Posttraumatic stress disorder (PTSD) is an anxiety disorder initiated by exposure to a traumatic event and characterized by intrusive thoughts about the event, attempts to avoid reminders of the event, and physiological hyperarousal. In a number of large prospective observational studies, PTSD has been associated with incident cardiovascular disease (CVD) and mortality. Also, in recent years, a number of studies have shown that cardiovascular events can themselves cause PTSD in more than 1 in 8 patients with acute coronary syndrome. Further, a few small studies suggest that PTSD secondary to an acute CVD event then places patients at increased risk for subsequent CVD events and mortality. In this article, we review the evidence for a link between PTSD and CVD, and discuss potential mechanisms for that association as well as future directions for research.

Background

Patients with post-traumatic stress disorder (PTSD) are at increased risk for adverse outcomes from comorbid medical conditions. Medication non-adherence is a potential mechanism explaining this increased risk.

Methods

We examined the association between PTSD and medication adherence in a cross-sectional study of 724 patients recruited from two Department of Veterans Affairs Medical Centers between 2008 and 2010. PTSD was assessed using the Clinician Administered PTSD Scale. Medication adherence was assessed using a standardized questionnaire. Ordinal logistic regression models were used to calculate the odds ratios (ORs) for medication non-adherence in patients with versus without PTSD, adjusting for potential confounders.

Results

A total of 252 patients (35%) had PTSD. Twelve percent of patients with PTSD reported not taking their medications as prescribed compared to 9% of patients without PTSD (unadjusted OR 1.85, 95% CI 1.37-2.50, P<0.001). Forty-one percent of patients with PTSD compared to 29% of patients without PTSD reported forgetting medications (unadjusted OR 1.90, 95% CI 1.44-2.52, P<0.001). Patients with PTSD were also more likely to report skipping medications (24% versus 13%; unadjusted OR 2.01, 95% CI 1.44-2.82, P<0.001). The association between PTSD and non-adherence remained significant after adjusting for demographics, depression, alcohol use, social support, and medical comorbidities (adjusted OR 1.47, 95% CI 1.03-2.10, P=0.04 for not taking medications as prescribed and 1.95, 95% CI 1.31-2.91, P=0.001 for skipping medications).

Conclusions

PTSD was associated with medication non-adherence independent of psychiatric and medical comorbidities. Medication non-adherence may contribute to the increased morbidity and mortality observed in patients with PTSD.

The notion that psychological states can influence physical health is hardly new, and perhaps nowhere has the mind-body connection been better studied than in cardiovascular disease (CVD). Recently, large prospective epidemiologic studies and smaller basic science studies have firmly established a connection between CVD and several psychological conditions, including depression, chronic psychological stress, posttraumatic stress disorder (PTSD), and anxiety. In addition, numerous clinical trials have been conducted to attempt to prevent or lessen the impact of these conditions on cardiovascular health. In this article, we review studies connecting depression, stress/PTSD, and anxiety to CVD, focusing on findings from the last 5 years. For each mental health condition, we first examine the epidemiologic evidence establishing a link with CVD. We then describe studies of potential underlying mechanisms and finally discuss treatment trials and directions for future research.

Objective

Elevated inflammation has been repeatedly observed in posttraumatic stress disorder (PTSD), and it may drive the development of both psychiatric symptoms and physical comorbidities. However, it is not clear if elevated inflammation is a feature of both remitted and current PTSD, and little is known about relationships between specific clusters of PTSD symptoms and inflammation. Exaggerated threat sensitivity, as indexed by threat reactivity and avoidance of perceived threats, may be particularly closely associated with inflammation.

Methods

We assessed PTSD symptoms and threat sensitivity using the Clinician Administered PTSD Scale in 735 Veterans Affairs patients (35% current PTSD; 16% remitted PTSD) who participated in the Mind Your Heart Study (mean age=59±11; 94% male). High sensitivity C-reactive protein (hsCRP), white blood cell count (WBC), and fibrinogen were used as indices of inflammation. Analysis of covariance models with planned contrasts were used to examine differences in inflammation by PTSD status, adjusting for age, sex, race, kidney function and socioeconomic status.

Results

Individuals with current PTSD had significantly higher hsCRP and WBC than patients with no history of PTSD, but there were no significant differences in inflammatory markers between those with remitted versus no history of PTSD. Within patients with current PTSD, higher threat reactivity was independently associated with higher hsCRP (β=0.16, p=0.01) and WBC count (β=0.24, <0.001), and higher effortful avoidance was associated with higher fibrinogen (β=0.13, p=0.04).

Conclusion

Our data indicate that elevated inflammation may be a feature of current, but not remitted, PTSD. Within patients with PTSD, higher threat reactivity was also associated with elevated inflammation. A better understanding of the relationship between threat sensitivity and inflammation may inform interventions for patients with PTSD.

INTRODUCTION: Traffic-related air pollution can trigger myocardial infarction (MI). However, the hourly hazard period of exposure to nitrogen dioxide (NO2), a common traffic tracer, for incident MI has not been fully evaluated. Thus, the current hourly US national air quality standard (100 ppb) is based on limited hourly-level effect estimates, which may not adequately protect cardiovascular health. OBJECTIVES: We characterized the hourly hazard period of NO2 exposure for MI in New York state (NYS), USA, from 2000 to 2015. METHODS: For nine cities in NYS, we obtained data on MI hospitalizations from the NYS Department of Health Statewide Planning and Research Cooperative System and hourly NO2 concentrations from the US Environmental Protection Agencys Air Quality System database. We used city-wide exposures and a case-crossover study design with distributed lag non-linear terms to assess the relationship between hourly NO2 concentrations over 24 h and MI, adjusting for hourly temperature and relative humidity. RESULTS: The mean NO2 concentration was 23.2 ppb (standard deviation: 12.6 ppb). In the six hours preceding MI, we found linearly increased risk with increasing NO2 concentrations. At lag hour 0, a 10 ppb increase in NO2 was associated with 0.2 % increased risk of MI (Rate Ratio [RR]: 1.002; 95 % Confidence Interval [CI]: 1.000, 1.004). We estimated a cumulative RR of 1.015 (95 % CI: 1.008, 1.021) for all 24 lag hours per 10 ppb increase in NO2. Lag hours 2-3 had consistently elevated risk ratios in sensitivity analyses. CONCLUSIONS: We found robust associations between hourly NO2 exposure and MI risk at concentrations far lower than current hourly NO2 national standards. Risk of MI was most elevated in the six hours after exposure, consistent with prior studies and experimental work evaluating physiologic responses after acute traffic exposure. Our findings suggest that current hourly standards may be insufficient to protect cardiovascular health.

Climate change is the greatest threat to global health in human history. It has been declared a public health emergency by the World Health Organization and leading researchers from academic institutions around the globe. Structural racism disproportionately exposes communities targeted for marginalization to the harmful consequences of climate change through greater risk of exposure and sensitivity to climate hazards and less adaptive capacity to the health threats of climate change. Given its interdisciplinary approach to integrating behavioral, psychosocial, and biomedical knowledge, the discipline of behavioral medicine is uniquely qualified to address the systemic causes of climate change-related health inequities and can offer a perspective that is currently missing from many climate and health equity efforts. In this article, we summarize relevant concepts, describe how climate change and structural racism intersect to exacerbate health inequities, and recommend six strategies with the greatest potential for addressing climate-related health inequities.

Background

Posttraumatic stress disorder (PTSD) symptoms can develop following acute, life-threatening medical events. This study explores a potential biomarker of PTSD risk that is novel to a medical trauma population: a noninvasive, mobile skin conductance (SC) measurement.

Methods

Participants (N=64) were enrolled in-hospital following a stroke or transient ischemic attack (TIA). Mobile measurement of SC reactivity to recalling the stroke/TIA traumatic event was conducted at hospital bedside in the days following the stroke/TIA. PTSD symptoms that developed in response to the stroke/TIA were measured at 1-month follow-up. We tested the association between SC reactivity and total 1-month PTSD symptoms, as well as PTSD symptom dimensions of fear and dysphoria.

Results

In unadjusted analyses, there were significant positive associations between in-hospital SC reactivity to recalling the stroke/TIA traumatic event and higher-order fear-related symptoms (r=.30, p=.016), as well as lower-order fear-related symptoms of anxious arousal (r=.27, p=.035) and avoidance (r=.25, p=.043) at 1 month. Associations between SC reactivity and the fear, anxious arousal, and avoidance symptom dimensions remained significant in multivariable regression models that adjusted for relevant covariates including age, gender, stroke severity, medical comorbidity, and psychosocial factors. Although there was a positive association observed between SC reactivity to recalling the stroke/TIA event and total PTSD symptom severity at 1-month follow-up, it did not reach the level of statistical significance (r=.23, p=.070). Further, no significant association was detected for dysphoria-related symptoms (r=.11, p=.393).

Conclusions

This is the first study to test the prospective association of SC reactivity with PTSD symptom development following a medical trauma. The findings indicate that mobile measures of SC reactivity may be useful for in-hospital identification of individuals at risk for fear-related PTSD symptom development following a medical event and highlight the potential mechanisms involved in the development of these symptoms following a medical event.