| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2006;114:e537.)
© 2006 American Heart Association, Inc.
Correspondence |
Department of Cardiovascular Medicine, Alfred Hospital, Melbourne, Australia, a.dart{at}alfred.org.au
University of Melbourne, Melbourne, Australia
Baker Heart Research Institute, Melbourne, Australia
We read with interest the recent article from the Conduit Artery Function Evaluation (CAFE) investigators1 on estimated central aortic blood pressure. The use of central arterial waveforms and estimates of central pressures in routine clinical practice would be justified if such measures materially add to the prognostic information provided by "routine" blood pressure measures, most usually obtained from brachial artery sphygmomanometry. The results from CAFE confirm our own recent findings from a substudy of The Australian National Blood Pressure Study 2 (ANBP2) 2 showing that this is not the case.3 In our study, neither central augmentation index nor central systolic or pulse pressure was a significant predictor of outcome, whereas brachial systolic and pulse pressures were. Diastolic pressure was not related to outcome in our study. In the CAFE study,1 central pulse pressure was either less predictive than brachial pulse pressure or of approximately similar predictive value. Augmentation index was not predictive of outcome in 2 of the 3 adjusted models. No information is provided regarding the predictive value of diastolic pressure.
There are several differences in the 2 studies that may account for the fact that central pressures and waveforms were of no predictive value in our cohort. Our study was in women, who only made up about 20% of the CAFE cohort. In our study, we did not include development of renal impairment as an end point, as they did in CAFE. The rationale for including this, a component of the tertiary end point of the parent Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) study,4 is unclear, as it is not obvious that estimated proximal aortic pressure would provide a good estimate of renal artery pressures. We would be interested to know how central pressures and augmentation index were related to the primary and secondary end points of the ASCOT study. In our study,2 all central pressure and waveform data were collected before treatment rather than during treatment, as in CAFE. Furthermore, we recorded carotid waveforms, whereas in CAFE, a radial waveform was used and transformed to give a putative central aortic pressure. It is interesting that despite the differences in study design, brachial pulse pressure, measured before treatment in our study and during treatment in CAFE, was similarly related to risk, with a hazard ratio of 1.19 (per 10 mm Hg) in our study and 1.23 in the CAFE study.
We concur with the editorial5 accompanying the CAFE study that the technique of radial tonometry is "not yet ready for prime time" (p 1163) in routine clinical practice, but we believe that along with other methods for assessing central arterial parameters, it should remain an area of active research.
| Acknowledgments |
|---|
Drs Dart and Kingwell have received NHMRC grants. Dr Gatzka reports no disclosures.
| References |
|---|
|
|
|---|
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2006 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |