Higher Pretreatment Blood Pressure Is Associated With Greater Posttraumatic Stress Disorder Symptom Reduction in Soldiers Treated With Prazosin.

Background: In a previously reported positive randomized controlled trial of the α-adrenoreceptor (αAR) antagonist prazosin for combat posttraumatic stress disorder (PTSD) in 67 active duty soldiers, baseline symptoms did not predict therapeutic response. If increased brain αAR activation in PTSD is the target of prazosin treatment action, higher brain αAR activation should predict greater prazosin efficacy. Although brain αAR activation is not measurable, coregulated peripheral αAR activation could provide an estimate of brain αAR activation. Standing blood pressure (BP) is an accessible biological parameter regulated by norepinephrine activation of αARs on peripheral arterioles.

Methods: Effects of baseline standing systolic and other BP parameters on PTSD outcome measures from the previously reported randomized controlled trial were analyzed using linear mixed-effects models. Prazosin participants (n = 32) and placebo participants (n = 35) were analyzed separately.

Results: In prazosin participants, each 10-mm Hg higher baseline standing systolic BP increment resulted in an additional 14-point reduction (improvement) of Clinician-Administered PTSD Scale total score at end point (p = .002). All other combinations of baseline BP parameters and PTSD outcome measures were similarly significant or demonstrated trends in the predicted direction. In placebo participants, there was no signal for a baseline BP effect on PTSD outcome measures.

Conclusions: These findings suggest that higher standing BP is a biomarker that helps identify persons with combat PTSD who are likely to benefit from prazosin. These results also are consistent with αAR activation contributing to PTSD pathophysiology in a subgroup of patients.