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 the CAFE study are consistent with their report of differential drug effects on central aortic pressures in the Preterax in Regression of Arterial Stiffness in a Controlled Double-Blind Study (REA-SON). 2 We concur with the view that vascular structural changes are likely to make an important contribution to the long-term hemodynamic effects of BP-lowering therapy, especially wave reflection, and we suggested in our article that different BPlowering treatments may modify central aortic pressures and hemodynamics through differential effects on vascular structure. 1 The fact that the most beneficial effects on central aortic pressure have been observed with vasodilator therapy, in contrast to ␤-blockade, supports the view that a reduction in vascular resistance, by vasodilation and subsequent vascular remodeling, is an important determinant of reduced wave reflection and central aortic pressure, thereby defining the characteristics of optimal BP-lowering therapy.Cameron and colleagues are concerned that the data in their article 3 may have been misinterpreted. We clarify that our reference to their work related to the accuracy and validation of the transfer function rather than the derivation of central aortic pressures, which are prone to and dependent on the same level of inaccuracy as the measurement of brachial BP by cuff sphygmomanometry.We thank Dr Dart et al for their comments and interest in our study but would like to point out fundamental differences between the design and objectives of the CAFE study and The Australian National Blood Pressure Study 2 (ANBP2). substudy of central aortic pressures. 4 The prespecified primary objective 5 of the CAFE study was to examine the hypothesis that 2 different BP-lowering regimens would have different effects on derived central arterial pressures and hemodynamics despite similar effects on brachial pressures. This was convincingly demonstrated by the findings of ...

Societies CVD risk-assessment programme/chart. Optimal cholesterol lowering should reduce the total cholesterol by 25% or LDL-cholesterol by 30% or achieve a total cholesterol of o4.0 mmol/l or LDL-cholesterol of o2.0 mmol/l, whichever is the greatest reduction (A). Glycaemic control should be optimised in people with diabetes, for example, HbA1c o7% (A). Advice is provided on the clinical management of hypertension in specific patient groups, that is, the elderly, ethnic minorities, people with diabetes mellitus, chronic renal disease, and in women (pregnancy, oral contraceptive use and hormone-replacement therapy). Suggestions for the improved implementation and audit of these guidelines in primary care are provided.