Abstract

We respond to recent correspondence relating to the Conduit Artery Function Evaluation study (CAFE),1 published in Circulation earlier this year. We thank Drs Nieminen, Kahonen, and Kobie for their remarks and suggestions. We agree that increased stroke volume at lower heart rates should be considered as a contributor to the elevated pulse pressure (PP) seen with atenolol-based treatment in the CAFE study. We did not assess stroke volume, and further studies are required to define the impact of blood pressure (BP)-lowering therapies on stroke volume and its contribution to central aortic pressures. Nevertheless, our data do suggest an important role for increased wave reflections in determining higher central aortic pressures with atenolol-based when compared with amlodipine-based treatment. Indeed, the higher central but not brachial PP with atenolol-based therapy in the CAFE study supports the hypothesis that the main driver of differential central aortic pressures was drug effects on pressure wave reflections rather than changes in stroke volume. We agree with Drs Safar and Fournier that the findings of …

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