an ensemble average after a procedure extensively described earlier.2 The relatively high dropout for the brachial measurements (virtually nonexistent for the other sites) is largely attributable to the pursued high standards, accepting only high-quality recordings with brachial and carotid/radial waveforms showing a similar number of accepted beats (minimally 10) and width of CIs of the ensemble average.
We do realize that measurability of brachial artery pulsations does not imply that they also adequately reflect the intra-arterial pressure. There is, however, consistency in our data.3 The form factor (FF=[mean−diastolic blood pressure]/pulse pressure), an indication of the peaking of the curve, decreases from the carotid to the radial artery (approximately progressive central-to-peripheral peaking), with, especially in men, brachial FF in between as one might anticipate (see Reference 2, Figure 1). The FF of 40% to 44% at the brachial artery is similar to the value of 40% proposed by Bos et al4 on the basis of invasive recordings. In addition, in an ongoing study in 148 subjects (mean age: 29.6 years), the carotid-to-brachial systolic pressure amplification measured with applanation tonometry was very similar to the amplification measured with diameter distension waveforms (16% and 13%, respectively; unpublished data).
Given all of the knowledge on wave travel and reflection, it appears most unlikely that the pulse travels unaltered from the elbow to the wrist. Figure 4 in Karamanoglu et al,5 for instance, clearly displays a higher modulus of the aorta-to-radial transfer function than of the aorta-to-brachial transfer function (eg, at 4 Hz: ≈3.2 versus ≈2.2 estimated from the figure for symbols representing the control data measured in their study), supporting brachial-to-radial pulse amplification. In the smaller radial artery, however, amplification and wave peaking may be counteracted by viscous friction forces leading to a decrease in mean blood pressure of a few millimeters of mercury.6
These complex aspects of brachial-to-radial pressure transfer come into play when calibrating a radial pressure waveform from data measured at the brachial artery. As such, they interfere with methods estimating central blood pressure from a mathematical transformation of this calibrated radial pressure waveform (as the SphygmoCor system does) and applied in studies like REASON (Preterax in Regression of Arterial Stiffness in a Controlled Double-Blind), CAFÉ (Conduit Artery Function Evaluation), and Strong Heart Study. Our approach via direct measurements at the brachial and carotid arteries avoids these problems when estimating central pressures.
Finally, we emphasize that it is not correct that the consequence of our method would be that there is no difference between brachial and carotid systolic or pulse pressures (Figure 2 in Reference 2). It is correct that the difference is smaller than what would be found when calculating central pressure following the approach as advocated by the SphygmoCor.
O'Rourke MF, Takazawa K. Flawed measurement of brachial tonometry for calculating aortic pressure? Hypertension. 2009; 54: e131.
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 PR, De Backer G, Gillebert TC. Rationale, design, methods and baseline characteristics of the Asklepios Study. Eur J Cardiovasc Prev Rehabil. 2007; 14: 179–191.
Segers P, Mahieu D, Kips J, Rietzschel E, De Buyzere M, De Bacquer D, Bekaert S, De Backer G, Gillebert T, Verdonck P, Van Bortel L; for the Asklepios investigators. Amplification of the pressure pulse in the upper limb in healthy, middle-aged men and women. Hypertension. 2009; 54: 414–420.
Karamanoglu M, O'Rourke M, Avolio A, Kelly R. An analysis of the relationship between central aortic and peripheral upper limb pressure waves in man. Eur Heart J. 1993; 14: 160–167.