Baroreflex dysfunction and augmented sympathetic nerve responses during mental stress in veterans with posttraumatic stress disorder (PTSD)

Abstract

Posttraumatic Stress Disorder (PTSD) is associated with increased cardiovascular (CV) risk. We tested the hypothesis that PTSD patients have augmented sympathetic nervous system (SNS) and hemodynamic reactivity during mental stress, and impaired arterial baroreflex sensitivity (BRS). 14 otherwise healthy Veterans with combat-related PTSD were compared to 14 matched Controls without PTSD.  Muscle sympathetic nerve activity (MSNA), continuous blood pressure (BP), and electrocardiography were measured at baseline, and during two types of mental stress:  combat-related mental stress using virtual reality combat exposure (VRCE); and noncombat related stress using mental arithmetic (MA). Cold pressor test (CPT) was administered for comparison. BRS was tested using pharmacologic manipulation of BP via the Modified Oxford technique at rest and during VRCE. Blood samples were analysed for inflammatory biomarkers. Baseline characteristics, MSNA and hemodynamics were similar between the groups. In PTSD versus Controls, MSNA (+8.2 ± 1.0 vs +1.2 ± 1.3 bursts/min P < 0.001) and heart rate (HR) responses (+3.2 ± 1.1 vs −2.3 ± 1.0 beats/min, P = 0.003) were significantly augmented during VRCE.  Similarly, in PTSD versus Controls, MSNA (+21.0 ± 2.6 vs +6.7 ± 1.5 bursts/min, P < 0.001) and diastolic BP responses (+6.3 ± 1.0 vs +3.5 ± 1.0 mmHg, P = 0.011) were significantly augmented during MA, but not during CPT (P = NS). In the PTSD group, sympathetic BRS (-1.2 ± 0.2 vs -2.0 ± 0.3 BI mmHg⁻¹, P = 0.026) and cardiovagal BRS (9.5 ± 1.4 vs 23.6 ± 4.3 ms mmHg⁻¹, P = 0.008) were significantly blunted at rest. PTSD patients had significantly higher hs-CRP levels compared to Controls (2.1 ± 0.4 vs 1.0 ± 0.3 mg L⁻¹, P = 0.047). Augmented SNS and hemodynamic responses to mental stress, blunted BRS, and inflammation may contribute to increased CV risk in PTSD.

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