ABSTRACT

HIGHLIGHTS

Abstract

Abstract

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

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.

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
R2=.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
R2=.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
R2=.257

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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.

References