Authors' response

We appreciate Gleim and Smith's review of studies comparing antihypertensive efficacy of amlodipine and losartan. However, we disagree with the assertion that notably different results were obtained in patient populations similar to those studied in our report.1 Indeed, Wilson et al.,2 found, as we did, that although ambulatory blood pressure was reduced to the same degree, trough sitting blood pressure was more effectively reduced by amlodipine than with losartan-based therapy. We agree that ambulatory blood pressure may be a better measure of risk, yet decisions in routine clinical practice about drug efficacy are made on the basis of the seated office blood pressure. Although we did not measure left ventricular (LV) mass regression, we believe the study cited by Gleim and Smith that compared the LV mass reduction by losartan and amlodipine is invalid.3 At baseline, the losartan group had LV mass that was 20% greater than the amlodipine group, and at the end of the study the amlodipine group still had lower LV mass. Greater LV mass reduction in the losartan arm most likely represents regression to the mean for the losartan group, rather than a true biologically different effect of treatments on LV mass.3 Furthermore, amlodipine has been shown to be quite effective in reversing LV hypertrophy.4 We agree that evidence-based medicine should guide clinical practice, and we were careful to point out in our conclusions that differences in drug efficacy may be found in different patient populations. In the recently published Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT), where the demographics of the patients were similar to our study, amlodipine was as effective as the angiotensin-converting enzyme inhibitor and diuretic in preventing the primary outcome of cardiovascular death and nonfatal myocardial infarction.5 Furthermore, in ALLHAT the angiotensin-converting enzyme inhibitor, but not amlodipine, was associated with more stroke than chlorthalidone. We also acknowledge that in patients with impaired renal function, blockade of the renin-angiotensin-aldosterone system with angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker therapy should be the basis of antihypertensive therapy6,7 and that in patients with ECG evidence of left ventricular hypertrophy, losartan reduced stroke more effectively than atenolol.8 In our study, patients with renal dysfunction were excluded, and ECG evidence of left ventricular hypertrophy was not an inclusion criteria.