This study investigated prevalence and predictors of PTSD three months after admission for ACS. We found that 14.8% of patients admitted for ACS could be classified as experiencing PTSD three months after admission. This falls within the range reported in previous studies.2,3,4,5,6
No demographic variables were predictive of PTSD or symptom severity at three months, whereas studies of PTSD in the general population have found education, female sex and younger age to be associated with PTSD.21
This does not appear to be the case in cardiac populations, however, suggesting that PTSD may have distinctive correlates in medically ill patients. Objective clinical severity of ACS was not predictive of PTSD, despite use of a broad range of indices, and this is in agreement with previous studies in cardiac populations2
and literature on PTSD after a wider range of medical events.9
Subjective severity or intensity of the ACS as indexed by degree of chest pain, however, was a predictor of PTSD severity.
In‐hospital psychological factors were the strongest predictors of PTSD at three months. Negative affect, whether measured in terms of depressive symptoms or a personality dimension, is the most robust predictor of PTSD in cardiac populations.5,6,7
Although in a previous study type D personality predicted PTSD,7
in our data only the dimension negative affect, rather than type D as a whole, predicted PTSD independently of other covariates. One other study found an association with hostility5
and, as with the present study, anxiety has not been found to be predictive.6
In addition, history of depression was associated with PTSD, and previous mental illness is a risk factor for PTSD in the general population.21
One limitation of the current study is that PTSD was assessed by questionnaire rather than by clinical interview. A full diagnostic interview was not possible within the confines of the study, given sample size and the two‐phase design. Standard clinical interviews tend to give lower prevalences than self‐report scales, causing some authorities to suggest that clinical PTSD is rare in cardiac patients. Two recent studies contradict this argument; O'Reilly et al4
found a 7% prevalence among patients with MI by using structured clinical interview diagnosis, and Ladwig et al22
recorded an exaggerated startle response, an established physiological marker of PTSD,23
in survivors of life threatening cardiac events with PTSD. The present study therefore provides only an estimate of PTSD frequency. Conservative scoring criteria were applied,19
however, and therefore only patients with frequent symptoms were assigned to the PTSD group. This method also avoids confounding by high scores on somatic items, which is problematic when assessing mood state in populations with chronic illness. From a clinician's perspective, in which the goal is to identify patients at risk of distress and poor outcomes, post‐traumatic stress severity may be a more useful concept than PTSD. PTSD symptoms occur on a continuum of severity, as do those of depression; therefore, subclinical PTSD may exert a detrimental effect on cardiac patients as does depression,24
where increasing severity predicts increasing risk of mortality. Another limitation is lack of psychological data on those patients who were clinically eligible but did not consent to take part, as those with severe traumatisation may have avoided participation, thus underestimating PTSD in this sample. Strengths of the study are the consideration of the full range of ACS rather than just MI, its sample size and the prospective design.
It is not surprising that depression (in‐hospital or before onset) is predictive of PTSD, given the high levels of co‐morbidity between the two and the finding that depression and PTSD are risk factors for one another.25
This raises a number of issues, the first being the specificity of the measures used in this study and the influence of “reporting bias” (the tendency to endorse any negative items). Although PTSD and depression may co‐occur, symptoms are distinct and the measures used in this study are specific to PTSD. Furthermore, the scales were adapted to refer to ACS as the index “traumatic event” and therefore reflect distress arising from ACS rather than pre‐existing distress. Statistical control for reporting bias on the PTSD scale was provided by entering acute stress symptoms into the regression model before other psychological predictors.
A second issue is whether psychological predictors identified by this study constitute a non‐specific dimension of vulnerability to PTSD. The predictors (depression, negative affect and hostility), however, were independent of one another. Rather than being a single factor of “distress”, these psychological factors may operate through different pathways to precipitate PTSD and may importantly require different kinds of intervention.
A third issue addresses the implications of PTSD in cardiac populations and concerns the value of screening for PTSD as well as for depression. PTSD in patients with cardiac disease is associated with a reduced quality of life, reduced adherence to drug treatment, and cardiac readmission after MI.2,3
Depression in patients with coronary heart disease has also been associated with poor outcomes,24
and plausible biological pathways leading to progression of coronary heart disease have been delineated. Neuroendocrine, immunological and autonomic pathways are found to be disrupted in PTSD; the proinflammatory cytokines tumour necrosis factor and interleukin 6 are raised26
and heart rate variability is reduced.27
Both of these patterns are established risk factors for coronary heart disease.28,29
Although cortisol concentrations are raised in patients with depression, however, studies of patients with PTSD but without cardiac disease find lower concentrations of cortisol and downregulation of the hypothalamic–pituitary–adrenal axis.25
Screening patients only for depression may overlook those with severe PTSD and the risks that this incurs. Furthermore, different types of treatment are required for depression and PTSD. Recently published national guidelines on the management of PTSD recommend “trauma‐focused therapy” as the first line of treatment, which differs from standard cognitive–behavioural techniques used to treat depression.20
One group investigated efficacy of administering corticosteroids to patients recovering from cardiac surgery, finding that the incidence of traumatic stress symptoms was lower in the treatment group.30
In conclusion, the association of PTSD with harmful behavioural and biological factors and with raised levels of depression means that, whatever the direction of causality, coexisting PTSD and coronary heart disease are a potentially malignant problem with a clear threat to well‐being and future risk of death.