PTSD and depression severity are associated with cardiovascular disease symptoms in trauma-exposed women

ABSTRACT

Background: Posttraumatic stress disorder (PTSD) and depression are associated with increased risk for cardiovascular disease (CVD), which is the leading cause of death and disability worldwide. Epidemiological studies have revealed these illnesses to be highly comorbid, particularly among women. In the current study, we explored associations between indices of cardiovascular health, PTSD, and depression among a sample of trauma-exposed individuals assigned female at birth.

Methods: Participants were N = 49 individuals without CVD who reported lifetime Criterion A trauma exposure. Blood pressure (BP), heart rate (HR), and high-frequency heart rate variability (HF-HRV) were collected during a 5-minute resting period. Symptoms of CVD (e.g. extremity pain and swelling, shortness of breath), PTSD, and depression were assessed, along with an exploratory measure of anhedonia.

Results: Trauma exposure was positively correlated with systolic BP (r = .32, p = .029) and diastolic BP (r = .30, p = .040). The number of reported CVD symptoms was positively correlated with symptoms of PTSD (r = .41, p = .004), depression (r = .40, p = .005) and anhedonia (r = .38, p = .007). CVD symptoms were also significantly associated with PTSD (β = .41, t = 2.43, p = .023), depression (β = .40, t = 2.76, p = .009), and anhedonia (β = .38, t = 2.51, p = .017) after controlling for age and trauma exposure. These associations were not moderated by HF-HRV in our sample.

Conclusions: Our results support the association between PTSD and depressive symptoms and worse cardiovascular functioning among an often-overlooked population that is particularly vulnerable to these illnesses. Future studies should investigate residual impacts of PTSD and depression treatment on CVD risk among trauma-exposed individuals, particularly women.

HIGHLIGHTS

• Trauma exposure and PTSD are associated with depression and cardiovascular disease (CVD) risk.

• We explored cardiovascular health, PTSD, and depression among 49 trauma-exposed individuals assigned female at birth.

• Trauma exposure positively correlated with blood pressure.

• CVD symptoms were positively correlated with PTSD, depression, and anhedonia.

• Associations were not moderated by heart rate variability.

Antecedentes: El trastorno de estrés postraumático (TEPT) y la depresión están asociados con un mayor riesgo de enfermedad cardiovascular (ECV), que es la principal causa de muerte y discapacidad en todo el mundo. Los estudios epidemiológicos han revelado que estas enfermedades son altamente comórbidas, particularmente entre las mujeres. En el estudio actual, exploramos las asociaciones entre los índices de salud cardiovascular, el TEPT y la depresión en una muestra de personas asignadas como mujeres al nacer, expuestas a traumas.

Métodos: Los participantes fueron N = 49 personas sin ECV que reportaron exposición a traumas del Criterio A durante la vida. Se recogieron la presión arterial (PA), la frecuencia cardíaca (FC) y la variabilidad de la frecuencia cardíaca de alta frecuencia (HF-HRV) durante un período de descanso de 5 minutos. Se evaluaron los síntomas de ECV (p. ej., dolor e hinchazón de las extremidades, dificultad para respirar), TEPT y depresión, junto con una medida exploratoria de anhedonia.

Resultados: La exposición al trauma se correlacionó positivamente con la PA sistólica (r = .32, p = .029) y la PA diastólica (r = .30, p = .040). El número de síntomas de ECV notificados se correlacionó positivamente con los síntomas de TEPT (r = 0,41, p = 0,004), depresión (r = .40, p = .005) y anhedonia (r = .38, p = .007). Los síntomas de ECV también se asociaron significativamente con TEPT (β = .41, t = 2,43, p = .023), depresión (β = .40, t = 2.76, p = .009) y anhedonia (β = .38, t = 2.51, p = .017) después de controlar por edad y exposición al trauma. Estas asociaciones no fueron moderadas por HF-HRV en nuestra muestra.

Conclusiones: Nuestros resultados respaldan la asociación entre TEPT, síntomas depresivos y peor funcionamiento cardiovascular entre una población a menudo ignorada que es particularmente vulnerable a estas enfermedades. Los estudios futuros deberían investigar los impactos residuales del TEPT y el tratamiento de la depresión en el riesgo de ECV entre las personas expuestas al trauma, en particular las mujeres.

背景：创伤后应激障碍 (PTSD) 和抑郁与全世界死亡和残疾主要原因——心血管疾病 (CVD) 的风险增加有关。流行病学研究表明，这些疾病是高度共病的，尤其是在女性中。在本研究中，我们在出生时被指定为女性的创伤暴露个体样本中探索了心血管健康指数、PTSD 和抑郁之间的关联。

方法：参与者是 49 名没有 CVD 的人，他们报告了终身标准 A 创伤暴露。在 5 分钟的休息期间收集血压 (BP)、心率 (HR) 和高频心率变异性 (HF-HRV)。评估了 CVD（例如，肢体疼痛和肿胀、呼吸急促）、PTSD 和抑郁症状，以及快感缺乏的探索性测量。

结果：创伤暴露与收缩压 (r = .32, p = .029) 和舒张压 (r = .30, p = .040) 呈正相关。报告的 CVD 症状数量与 PTSD（r = .41，p = .004）、抑郁（r = .40，p = .005）和快感缺失（r = .38，p = .007）症状呈正相关 。在控制了年龄和创伤暴露后，CVD 症状也与 PTSD (β = .41, t = 2.43, p = .023)、抑郁 (β = .40, t = 2.76, p = .009) 和快感缺失 (β = .38, t = 2.51, p = .017)相关。在我们的样本中，这些关联不受 HF-HRV 的调节。

结论：在一个对相关疾病易感却经常被忽视的群体中，我们的结果支持了 PTSD 与抑郁症状和心血管功能恶化之间的关联。未来的研究应该考查 PTSD 和抑郁治疗对创伤暴露个体（尤其是女性）CVD 风险的残余影响。

KEYWORDS:

• PTSD
• Depression
• Anhedonia
• Cardiovascular
• Blood pressure

PALABRAS CLAVE:

• TEPT
• depresión
• anhedonia
• cardiovascular
• presión arterial

关键词:

• PTSD
• 抑郁
• 快感缺失
• 心血管
• 血压

1. Introduction

Cardiovascular disease (CVD) has been identified as the leading cause of death and disability worldwide (World Health Organization, 2021). Beyond afflicting the heart and blood vessels, CVD shares a reciprocal relationship with mental health concerns like depression and traumatic stress, such that the presence of one condition is associated with an increased risk of developing the other (Lichtman et al., 2008; Nemeroff & Goldschmidt-Clermont, 2012; Thomas et al., 2004; Thombs et al., 2006). Given its impact on the prevalence of mental illness, gender may further compound one’s risk for CVD. For example, women experience higher rates of major depressive disorder (MDD) compared to men (Weissman et al., 1996), and they are more susceptible to developing post-traumatic stress disorder (PTSD) following a traumatic event (Kilpatrick et al., 2013). To better understand the presentation of comorbid mental illness and CVD among more vulnerable populations, further research involving trauma-exposed women is warranted.

Several epidemiological studies have highlighted the debilitating cycle of CVD and depression. When assessing patients with acute myocardial infarction (AMI), Thombs and colleagues (2006) reported that nearly 20–30% of their sample met criteria for MDD, a figure that far exceeded the 5% prevalence rate reported in the general population. In another study, Celano and Huffman (2011) discovered that 50–70% of sampled CVD patients reported experiencing a depressive episode prior to their first cardiac event. Anhedonia, a blunted affective state characterized by a lack of pleasure or interest in daily activities, may serve as a particularly cardiotoxic symptom cluster of depression. In two separate studies involving patients with acute coronary syndrome, anhedonia was associated with future severe adverse cardiac events above and beyond depressed mood (Davidson et al., 2010; Leroy et al., 2010). Among a sample of adolescents, anhedonia was also the strongest predictor of low high-frequency heart rate variability (HF-HRV; Vazquez et al., 2016), a measure of parasympathetic control. Further investigation of anhedonia as a potential subtype of depression may offer valuable insight into cardiovascular outcomes, particularly among at-risk populations.

Traumatic stress is another mental health condition that may exacerbate CVD risk (Cohen et al., 2015). For some, the stress associated with trauma exposure does not dissipate over time and instead contributes to adverse psychological outcomes, such as PTSD and depression (Copeland et al., 2018; Cougle et al., 2009; Do et al., 2019; Rytwinski et al., 2013). A comparison study of first responders and civilians with PTSD suggests that prolonged trauma exposure may also be linked to anhedonia, such that first responders reported higher rates of blunted psychological reactivity, loss of interest, and emotional numbing (Bryant, 2022). Given the close relationship between traumatic stress and depression, it is not surprising that trauma exposure and PTSD have also been linked to heightened CVD risk (Hendrickson et al., 2013; Sumner et al., 2015) and altered cardiovascular physiology, such as elevated heart rate (HR) and blood pressure (BP), and lower HF-HRV (see O'Donnell et al., 2021 for a review). It is therefore critical to consider the severity of both PTSD and depression symptoms when examining CVD risk among trauma-exposed individuals.

Gender is also important to consider when examining relationships among traumatic stress, depression, and CVD. The cycle of these conditions has been shown to disproportionately burden women, even as men in the general population experience a higher incidence of CVD than do premenopausal women. Compared to affected men, women with CVD experience more severe depression, while women with depression face a greater risk of developing CVD (Möller-Leimkühler, 2007). Women are also more vulnerable to the effects of trauma exposure. While men report higher rates of trauma exposure, women report higher rates of interpersonal trauma (e.g. assault) and higher levels of distress following traumatic events (Frans et al., 2005). Given these gender disparities, it is particularly important to focus on women when studying the links between psychiatric illnesses and CVD.

To address this gap, the current study examined associations between PTSD and depression symptoms with cardiovascular physiology in a sample of trauma-exposed individuals assigned female at birth. In light of emergent evidence for the cardiotoxic nature of anhedonia (Davidson et al., 2010; Leroy et al., 2010), we included an exploratory measure of anhedonia in our assessment of depressive symptoms. Cardiovascular measures included BP, HR, and HF-HRV. Participants were also asked to report somatic symptoms associated with CVD risk (e.g. chest pain, shortness of breath). We expected symptoms of PTSD, depression, and anhedonia to be positively correlated with BP, resting HR, and CVD symptoms. On the other hand, we expected a negative correlation between these symptoms and HF-HRV. Given prior work implicating low HF-HRV as a moderator of stress and increased HR (Sack et al., 2004), we expected that the associations between all three psychological self-reports and BP, HR, and CVD symptoms would be stronger among those with low HF-HRV.

2. Methods

2.1. Participants and procedure

Participants were 49 trauma-exposed individuals assigned female at birth (M age = 31.58, SD = 9.64). In terms of gender, 44 (90%) self-identified as women, three (6%) identified as non-binary, one (2%) identified as genderqueer, and one (2%) did not provide a gender. Extent of trauma history was calculated as the total number of traumatic event types experienced across the lifetime, as reported on the Life Events Checklist (LEC-5; Weathers et al., 2013). Trauma types include but are not limited to natural disaster, physical assault, sexual assault, combat, and life-threatening illness. PTSD status was assessed with the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5; Weathers et al., 2018). Participants with existing CVD were excluded, as the goal of this study was to study cardiovascular physiology and CVD risk in trauma-exposed women without overt CVD. In terms of race, 42 participants (85.7%) identified as White, three (6.1%) identified as Asian or South-Asian, two (4.1%) indicated that their race was not listed, one (2.0%) identified as Black or African American, and one participant (2.0%) chose not to respond.

Participants completed a battery of self-report measures evaluating symptoms of CVD (Health Questionnaire), PTSD, depression, and anhedonia (described below). Approximately twenty minutes after arrival, participants completed five-minute assessments of BP (average of three measurements), followed by assessments of resting HR and HF-HRV. All procedures were in accordance with the ethical standards of the Institutional Review Board, and the United States Federal Policy for the Protection of Human Subjects. Written informed consent was obtained from all participants following an explanation of the study’s procedures, and participants were compensated $100 for completion of the study.

2.2. Measures

PTSD Checklist – 5. The PCL-5 is a 20-item self-report survey of PTSD symptoms using the four DSM-5 symptom clusters (Intrusions, Avoidance, Negative Alterations in Cognition and Mood, and Alterations in Arousal and Reactivity). All items are rated on a 5-point Likert-type scale from 0 to 4, with higher scores indicating worse PTSD symptoms. Cronbach’s alphas in the current study were .93 (Total), .85 (Intrusions), .70 (Avoidance), .89 (Negative Alterations in Cognition and Mood), and .77 (Alterations in Arousal and Reactivity).

Beck Depression Inventory-II. The BDI-II is a 21-item self-report survey used to measure the severity of depression symptomatology. The survey has demonstrated high internal consistency and retest reliability, as well as improved concurrent, content, and structural validity when compared with the original BDI (Wang & Gorenstein, 2013). Each item of the BDI-II is rated on a 4-point scale ranging from 0 to 3, with a maximum total score of 63. A total score between 0 and 13 is considered minimal depression, 14–19 is mild, 20–28 is moderate, and 29–63 is severe. Cronbach’s alpha in the current study was .95.

Inventory of Depressive Symptomatology-Self Report. The IDS-SR is a 30-item self-report survey of depressive symptoms. In terms of psychometric properties, this measure has demonstrated adequate face validity and reasonable internal consistency, interrater reliability, and concurrent and discriminant validity (Rush et al., 1996). Cronbach’s alpha in the current study was .94.

Exploratory Measure of Anhedonia. Drawing upon prior research involving a BDI anhedonia sub-score (Pizzagalli et al., 2005), four items from the BDI-II were included in our exploratory self-report measure of anhedonia: Item 4 (loss of pleasure), Item 12 (loss of interest), Item 15 (loss of energy), and Item 21 (loss of interest in sex). Additionally, four overlapping items from the IDS-SR were also included: Item 19 (general interest), Item 20 (energy level), Item 21 (capacity for pleasure or enjoyment), and Item 22 (interest in sex). Our 8-item measure demonstrated high internal consistency (α = .922).

Health Questionnaire. The Health Questionnaire was developed based on several pre-existing measures to comprehensively assess participant physical health (e.g. perceived health, medical history, menstrual cycle information). Specifically relevant to the present analysis is this questionnaire’s assessment of CVD symptoms, including ankle swelling, shortness of breath, irregular heart rate, and pain in the calves, chest, or lower extremities.

2.3. Physiological data collection and processing

Blood Pressure. BP data were collected using an IntelliSense blood pressure monitor (Omron Corporation). The device measures BP three times, and the average of these three systolic and diastolic blood pressures is displayed. BP measurements occurred following five minutes of seated rest.

Heart Rate and High Frequency-Heart Rate Variability. Biopac MP150 for Windows (Biopac Systems Inc.) was used to collect resting cardiovascular physiological data (e.g. HR and HF-HRV) at a sampling rate of 1 kHz, amplified and digitized using the Biopac system. Following BP assessments, these data were collected over the course of a five-minute resting state recording. These data were processed using MindWare software (MindWare Technologies, Inc.). To obtain HR and HF-HRV data, MindWare identifies electrocardiogram R-peaks and R-R intervals (i.e. the time between successive heart beats). The system flags R-peaks that have been identified as improbable, and these R-peaks can then be manually examined and corrected. HF-HRV was derived by spectral analysis of one-minute epochs with a Hamming windowing function, a baseline and muscle noise filter, and log transformed. Settings for the high frequency band were based on standard recommendations for HF-HRV data (0.12–0.40 Hz; Task Force, 1996).

2.4. Data analysis

No significant outliers were identified for study variables (≥3 SDs). Bivariate correlations were used to probe the associations between CVD symptoms, resting HR, resting HF-HRV, average diastolic and systolic BP, extent of traumatic experiences, symptoms of PTSD, depression, and anhedonia. Next, three linear regressions were conducted with PTSD symptoms, depression symptoms, and anhedonia symptoms as outcome variables. For all models, predictor variables included CVD symptoms, resting HR, resting HF-HRV, and average diastolic and systolic BP. Age and extent of trauma history were included as covariates in Step 2 for all models. All calculations were computed using SPSS version 28 with a significance level of p < .05.

3. Results

Participants in this study ranged between 20 and 54 years old, with an average age of 31.58. Over half of the sample met criteria for PTSD (n = 29, 59.2%). Similarly, all participants were pre-menopausal, and a slight majority were naturally cycling (n = 28, 57.1%). In terms of medications, n = 18 (36.73%) reported using anti-depressants and n = 16 (32.65%) reported using anti-anxiety medications. The number of reported CVD symptoms was significantly positively correlated with PTSD (r = .41, p = .004), depression (r = .40, p = .005), and anhedonia (r = .38, p = .007). Significant positive correlations were also observed between trauma exposure and both systolic BP (r = .32, p = .029) and diastolic BP (r = .30, p = .040). See Table 1 for additional bivariate correlations and descriptive statistics.

Table 1. Correlations and descriptive statistics for study variables.

	1	2	3	4	5	6	7	8	9	10	11	12	13	14	15
1. Systolic BP	–
2. Diastolic BP	.769**	–
3. Heart Rate	.154	.184	–
4. HF-HRV	−.256	−.197	−.602**	–
5. CVD Symptoms	.008	−.079	.059	−.026	–
6. Anhedonia Score	.191	.228	.155	.069	.382**	–
7. BDI-II Score	.228	.236	.220	.050	.396**	.913**	–
8. LEC-5-E	.524**	.491**	−.201	−.273	.182	.147	.185	–
9. PCL-5 Total Score	.201	.216	.095	.041	.407**	.722**	.782**	.157	–
10. PCL-5 Cluster B	.186	.210	.129	−.042	.462**	.564**	.628**	.223	.878**	–
11. PCL-5 Cluster C	−.039	.002	−.097	.077	.088	.385**	.378**	.178	.696**	.494**	–
12. PCL-5 Cluster D	.265	.256	.055	.020	.294*	.710**	.766**	.138	.924**	.734**	.588**	–
13. PCL-5 Cluster E	.136	.157	.147	.108	.457**	.697**	.755**	.068	.896**	.731**	.606**	.721**	–
14. STAI-S Score	−.016	−.089	−.003	.083	.131	−.191	−.151	−.035	−.165	−.101	−.198	−.257	−.015	–
15. STAI-T Score	−.037	−.007	−.009	.293	.160	.347*	.444**	−.179	.431**	.272	.271	.398**	.490**	.245	–
Mean	120.29	78.58	72.97	6.01	.76	7.81	19.17	3.76	34.98	8.38	3.46	13.08	10.06	41.27	46.15
SD	13.74	12.19	11.69	1.21	1.05	6.07	13.32	1.76	17.23	4.80	2.06	7.25	5.46	5.36	4.49
Minimum	97.00	55.00	50.98	2.93	0.00	0.00	0.00	0.00	0.00	0.00	0.00	0.00	0.00	31.00	37.00
Maximum	154.00	106.00	102.72	8.27	3.00	23.00	52.00	7.00	75.00	20.00	8.00	28.00	24.00	57.00	56.00

Note: *p < .05; **p < .01; BP = Blood Pressure; HF-HRV = high frequency heart rate variability; CVD = cardiovascular disease; BDI-II = Beck Depression Inventory II; LEC-5-E = Life Events Checklist for DSM-5-Experienced; PCL-5 = PTSD Checklist for DSM-5; STAI-S = State-Trait Anxiety Inventory-State; STAI-T = State-Trait Anxiety Inventory-Trait.

A summary of the three regression models can be found in Table 2. The first model with PTSD symptoms as the dependent variable was not significant (R² = .39, p = .069). While systolic BP, HR, and HF-HRV were not significant in this model, diastolic BP (β = .66, t = 2.07, p = .05) and reported CVD symptoms (β = .41, t = 2.43, p = .023) were significantly associated with PTSD symptoms. The second regression model with depression symptoms as the dependent variable was significant and accounted for 32% of the variance in depression symptoms (R² = .32, p = .047). As expected, the number of reported CVD symptoms was significantly associated with depression symptoms (β = .40, t = 2.76, p = .009). However, BP, HR, and HF-HRV were not significantly associated with depression symptoms. Finally, the third regression model with anhedonia symptoms as the dependent variable was not significant (R² = .26, p = .135), and neither were BP, HR, or HF-HRV. However, the number of reported CVD symptoms was significantly associated with anhedonia total score (β = .38, t = 2.51, p = .017).

Table 2. Linear regression models.

	β	t	p
Dependent Variable: PCL-5 Score
Systolic Blood Pressure	−.430	−1.305	.204
Diastolic Blood Pressure	.662	2.065	.050*
Heart Rate	.101	.406	.689
HF-HRV	.181	.685	.500
CVD Symptoms	.412	2.428	.023*
Age	−.116	−.429	.672
LEC-5 – Experienced	.181	.790	.437
R^2= .393
Dependent Variable: BDI-II Score
Systolic Blood Pressure	.094	.332	.742
Diastolic Blood Pressure	.246	.956	.346
Heart Rate	.282	1.203	.237
HF-HRV	.276	1.167	.251
CVD Symptoms	.401	2.764	.009*
Age	−.025	−.097	.923
LEC-5 – Experienced	−.087	−.475	.638
R^2= .317
Dependent Variable: Anhedonia Score
Systolic Blood Pressure	.086	.292	.772
Diastolic Blood Pressure	.249	.927	.360
Heart Rate	.133	.541	.592
HF-HRV	.170	.687	.497
CVD Symptoms	.379	2.508	.017*
Age	−.142	−.531	.599
LEC-5 – Experienced	−.039	−.206	.838
R^2= .257

Note: *p < .05; PCL-5 = PTSD Checklist for DSM-5; HF-HRV = high frequency heart rate variability; CVD = cardiovascular disease; LEC-5 = Life Events Checklist for DSM-5; BDI-II = Beck Depression Inventory II.

To probe moderation by HF-HRV, an interaction term was created using HF-HRV and CVD symptoms given that CVD symptoms were significantly associated with PTSD, depression, and anhedonia, while HR and BP were not. The HF-HRV × CVD symptoms interaction was calculated by mean-centering the variables and then multiplying these mean-centered values. The interaction term was not significant for the PTSD model (β = .062, t = .197, p = .845), depression model (β = −.17, t = −.92, p = .365), or anhedonia model (β = −.10, t = -.531, p = .599). This suggests that while CVD symptoms were significantly associated with PTSD, depression, and anhedonia symptoms, these associations were not stronger for individuals with low HF-HRV. In other words, our findings did not support moderation by HF-HRV.

4. Discussion

It is well documented that traumatic stress and depression are closely linked to CVD, and that they disproportionately affect women. Recognizing this gender gap, our study examined the relationships between PTSD and depressive symptoms and cardiovascular physiology among trauma-exposed individuals assigned female at birth. Overall, indices of cardiovascular health (i.e. BP and CVD symptoms) were worse among those who reported experiencing a higher volume of traumatic events and more severe symptoms of PTSD and depression. This connection between psychological and cardiovascular health may compound the importance of early intervention among women experiencing depression and traumatic stress.

Preliminary correlation analyses supported our hypothesis that individuals with worse PTSD and depressive symptoms, as well as anhedonia, would report experiencing more CVD symptoms. Previous studies involving CVD populations have linked depression symptoms to chest pain (Barnett et al., 2017; Hayek et al., 2017), shortness of breath (Barnett et al., 2017), and impaired lower extremity functioning (McDermott et al., 2003). Anhedonia has also been associated with increased somatic symptoms in CVD patients (Pelle et al., 2011). Furthermore, research involving acute coronary syndrome patients has highlighted anhedonia as a particularly cardiotoxic symptom cluster of depression (Davidson et al., 2010; Leroy et al., 2010). As discussed by Davidson and colleagues (2010), separate biological correlates (i.e. serotonergic dysfunction in depressed mood and catecholaminergic dysfunction in anhedonia) may help explain differences in clinical outcomes among these groups. Unlike prior studies highlighting the heightened cardiotoxicity of anhedonia, the association between anhedonia and reported CVD symptoms was not stronger than the association involving depression in our sample. In contrast to existing literature on PTSD, depression, and CVD comorbidity (Carney et al., 1999; Tessier et al., 2017), no link between HR and PTSD or depression symptom severity was observed in our sample. However, BP did increase with number of trauma exposures, replicating prior work suggesting that trauma and PTSD are associated with altered cardiovascular physiology and hypertension (O'Donnell et al., 2021).

Despite our initial correlation findings involving systolic and diastolic BP, these physiological indices were not significant in any regression model. However, the number of self-reported CVD symptoms was significant in the regression models with PTSD and depression symptom severity as dependent variables, controlling for age and number of traumatic exposures. It is possible that noticeable CVD symptoms, such as pain or swelling in the chest and lower extremities, may be stronger indicators of poor cardiovascular health than the physiological indices measured. Our model with anhedonia was not significant, which was not expected given prior studies that linked anhedonia to adverse cardiac events (Davidson et al., 2010; Leroy et al., 2010) and all-cause mortality (Damen et al., 2013; Doyle et al., 2012) among CVD patients, even when controlling for the presence and severity of depression. In the future, the use of a standardized anhedonia measure rather than sub-scores of the BDI-II and IDS may help clarify the cardiotoxicity of anhedonia.

Finally, although extensive literature has linked low HF-HRV to PTSD (Hauschildt et al., 2011; Sack et al., 2004) and depression (Brunoni et al., 2013; Carney et al., 1995; Koch et al., 2019; Wagner et al., 2019), HF-HRV was not a significant variable in our correlation, regression, or moderation analyses. Differences in the populations sampled may help explain these inconsistent results. For example, studies included in a meta-analysis conducted by Koch et al. (2019) consisted of clinically depressed individuals, whereas our sample included women with a range of PTSD and depression symptoms from the general population (i.e. not a clinical sample). Stress induced from the commute to the site, as well as preliminary questions regarding trauma history, may have also influenced HF-HRV readings within our sample. Additionally, nearly half of the participants included in our study were not naturally cycling, a factor that may also impact HF-HRV (Teixeira et al., 2015). Lastly, patterns in HF-HRV levels may have been obscured by medication status. Roughly 55% (n = 27) of our sample reported taking antidepressant or anti-anxiety medications, which have been associated with altered HF-HRV in clinical populations (Licht et al., 2008; O'Regan et al., 2015). While prior studies found that antidepressant use was associated with lower HF-HRV among clinical samples, we did not observe this association. However, this may be due to our sample being a general trauma-exposed sample and not a clinical sample.

While treatment implications from the current study are limited, it is worth noting that studies of cognitive behavioural therapy (CBT) for PTSD and depression show promise for reducing CVD risk. For example, preliminary studies have demonstrated that CBT appears to reduce HR and BP and improve HRV (Bourassa et al., 2020; Dunne et al., 2012; Fecteau & Nicki, 1999; Rabe et al., 2006; Wells et al., 2015). Further, exercise is one of the primary behavioural interventions for CVD risk and is also used as a psychiatric intervention (e.g. within the context of behavioural activation). Given the high comorbidity of PTSD and depression, and the potential for both CBT and exercise to ameliorate symptoms, future studies examining the effects of CBT and exercise (and their combination) on CVD risk are warranted in this population.

Several study strengths and limitations should be considered alongside the results presented here. First, our sample was comprised exclusively of trauma-exposed individuals assigned female at birth, most of whom identified as women, a high-risk and under-examined population. While providing valuable insight into psychiatric symptoms and cardiovascular risk experienced by this population, the novelty of our sample reduces the generalizability of our results and necessitates replication. Additionally, our reduced statistical power limited our ability to consider the potential impact of important individual characteristics, such as race and trauma type. Next, the high correlation between BDI-II and PCL-5 scores, though expected, challenged our ability to differentiate the relationship between CVD and depression from the relationship between CVD and traumatic stress. Finally, while our measure of CVD symptoms was not significantly associated with state or trait anxiety, it is possible that they are more reflective of general anxiety and not actual CVD risk. Future research would benefit from the inclusion of more specific and objective CVD risk measures in addition to self-report.

The present study provided support for the link between PTSD and depressive symptoms with worse CVD symptoms. Our sample represented an often-overlooked population that is particularly vulnerable to trauma-related sequalae and CVD. Given that participants with more severe PTSD and depressive symptoms displayed worse cardiovascular health, future studies should investigate residual impacts of treatment options in this population. More specifically, it may be the case that early psychiatric intervention among trauma-exposed individuals, particularly women, also has the potential to lower CVD risk.

Disclosure statement

KJR has received consulting income from Alkermes, research support from NIH, Genomind and Brainsway, and he is on scientific advisory boards for Janssen and Verily, all of which is unrelated to the present work.

Data availability statement

The data that support the findings of this study are available from the corresponding author, [AVS], upon reasonable request.

Additional information

Funding

AVS supported by NIH K23MH125920-01 and AHA 20CDA35310031. KJR supported by the Frazier Foundation Grant for Mood and Anxiety Research, and Partners Healthcare Biobank.