Author + information
- Athanase Benetos, MD,
- Harold Smulyan, MD and
- Michel E. Safar, MD⁎ ()
- ↵⁎Diagnosis Center, Hôpital Hôtel-Dieu, 1 place du Parvis Notre-Dame, 75181 Paris Cedex 04, France
In the past, blood pressure measurements were devoted to the diagnosis and treatment of threatening accidents. Currently, the goal of measurements has changed and became prevention, but the devices remained almost identical. For example, pulse pressure (PP) amplification (1,2), described 50 years ago, is yet poorly used in clinical practice. The remarks of our 2 colleagues are important in this context and should be developed.
First, it must be clarified that our equation (2) predicts carotid PP and then was used only to assess PP amplification. Second, as previously shown (1), PP amplification depends on most major modifiable and nonmodifiable cardiovascular (CV) risk factors; in the present equation, glucose was the only modifiable CV risk factor beyond blood pressure. Third, both carotid PP and amplification provided higher predictive value than brachial PP regarding CV mortality by 3% to 5% and 13% to 25%, respectively (depending on the adjusted model), whereas only 2.3% of the variability of predicted carotid PP was due to these factors. This is far less than the expected contribution of these factors (i.e., age, sex, glucose) on CV mortality. Fourth, the equation used for assessing carotid PP, and thus PP amplification, was introduced in multivariate model further adjusting for other classical CV risk factors: smoking, physical activity, pulse rate, cholesterol, as well as de novo adjusted for age and sex.
Finally, the reported equation was not proposed as a substitute of the actual assessment of central hemodynamics but as an indirect proof of the value of PP amplification, deriving from a large epidemiological study with a population of 125,151 subjects. The weight of evidence from the present study (1) as well as the review of the available data (2) suggest that PP amplification integrates the synergistic effect of known or potentially unknown CV risk factors on blood pressure and arterial wall structural and functional properties. Thus, this is not just a mathematical association but an association based on the pathophysiology of the arterial disease. We agree with the view (3) that direct assessment of PP amplification will possibly provide more solid results by avoiding mathematical controversies and less “dilution” of the biophysical mechanisms. Our goal was not to provide evidence in terms of methodological gold-standard precision (e.g., by receiver operator characteristics curves analysis) but in terms of pathophysiological applicability.
Certainly as suggested (3), biomedical innovation on the field is warranted. The confirmation of the validity of the present model and results using other methodologies and population by the group of Philadelphia would also be of great help.
- American College of Cardiology Foundation