Pulse pressure and dual angiotensin blockade.

I n diabetes mellitus type 2, macrovascular complications are often predicted from a significant increase in aortic stiffness, which is higher than in essential hypertension for the same level of mean arterial pressure (MAP).1 Pulse pressure (PP) is increased due to an increase in systolic blood pressure (SBP), frequently associated with decreased diastolic blood pressure (DBP). Thus, a decrease in BP under drug treatment may result from: a decrease in vascular resistance (which reduces SBP and DBP); a decrease in aortic stiffness (which reduces SBP but maintains or even increases DBP); a combination of both.1 In the recent issue of this Journal, Knudsen et al.2 compared (in subjects with hypertension and diabetes mellitus), the angiotensin-converting enzyme inhibitor (ACEI) lisinopril (40 mg daily) with the same agent (20 mg daily) associated with the angiotensin antagonist candesartan (16 mg daily). Under dual therapy, PP decreased significantly, due to reduction of SBP without DBP modification. Lisinopril did not modify PP and decreased DBP significantly, but not SBP. Because angiotensin blockade poorly modifies ventricular ejection, the results indicate that lisinopril mainly reduced vascular resistance, whereas dual blockade acted predominantly on aortic stiffness and/or wave reflections. In the paper by Knudsen et al.,2 the duration of treatment was one year and the reduction of MAP was similar, whatever the drug regimen. Thus it seems reasonable to expect that the decrease in aortic stiffness would be similar for both treatments, as is usually observed under angiotensin blockade.1 In contrast, the PP reduction under dual blockade may rather result from disturbed wave reflections. Indeed, insulin administration not only causes arteriolar vasodilatation but also reduces wave reflections.3 Furthermore, subjects with diabetes mellitus type 2 are characterized by hypertrophic remodeling of resistance arteries, a histomorphometric pattern distinct from that of essential hypertension (where eutrophic remodeling is present).1 Vessel hypertrophy declines under angiotensin blockade, modifying the geometry and stiffness of arteriolar vessels