Central aortic pressure influences pulse wave velocity.

Central Aortic Pressure Influences Pulse Wave Velocity To the Editor: The study reported by Lantelme and colleagues1 suggests that increasing heart rate is independently associated with higher aortic pulse wave velocity (PWV). We are concerned that the authors of this study have neither addressed the impact of central aortic pressure changes on PWV nor the presence of potential bias in their study. In Lantelme’s study, PWV represented the average wave speed from the carotid artery, through the aorta, and down to the common femoral artery. Local wave speed varies between different arteries and along the length of the aorta,2 and, furthermore, may alter in response to changes in local pressure.3 Knowledge of central aortic pressure is therefore an essential requirement for the interpretation of studies using PWV. Central aortic pressure is influenced by left ventricular ejection and the phenomenon of wave reflection.3 Systolic pressure in peripheral muscular arteries tends to be higher than in those measured centrally,4 particularly in younger subjects, and amplification of the central pressure pulse toward the periphery may be influenced by a number of factors, including heart rate.5–7 Previous work using similarly aged subjects5,6 suggested that, over a similar range of heart-pacing rates, there was a significant increase in both diastolic and mean central pressures. Only one study measured PWV,5 where it was noted to increase nonsignificantly with increasing heart rate. There is also evidence that in younger subjects increased heart-pacing rates are associated with elevation of central diastolic blood pressure.7,8 It is possible therefore that central pressures, and particularly diastolic blood pressure, which were not controlled for in Lantelme’s study, contributed to the change in PWV seen with different pacing rates. In this small group of elderly subjects, Lantelme et al found no significant changes in brachial pressures over paced heart rates of 60 to 100 bpm. In contrast, however, the 2 studies5,6 that recruited subjects of similar age to those in Lantelme’s group showed that both brachial systolic and diastolic pressures increased significantly over a range of physiological heart rates. A potential contributing factor to this important difference between the studies is the method used to measure brachial blood pressure. Lantelme’s use of a mercury sphygmomanometer exposes the results to significant operator bias. On the other hand, the use of a validated semiautomated blood pressure monitor, as used in the other studies, removes this problem and may explain the differences in peripheral blood pressure observed in these studies. There is further evidence for potential bias in this study supported by the data presented as a Bland-Altman plot. There is a discernible trend for the difference between the 2 measurements of PWV to increase with increasing values of PWV. This is further supported by the correlation data, where the slope of the regression line is approximately 0.7. Although epidemiological and observational data have suggested that heart rate is an independent determinant of PWV, few conclusions can be made from Lantelme’s study because of potential methodological bias and the failure to address the effects of central arterial pressure. Andrew Zambanini Simon A. McG Thom Alun D. Hughes Department of Clinical Pharmacology Faculty of Medicine, Imperial College London, United Kingdom E-mail [email protected]