Response to Brachial and Central Arterial Pressure
Thank you for giving us the opportunity to respond to the letter of Dr O’Rourke et al.1 Contrary to the assertions of Dr O’Rourke and colleagues, our recently published study2 does not contradict previous findings of our group because this is the only study we have undertaken relating central waveforms to outcome. The study of Waddell et al3 was not an outcome study (and was in men with proven coronary disease). Also, our study clearly predated the Conduit Artery Function Evaluation (CAFE) study,4 as all data collection in the Australian National Blood Pressure Study 2 (ANBP2) trial was completed before CAFE had started. Although, in contrast to our study, CAFE did not obtain any central arterial measurements before drug treatment, the results of the 2 studies were similar. Thus, central augmentation index, when adjusted for other factors, was not predictive of outcome in either study. In neither study did central pressure estimates prove superior in predicting outcome to the much more easily measured brachial pressures. Also contrary to the claims made by O’Rourke and colleagues, there are not equivalent “multiple previous studies” (none of which is, however, cited) for which our study is an “outlier.”1 Again contrary to the contents of the letter from O’Rourke and colleagues, our publication contained no claims that the decision to report the data for females was made prospectively.
Furthermore, Dr O’Rourke and colleagues appear to have either misread or misunderstood the study of Gatzka et al.5 The times quoted (5 to 290 ms) were not times to the augmentation point but time differences between the forward and backward waves (as is clearly stated in the figure legends). Comparison of variance between aortic and radial measurements in CAFE would be essentially tautologous since aortic pressures are derived from the peripheral measures and are not independently measured. Actually, there appears to be no data presented in CAFE on the standard deviation of radial pressures (but only of brachial).
The question we posed when formulating the arterial mechanics substudy of ANBP2 was: Would knowledge of central pressures and augmentation index prove more prognostically informative than simple measurement of brachial pressures? The answer from both ANBP2 and CAFE is “no.”
O’Rourke MF, Nichols WW, Safar ME. Brachial and central arterial pressure. Hypertension. 2006; 48: e1.
Dart AM, Gatzka CD, Kingwell BA, Willson K, Cameron JD, Liang Y-L, Berry KL, Wing LMH, Reid CM, Ryan P, Beilin LJ, Jennings GLR, Johnston CI, McNeil JJ, MacDonald GJ, Morgan TO, West MJ. Brachial blood pressure but not carotid arterial waveforms predict cardiovascular events in elderly female hypertensives. Hypertension. 2006; 47: 785–790.
Waddell TK, Dart AM, Medley TL, Cameron JD, Kingwell BA. Carotid pressure is a better predictor of coronary artery disease severity than brachial pressure. Hypertension. 2001; 38: 927–931.
Williams B, Lacy PC, Thom SM, Cruickshank K, Stanton A, Collier D, Hughes AD, Thurston H, O’Rourke M. Differential impact of blood pressure–lowering drugs on central aortic pressure and clinical outcomes. Principal results of the Conduit Artery Function Evaluation (CAFE) study. Circulation. 2006; 113: 1213–1225.
Gatzka CD, Cameron JD, Dart AM, Berry KL, Kingwell BA, Dewar EM, Reid CM, Jennings GL. Correction of carotid augmentation index for heart rate in elderly essential hypertensives. ANBP2 Investigators. Australian comparative outcome trial of angiotensin-converting enzyme inhibitor- and diuretic-based treatment of hypertension in the elderly. Am J Hypertens. 2001; 14: 573–577.