Published online before print November 19, 2007, doi: 10.1161/HYPERTENSIONAHA.107.098681
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(Hypertension. 2008;51:37.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
Peripheral Augmentation Index
Shouldering the Central Pressure Load
From the Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom.
Correspondence to David J. Webb, Centre for Cardiovascular Science, University of Edinburgh, Queen’s Medical Research Institute, 47 Little France Crescent, Edinburgh, EH16 4TJ, United Kingdom. E-mail d.j.webb{at}ed.ac.uk
Peripheral blood pressure (BP) measurement has remained essentially unchanged over the last century, and many researchers believe that changes in such measurements fully account for the benefits of antihypertensive treatment in clinical trials.1 Indeed, the wealth of data supporting a strong association between cuff measurements and adverse cardiovascular outcome may well have hindered the quest for alternative, and indeed potentially better, measures of arterial pressure. Over the last few years, however, advances in technology have enabled the routine assessment of BP in previously inaccessible central arteries. Central BP is not the same as peripheral BP. After cardiac contraction, a pressure wave propagates distally through the arterial tree. At points of impedance mismatch (arterial branch points), the wave is reflected, interacting with the incident wave and determining the overall measured pressure. The velocity and magnitude of the incident and reflected waves, and, hence, the nature of this interaction at different anatomic sites, are affected by various factors, including mean distending pressure, the intrinsic properties of the arterial wall, arterial path length, and the degree of impedance mismatch. From the pathophysiological perspective, central BP is likely to be more relevant than peripheral BP to the risk of left ventricular hypertrophy, heart failure, myocardial infarction, and stroke. Proximal aortic pressure determines left ventricular work and influences myocardial perfusion during diastole. Furthermore, degenerative changes characteristic of hypertension are observed in the wall of the large elastic arteries rather than in peripheral conduit vessels. There is increasing evidence that central pressure may be a stronger predictor of vascular events and disease severity2 than brachial pressure. Moreover, variations in outcome between drug regimens may be explained by differences in the degree of central BP lowering, independent of peripheral BP reduction.3,4
Two main methods have been developed for noninvasively determining central BP using transcutaneous pressure transducers. The first approach is to use the carotid waveform as a surrogate for that of the aorta, calibrating the wave to brachial diastolic and mean pressure, which are assumed to be constant throughout the arterial tree.5 The second method is to use a generalized transfer function to derive an aortic waveform from measurements made at more easily accessible peripheral sites, such as the radial artery.6 A transfer function is a mathematical description of the change from the input (in this case, radial) to output (aortic) signals of a system and is widely used in engineering sciences. Neither system is ideal, however. Carotid measurement can be technically challenging, makes assumptions about the constancy of diastolic and mean pressure throughout the vasculature and, it must be remembered, is only a surrogate for aortic pressure. Measurements at the radial artery are more straightforward, and waveform calibration using brachial BP is less problematic. However, the generalized nature of the transfer function assumes that the properties of the upper limb arteries are identical among all the individuals. Most validation work on the transfer function has, understandably, been carried out in patients undergoing clinically indicated cardiac catheterization. The transfer function, therefore, reflects an older population at increased risk of vascular disease, and inconsistencies have been observed between sexes, patients with and without diabetes or coronary disease, and before and after exercise.
Millasseau et al7 have been staunch critics of the need for a transfer function, arguing that the information contained within the central pressure wave is available from the peripheral waveform without the requirement for previous mathematical manipulation. In this issue of Hypertension, they present an alternative approach to the measurement of central systolic BP.8 This involves identifying what they refer to as the late systolic shoulder on the peripheral waveform. Two studies are described, the first comparing radial waveforms obtained using applanation tonometry against aortic waveforms derived using a transfer function in patients undergoing coronary angiography. Considerable similarity was observed between derived aortic systolic pressure and the late systolic shoulder of the radial waveform. These findings are endorsed by a second study comparing peripheral finger pressure waveforms with invasively measured aortic waveforms, including following hemodynamic perturbation using atrial pacing and the administration of intravenous nitrates. These observations support and expand on previous work. Takazawa et al9 studied patients undergoing cardiac catheterization and observed similar decreases in central systolic BP and the radial late systolic shoulder in response to sublingual nitroglycerin. They proposed a potential association between the 2 measurements, although they did not make direct comparisons. Pauca et al10 made simultaneous invasive measurements of radial and aortic pressure in a group undergoing cardiac surgery. Waveform analysis was less than ideal because of the paper recording methods used and the problems of manually identifying wave inflection points, but similar conclusions were reached.
An alternative method of measuring central BP that does not involve the use of a transfer function is very attractive. The increasing evidence of an independent prognostic value of central systolic BP was acknowledged in a consensus document published earlier this year, which supported the need for adoption of central hemodynamic measures into clinical practice.11 Certainly, studies of the effects of novel BP-lowering agents should take into account changes in central BP. Furthermore, drugs that directly target intrinsic arterial wall stiffness may affect pulse wave propagation and, thus, reduce central BP, independent of any effects on peripheral BP. This technique provides an additional tool for achieving these measurements. It also has the potential to be retrospectively applied to the large database of existing pulse wave data, both for validation purposes and to examine its prognostic role. Indeed, we have shown recently that peripheral waveform measurements might be obtained during sphygmomanometry; measurement of the systolic shoulder in this situation would provide central BP values in patients having routine cuff BP recordings.12
One interesting question to arise from this work is why there should be such a close association between the 2 measures. It seems hard to believe that this relationship will necessarily hold in all physiological and pathological circumstances. Munir et al8 offer an explanation in terms of analysis in the frequency domain. Any pulsatile signal can be considered to be the sum of a series of sine waves, known as the harmonic components. As the pulse travels from the aorta to the radial artery, changes in higher-frequency harmonics occur. In contrast, lower-frequency components, which comprise the aortic pressure peak, are affected less.6 This peak, therefore, maintains its identity, manifesting distally as the systolic shoulder of the radial pulse. Indeed, lower-frequency harmonics are minimally attenuated as they travel through the arterial system, supporting this supposition.13 These changes in harmonics are described by the transfer function, which appears to remain relatively constant even in the presence of varying hemodynamic conditions (eg, Valsalva maneuver or nitrates). Therefore, one might hypothesize that the close relationship between central pressure and the peripheral systolic shoulder will also be maintained in differing pathophysiological circumstances. However, this makes the assumption that there are no high-frequency components to the aortic peak. Higher-frequency harmonics are attenuated, and, therefore, the aortic peak and its corresponding reflection might, thus, not be expected to be of equivalent magnitude. By using methods to decompose the overall pressure wave into its forward and backward components or by using the various 1D arterial models that have been described, one may be able to gain a better understanding of the mechanisms associating these 2 pressure parameters and theoretically substantiate the potential for this association to remain constant.
Despite extensive clinical research using transfer functions, the technique remains widely criticized, and skeptics are likely to be equally judgmental of the peripheral systolic shoulder method. The problem of validating the technique in groups in whom invasive measurements cannot be ethically justified will be as challenging as for the transfer function and raises similar questions. Does the association hold in hypertensive patients with no overt vascular disease? How about healthy volunteers, who are often used in physiological and drug studies? What of the effects of antihypertensive agents? Nevertheless, the accuracy and prognostic value may still be compared directly with the transfer function, and it is possible to conduct formal validation work to examine the effects of factors such as gender, hypercholesterolemia, or diabetes. Even if the peripheral systolic shoulder is not consistently related to aortic systolic pressure, it may still prove useful as a means of risk stratification. Cuff BP has proven invaluable over the last century, but we must avoid becoming mired by sentimental affection for what could be regarded as an outdated technique. It is essential that methods such as those described by Munir et al8 receive the attention they deserve to develop better approaches to assessing BP suited to the next hundred years.
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Acknowledgments |
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Disclosures
None.
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Footnotes |
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The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
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References |
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