Evaluating clinical and neuroimaging predictors for cognitive-behavioral therapy outcome in obsessive-compulsive disorder.
Authors: Tochadse M, Klawohn J, Kaufmann C, Grützmann R, Riesel A, Heinzel S, Rane RP, da Silva SP, Wellan S, Gijsen S, Ritter K, Kathmann N
Journal: Scientific reports
mental health
psychology
open access
Abstract
Posttraumatic stress disorder (PTSD) is a psychiatric condition impacting 8% of civilians and 23% of military personnel (–). PTSD symptoms adversely impact personal relationships, occupational functioning, and quality of life (, ). Importantly, beyond its psychological and social impact, individuals with PTSD have an elevated risk of developing hypertension and cardiovascular diseases (CVD) (). Multiple large, well-controlled studies have shown that PTSD is independently associated with increased CVD risk and that this risk increases with worsening PTSD symptoms (–). Importantly, PTSD often co-occurs with other psychiatric symptoms, particularly anxiety and depression, which not only worsen overall symptom burden but are independently linked to increased CVD risk (, ). Thus, there is a need to identify mechanisms and biomarkers underlying CVD risk in PTSD so that early interventions can be developed and implemented to improve CVD risk in this growing patient population. Increased fluctuations in blood pressure (BP), termed blood pressure variability (BPV), are a potential early marker of CVD risk (). BPV can be assessed across several timescales, including very short-term (beat-to-beat), short-term [24-h ambulatory blood pressure (ABPM)], and long-term (visit-to-visit) clinic measures, each of which may reflect distinct physiological mechanisms. Prior work has shown that wider fluctuations in beat-to-beat, 24-h ABPM, and visit-to-visit BP are all associated with increased CVD risk, independent of mean BP (–). Compared with short-term and long-term methodologies, very short-term BPV has the advantage of being feasibly obtained within a single clinic visit; BPV indices can be quantified by capturing dynamic oscillations in resting BP over a period of 5–10 min. Beat-to-beat BPV is closely regulated by autonomic function and baroreflexes to maintain arterial BP in a very narrow range (). Individuals with PTSD have impaired baroreflex sensitivity (BRS) that manifests before the onset of overt hypertension (, ). However, whether this BRS dysfunction is associated with an augmented BPV in PTSD remains unexplored. Therefore, the present study evaluates very short-term BPV at rest in individuals with and without PTSD for comparison. We hypothesized that individuals with PTSD would exhibit greater beat-to-beat BPV indices compared with controls without PTSD. In addition, we hypothesized that higher beat-to-beat BPV is associated with lower cardiac BRS and higher severity of PTSD, anxiety, and depression symptoms.