Pressor effects of beta-blockers on standing blood pressure may be harmful for older patients with orthostatic hypertension.

Pressure May Be Harmful for Older Patients With Orthostatic Hypertension To the Editor: Cleophas et al1 reported an interesting pressor effect of -blockers in elderly patients with mild hypertension on standing such that pulse pressure, which decreased on standing when treated, showed an increase after -blockade. Although they considered this pressor effect to be beneficial, we think that this is not always the case. The orthostatic blood pressure (BP) reaction varies greatly among older individuals. In addition to orthostatic hypotension, which is a well-known risk factor for falls, syncope, and cardiovascular events in the elderly,2 in a recent study,3 we found orthostatic hypertension to be a new risk factor for stroke in elderly hypertensive patients. We performed a head-up tilt test and brain MRI in 241 elderly subjects with sustained hypertension confirmed by ambulatory BP monitoring. We classified the patients into an orthostatic hypertension group with an orthostatic increase of systolic BP (SBP) of 20 mm Hg (n 26), an orthostatic hypotension group with an orthostatic SBP decrease of 20 mm Hg (n 23), and a normal group with neither of these 2 patterns (n 192). Silent cerebral infarcts detected by brain MRI were more common in the orthostatic hypertension (3.4 per person, P 0.0001) and orthostatic hypotension groups (2.7 per person, P 0.04) than in the normal group (1.4 per person). Thus, we think that the pressor effect of -blocker could be potentially harmful for the elderly hypertensive patients with orthostatic hypertension. In our study, the orthostatic BP increase found in the elderly hypertensive patients with orthostatic hypertension was selectively abolished by -adrenergic blockade.3 This result indicates that -adrenergic activity is the predominant pathophysiological mechanism of orthostatic hypertension. As mentioned by Cleophas et al,1 this pressor effect of -blockers might be because of the imbalance between -adrenergic vasoconstrictor activity and -adrenergic vasodilator activity. In our study, morning SBP, which is predominantly determined by -adrenergic activity, was higher in the orthostatic hypertension group than in the normal group (159 versus 149 mm Hg, P 0.007), whereas there were no significant differences in ambulatory BP between the 2 groups during other periods.3 Thus, -blockers might further enhance the increased orthostatic BP response in elderly hypertensive patients with orthostatic hypertension and -adrenergic hyperactivity, particularly in the morning. The morning surge of BP coincides with the time of greatest susceptibility to stroke and other cardiovascular events.