Effect of PTSD treatment on cardiovascular reactivity during trauma memory recall and correspondence with symptom improvement

ABSTRACT

Background: Prior research has shown PTSD treatment leads to reductions in cardiovascular reactivity during trauma recall, but the extent to which such reductions are associated with changes in PTSD symptoms is less clear. Moreover, such relationships have not been investigated in a cognitively focused PTSD treatment.

Objective: To examine changes in cardiovascular reactivity to the trauma memory in patients receiving cognitive processing therapy (CPT), CPT with a written trauma account, and a written account only condition. We also examined the association of such changes with symptom improvement.

Method: 118 women with PTSD secondary to interpersonal violence completed pre- and post-treatment assessments of PTSD symptoms and cardiovascular reactivity during a script-driven imagery task.

Results: Results indicated a significant but modest reduction in cardiovascular reactivity in CPT conditions. Changes in cardiovascular reactivity and reexperiencing symptoms were significantly associated among the whole sample. Among individuals with the greatest reactivity to the trauma memory at pretreatment, associations were also seen with changes in total PTSD, numbing, and trauma-related guilt.

Conclusions: Results indicate that previous findings on the effect of PTSD treatment on cardiovascular reactivity during trauma recall extend to cognitively oriented treatment. Baseline cardiovascular reactivity may influence the extent to which reductions in PTSD symptoms and reactivity during trauma recall are related.

HIGHLIGHTS

• Cognitive Processing Therapy leads to reduced heart rate reactivity when recalling a trauma memory.

• Decreases in heart rate reactivity are associated with reduced reexperiencing symptoms.

• Changes in heart rate reactivity and PTSD symptoms are more closely related among patients with greater pretreatment reactivity.

Antecedentes: Investigaciones anteriores han demostrado que el tratamiento del TEPT conduce a reducciones en la reactividad cardiovascular durante el recuerdo del trauma, pero el grado en que dichas reducciones se asocian con cambios en los síntomas del trastorno de estrés postraumático es menos claro. Además, tales relaciones no se han investigado en un tratamiento de TEPT centrado cognitivamente.

Objetivo: Examinar los cambios en la reactividad cardiovascular ante el recuerdo de la memoria traumática en pacientes que reciben terapia de procesamiento cognitivo (CPT por sus siglas en inglés), CPT con un relato escrito del trauma y una condición de solo relato escrito. También examinamos la asociación de tales cambios con la mejoría de los síntomas.

Método: 118 mujeres con TEPT secundario a violencia interpersonal completaron evaluaciones de los síntomas de TEPT y la reactividad cardiovascular antes y después del tratamiento durante una tarea de imaginería guiada por guión.

Resultados: Los resultados indicaron una reducción significativa pero modesta en la reactividad cardiovascular en condiciones de CPT. Los cambios en la reactividad cardiovascular y la reexperimentación de síntomas se asociaron significativamente en toda la muestra. Entre los individuos con mayor reactividad al recuerdo traumático en el momento previo al tratamiento, también se observaron asociaciones con cambios en el trastorno de estrés postraumático total, adormecimiento y culpa relacionada con el trauma.

Conclusiones: Los resultados indican que los hallazgos previos sobre el efecto del tratamiento del TEPT sobre la reactividad cardiovascular durante el recuerdo del trauma se extienden al tratamiento de orientación cognitiva. La reactividad cardiovascular inicial puede influir en el grado en que se relacionan las reducciones en los síntomas de TEPT y la reactividad durante el recuerdo del trauma.

KEYWORDS:

• PTSD
• cognitive processing therapy
• physiological reactivity
• trauma memory
• heart rate
• treatment outcomes

PALABRAS CLAVE:

• TEPT
• terapia de procesamiento cognitivo
• reactividad fisiológica
• memoria del trauma
• frecuencia cardíaca
• resultados del tratamiento

1. Introduction

Posttraumatic stress disorder (PTSD) is associated with elevated cardiovascular reactivity (CVR) to trauma-related stimuli (Pole, 2007). Although evaluation of PTSD treatment efficacy is typically based on patient report of symptoms, physiological measures such as CVR can further our understanding of response to PTSD interventions (Bourassa et al., 2021). In particular, assessing CVR during trauma memory recall before and after treatment can provide insight into changes in emotional reactivity to the trauma memory without relying on a patient’s awareness or subjective assessment of their emotional state (Yang et al., 2021).

Previous studies have consistently found that trauma-focused therapy is associated with significant reductions in CVR during voluntary trauma memory recall (Blanchard et al., 2002; Bourassa et al., 2020; Dunne et al., 2012; Wangelin & Tuerk, 2015). The extent to which such reductions are associated with symptom improvement, however, is less clear. Some studies have found significant but modest correlations between the two (Blanchard et al., 2002; Rabe et al., 2006), while others have found null results (Bourassa et al., 2020; Maples-Keller et al., 2019) or variability across symptom measures (Davis et al., 2011). Notably, the above-mentioned studies all examined treatments that involve systematically revisiting the traumatic event via imaginal exposure, which explicitly aims to reduce reactivity to a trauma memory. Cognitively based treatments such as cognitive processing therapy (CPT), in contrast, focus on changing trauma-related beliefs. Nonetheless, CPT would still be expected to reduce trauma memory CVR given that shifting maladaptive beliefs about the cause and meaning of the trauma should lead to a corresponding reduction in trauma memory reactivity (Resick et al., 2017). Correspondence between changes in trauma memory CVR and symptom would also be expected in CPT given that both are thought to be driven by belief change (Schumm et al., 2015).

Accordingly, the first aim of this study was to examine whether CPT and its components led to significant reductions in CVR to an identified worst trauma memory. We examined this across treatments and within three separate treatment conditions: CPT with the written trauma account (CPT + A), CPT with no written account, (CPT), and Written Account only (WA), hypothesizing significant reductions in CVR in all three treatments. The written account in CPT involves repeatedly revisiting details of the trauma and experiencing associated emotions, with the WA intervention being designed to isolate the specific effects of such procedures (Resick et al., 2008). Thus, examining the above interventions separately enables an investigation of CVR changes in treatments with varying amounts of cognitive intervention and systematic revisiting of the trauma memory. Although we did test for differences in CVR effects between conditions, due to limited power for this comparison our emphasis was on estimating effects of each treatment individually rather than making a definitive comparison between treatments.

Our second aim was to examine the hypothesis that change in CVR to the trauma memory would be positively associated with change in PTSD symptoms. We then conducted two sets of exploratory follow-up analyses to examine factors potentially contributing to mixed findings on this relationship in prior research. First, we investigated if associations between CVR and symptom change would differ when examining PTSD symptom clusters and other trauma-related difficulties, specifically depression, trauma-related guilt, and sleep. Second, we explored whether baseline CVR moderates the relationship between symptom and CVR change, as some PTSD patients exhibit blunted CVR (D’Andrea et al., 2013) that could preclude or weaken such a relationship.

2. Method

2.1. Participants

Participants included 118 women who met DSM-IV criteria for PTSD secondary to interpersonal violence and consented to participate in one of two randomized controlled trials (RCTs) examining CPT (Galovski et al., 2016; Resick et al., 2008). Trials took place at the same location, recruited from the same community, and used identical inclusion and exclusion criteria, except for an additional requirement of clinically significant sleep impairment in Galovski et al (Galovski et al., 2016). Participants in the Resick et al. (Resick et al., 2008) trial were randomly assigned to receive CPT + A, CPT, or WA. Participants in Galovski et al. (Galovski et al., 2016) received CPT + A, with a subset also receiving three weeks of sleep-directed hypnosis prior to CPT, though this did not impact PTSD outcomes (Galovski et al., 2016).

Participants were included in this study if they had valid heart rate (HR) data during the script-driven imagery (SDI) assessments at pre- and post-treatment. Of the 242 participants in the intent-to-treat (ITT) samples, 68 did not complete a pretreatment SDI assessment, 45 did not complete a post-treatment SDI assessment, and 11 had invalid HR data due to equipment malfunction or movement artefacts, leaving a final sample of 118 (88 completers and 30 treatment dropouts who completed post-treatment assessments). There were no significant differences in baseline characteristics between participants included vs. excluded from analysis (see Supplementary Table 1). Sample sizes per condition were CPT + A: n = 73; CPT: n = 20; WA: n = 25. See Table 1 for demographics.

Table 1. Demographics.

	M (SD) or %
Age	37.3 (12.1)
Years of Education	14.2 (2.6)
Income (median)	$10–20,000/yr
Race
White	62%
Black	37%
American Indian or Alaska Native	1%
Asian	0%
Other	1%
Index Trauma Type
Childhood sexual abuse	37%
Childhood physical abuse	8%
Adult sexual assault	29%
Adult physical assault	26%
Exposure to Interpersonal Violence
Childhood sexual abuse	74%
Childhood physical abuse	68%
Adult sexual assault	69%
Adult physical assault	78%

2.2. Treatment

Both CPT and CPT + A were delivered via twelve 60-minute sessions occurring weekly or twice-weekly, whereas WA occurred weekly and consisted of two 60-minute sessions followed by five 2-hour sessions. CPT involves teaching patients to identify and challenge maladaptive beliefs about trauma, themselves, others, and the world. Initial sessions focus on beliefs about the cause and meaning of the trauma, whereas latter sessions focus on trauma-related beliefs about safety, trust, power/control, esteem, and intimacy. In CPT + A, patients also completed two written trauma narratives, which were read in session and for homework. In WA, no cognitive interventions were used. Instead, patients wrote detailed accounts of their trauma(s) in session, then read their account aloud with the therapist and discussed their reactions. Therapists were allowed to use nondirective, supportive statements, but were not permitted to engage in any cognitive challenging of patient’s beliefs. See Resick et al. (Resick et al., 2008) for further detail.

2.3. Measures

The following measures were administered at pre- and post-treatment.

Cardiovascular Reactivity. CVR to the trauma memory was measured using the Script Driven Imagery (SDI) procedure (Pitman et al., 1987), a common assessment of physiological trauma memory reactivity that is associated with PTSD diagnosis and severity (Pole, 2007). Participants listened to two 30-second audio recordings narrating their trauma and then were instructed to imagine the scene just described for another 30 s. To calculate CVR, mean HR during the imagery periods was subtracted from mean HR during the 30 s baseline period prior to each script reading. See Supplemental Materials for full SDI procedures. HR was measured via Ag/AgCl leads attached to the left wrist and right ankle, which were connected to a Coulbourn bioamplifier (S75-01). Peak R-wave signals were detected and interbeat intervals were converted to HR (beats per minute). Data were continuously sampled at 500 Hz. CVR values were square-root transformed to reduce variance caused by extreme scores.

Symptom Measures. Past-month PTSD symptoms were assessed via the Clinician Administered PTSD Scale (CAPS) (α = .91) (Blake et al., 1995) by evaluators blind to treatment condition. Symptom cluster scores were calculated using the King et al. (King et al., 1998) 4-factor model (Reexperiencing, Avoidance, Numbing, and Arousal; α = .72-.82) to more closely approximate DSM-5 clusters. Additional symptom measures included the Beck Depression Inventory (BDI) (α = .91; anchored to past two weeks) (Beck et al., 1996), Pittsburgh Sleep Quality Index (PSQI) (α = .79; anchored to past month) (Buysse et al., 1989) and the Trauma Related Guilt Inventory guilt cognitions subscale (TRGI) (α = .92; no time frame specified) (Kubany et al., 1996).

2.4. Data analysis

Mixed effects models were used to examine the effect of time (i.e. assessment point) and its interaction with variables of interest on trauma memory CVR, with the intercept (i.e. baseline CVR) and slope included as random effects. Prior to running primary analyses, we confirmed there were no significant differences in CVR change between RCTs or due to receipt of sleep-directed hypnosis before CPT (p’s > .20). For Aim 1, we examined the effect of time across the full sample and within each condition to examine if CVR significantly reduced during treatment. This was followed by a test of the interaction between treatment condition and time. For Aim 2, we tested separate models examining fixed effects of each symptom change variable (i.e. post-treatment minus pre-treatment values for CAPS total, CAPS subscales, BDI, TRGI, and PSQI), time, and their interaction on CVR. Significant interactions between symptom change and time indicate a significant relationship with the slope of pre- to post-treatment trauma memory CVR. For our Aim 2 exploratory analyses, we then examined the three-way interaction between time, symptom change, and a categorical variable reflecting baseline CVR. Variables were z-scored to aid in interpretation.

3. Results

3.1. Aim 1: effects of treatment

The baseline model examining the effect of time on trauma memory CVR across treatment conditions indicated that CVR significantly decreased at post-treatment compared to pre-treatment, Est = −0.53, 95% CI = −0.75–−0.31, p < .001. Within conditions, this effect was significant for CPT + A, Est = −0.59, 95% CI = −0.89–−0.29, p < .001, and CPT, Est = −0.66, 95% CI = −1.14–−0.17, p = .01, but not WA, Est = −0.39, 95% CI = −0.92–0.14, p = .14. However, the Time × Treatment Condition interaction indicated no significant differences between conditions on change in trauma memory CVR, F (2,115.00) = 0.33, p = .72. Within-subjects t-tests comparing pre- with post-treatment CVR indicated a medium-sized effects for CPT (d = 0.61, 95% CI = 0.12–1.08), and small effects for CPT + A (d = 0.42, 95% CI = 0.34–0.84) and WA (d = 0.34, 95% CI = −0.07–0.74).

3.2. Aim 2: associations with symptom change

Table 2 presents fixed effects of Time × Symptom Change interactions, reflecting relationships with CVR slope. The effect of PTSD total symptom-change on CVR slope was not significant (p = .06). When examining PTSD clusters separately, there was a significant relationship with reexperiencing (p = .03) indicating greater reductions in reexperiencing symptoms were associated with greater reduction in trauma memory CVR. The effect size indicated that reexperiencing change accounted for 10.5% of the variance in CVR change. No other symptom-change measures emerged as significant predictors.

Table 2. Fixed effects of symptom change variables on slope of trauma memory CVR.

Symptom Change Variable	Estimate	95% CI	p	f^2
Total PTSD (CAPS)	0.22	−0.00–0.44	.055	.072
Reexperiencing (CAPS)	0.26	0.04–0.48	.021	.105
Avoidance (CAPS)	0.20	−0.02–0.43	.069	.065
Numbing (CAPS)	0.17	−0.05–0.39	.128	.044
Hyperarousal (CAPS)	0.07	−0.15–0.29	.541	.008
Depression (BDI)	0.13	−0.08–0.36	.219	.029
Guilt (TRGI)	0.19	−0.04–0.40	.103	.062
Sleep difficulties (PSQI)	0.10	−0.14–0.33	.407	.013

Notes: Each row reflects a separate model that includes main effects of time and the respective symptom change variable. See Supplementary materials for full results. Symptom change variables were scored such that larger negative values reflect greater reduction in symptoms, thus positive effect estimates indicate that greater reductions in symptoms are associated with a steeper slope (i.e. greater reduction) in trauma memory CVR pre- to post-treatment.

To examine whether correspondence between changes in symptoms and CVR differed based on pretreatment CVR, the sample was divided into terciles. Trauma memory CVR values for the lowest group (Suppressors) were all negative (M = −2.47, SD = 1.64), reflecting suppression of HR, whereas the middle group (Low Reactors) exhibited minimal levels of reactivity (M = 0.98, SD = 0.99), and the highest group (High Reactors) exhibited strong reactivity (M = 7.54, SD = 4.34). The three-way interaction between pretreatment CVR group, time, and total PTSD change was significant, F (2,142.48) = 3.18, p = .045, indicating a smaller association between PTSD change and the slope of trauma memory CVR among Low Reactors, Est = −0.42, 95% CI = −0.80–−0.04, p = .032, and Suppressors, Est = −0.36, 95% CI = −0.69–−0.02, p = .037, compared to High Reactors. Similar three-way interactions were observed for reexperiencing, F (2,141.70) = 3.97, p = .022, and numbing clusters, F (2,144.16) = 4.42, p = .014, and for trauma-related guilt, F (2,137.52) = 5.00, p = .008, but not other symptom measures (p’s > .23) (see Supplemental Materials). Post-hoc analyses indicated that among High Reactors only, the slope of CVR change was significantly predicted by reductions in total PTSD, Est = 0.34, 95% CI = 0.03−0.64, p = .030, f² = .13, reexperiencing, Est = 0.32, 95% CI = 0.05–0.60, p = .023, f² = .14, numbing, Est = 0.36, 95% CI = 0.04–0.68, p = .030, f² = .13 and trauma-related guilt, Est = 0.55, 95 CI = 0.22–0.88, p = .001, f² = .28. Moderator results for total PTSD symptoms and trauma-related guilt are depicted in Figure 1.

Figure 1. Scatter plots of changes in trauma memory CVR in relation to changes in PTSD symptoms and trauma-related guilt across High reactors, Low reactors, and Suppressors. CVR = Cardiovascular Reactivity; CAPS = Clinician Administered PTSD Scale; TRGI = Trauma-Related Guilt Inventory. * p < .05; **p < .01. CVR data reflect change in square-root transformed values. TRGI values reflect reduction in mean item score (range 0-4), whereas CAPS values reflect reduction in summed CAPS (range 0–136). More positive numbers reflect greater CVR and symptom reduction pre-to-post-treatment.

4. Discussion

The present study found a significant, moderate reduction in CVR during trauma memory recall over the course CPT with or without the written trauma account. To our knowledge this is the first demonstration of a reduction in physiological trauma memory reactivity in cognitively focused PTSD treatment, extending research on interventions involving imaginal exposure (e.g. prolonged exposure) that have similarly found treatment-related reductions in CVR (Blanchard et al., 2002; Bourassa et al., 2020; Dunne et al., 2012; Wangelin & Tuerk, 2015). These results also add to the body of research on other physiological impacts of CPT, which has found reductions in physiological reactivity to stimuli not directly related to the trauma (loud tones) among CPT responders (Griffin et al., 2012), as well as improved 24-hour heart rate variability (Watkins et al., 2023). A significant reduction in CVR was not found in WA, which notably saw inferior symptom outcomes in the parent trial (Resick et al., 2008), though this null result should be interpreted cautiously given the small sample size and lack of significant differences in CVR change between treatments.

When examining relationships between reductions in CVR and symptom change, the only significant association that emerged was with reexperiencing symptoms, potentially because the reexperiencing cluster includes the symptoms most closely related to physiological reactivity to the trauma memory. Moderator analyses, however, suggested such relationships varied based on pretreatment trauma memory CVR, and a significant association with changes in PTSD symptoms, numbing, and trauma-related guilt emerged among High Reactors. It is possible that null results across the full sample resulted from the substantial portion of participants who exhibited either minimal or suppressed CVR at pretreatment (Suppressor and Low Reactor groups), causing a floor effect for CVR change. Blunted CVR to the trauma memory and other emotional stimuli is not atypical in PTSD (Sack et al., 2012), and may reflect dissociative processes 24. It has also been found to be associated with chronic childhood exposure to trauma 14, which was prevalent in the present sample. Variability in pretreatment trauma memory reactivity could contribute to conflicting findings in this area (Blanchard et al., 2002; Bourassa et al., 2020; Maples-Keller et al., 2019; Rabe et al., 2006). Even among High Reactors, however, relationships with PTSD symptoms were modest (r = 0.29), mirroring prior studies (Blanchard et al., 2002; Rabe et al., 2006). Such results suggest that reductions in trauma memory CVR and PTSD symptoms reflect distinct change process.

A somewhat stronger relationship emerged between changes in trauma-related guilt and reduction in CVR among High Reactors (r = 0.43), which is notable given that challenging guilt-related beliefs about the trauma is a core component of CPT (Resick et al., 2017). Such a link between reductions in trauma-related guilt and trauma memory CVR is consistent with evidence that resolving self-blame and other guilt-related cognitions in CPT facilitates a positive treatment response (Schumm et al., 2015) which may extend to CVR.

Limitations to this study include DSM-IV-based PTSD assessment, reliance on HR as the sole indicator of physiological reactivity, limited generalizability of findings beyond women with PTSD secondary to interpersonal violence, and a limited sample size for comparing treatment conditions. It is worth noting, however, that the present sample is larger than most prior investigations of CVR change in PTSD treatment (Bourassa et al., 2021). Implications of this research include support for the idea that physiological trauma memory reactivity can be reduced through cognitive techniques, and that changes in trauma memory CVR appear to be a relevant correlate of clinical improvement for a subgroup of women with PTSD secondary to interpersonal violence. Future research would benefit from a control condition to isolate specific effects of CPT on CVR and should attend to individual differences in baseline trauma memory reactivity when examining physiological change during treatment. Assessing changes in additional psychophysiological (e.g. fear-potentiated startle, skin conductance) and subjective (e.g. subjective distress, cognitive avoidance) measures during trauma recall would also help further illuminate the nature of changes in trauma memory reactivity during CPT.

Disclosure statement

Dr Resick receives royalties from Guildford Press for sales of the Cognitive Processing Therapy manual. The other authors have no competing interests to report.

Data availability statement

Data can be made available pending a Data Use Agreement with VA Boston Healthcare System.

Additional information

Funding

This research was supported by funding from the National Center for Complementary and Integrative Health (NCCIH) grant R34-MH-074-937 awarded to Tara E. Galovski, the National Institute of Mental Health (NIMH) grant 2-R01-MH51509 awarded to Patricia A. Resick, and NIMH grant K23-MH129878 awarded to Joseph K. Carpenter. The contents of this research are the sole responsibility of the authors and do not necessarily represent the views of the NCCIH or NIMH.