Diagnosis of MI, TIA or stroke means confrontation with a life-threatening event for those affected and can therefore be regarded as a traumatic event. Cerebral and cardiovascular events may increase the risk of developing chronic PTSD. There has been an abundance of evidence, particularly in recent years, demonstrating the enormous influence of psychological factors not only on HRQoL but also on the course of the disease and the survival chances of patients with MI, TIA or stroke [
44‐
46]. These concepts and the corresponding therapeutic approaches are hardly known in the routine medical care of these patients. In addition to medical treatment, a particular challenge is the early detection of high-risk patients who may develop symptoms of PTSD in the future. Only early detection of these symptoms enables fast and effective therapy. This is the only way to prevent further chronification, therapy delay and prolongation of the length of hospital stay followed by a poorer prognosis.
In our study, the prevalence of chronic PTSD in MI, TIA and stroke patients was 23.2%, which is more than 4 to 40 times higher than the lifetime prevalence in the general population in Europe (0.56 to 6.67%) [
47]. This indicates an outstanding high-risk population for PTSD hampering their overall prognosis. Our findings highly emphasize the need for an early screening and diagnosis of PTSD in cardiovascular and neurovascular patients, which should be followed by a specialized treatment of any identified PTSD symptoms. The sociodemographic characteristics of our patients, e.g., age, family status, number of children, level of education or occupation of the sample, were not associated with the PTSD prevalence estimates. Moreover, we did not find significant statistical relationships between the severity of the disease, i.e., MI, TIA or stroke, and the development of chronic PTSD. Numerous studies did not find correlations between disease severity and later manifestations of PTSD symptoms [
48‐
50]. However, structured prospective examinations with larger cohorts should be conducted in the future. The prevalence of depression in MI, TIA and stroke patients was 29.5%, which is more than twice as high as in the general population (2–12%) [
51,
52].
In the comparisons between the groups, we observed highly significant differences. The prevalence of depression was 13.0% in MI patients, 33.3% in TIA patients and 50.0% in stroke patients. Previous studies have shown similarly increased depression rates after stroke (3–39%) [
53‐
55]. This is probably because the diagnostic symptoms of depression and stroke overlap in the DSM-5 [
56], and our sample consisted mainly of patients with moderate stroke severity. Stroke severity and physical disability are the most consistent predictors of poststroke depression [
54,
57]. In contrast to anxiety disorder, depression may increase the mortality and disability of stroke patients [
58]. Probably due to the increased depression rate, the mental and physical HRQoL of our patient groups were significantly lower than the quality of life of the general population. This is confirmed by the results of other studies on HRQoL and depression in adults [
59]. In addition, the results of our study are in line with previous findings that depression is associated with increased comorbidity [
47,
60]. More than half (52.8%) of our PTSD-positive patients showed depressive symptoms. This is again in line with results from the literature, according to which about half of the patients with PTSD also suffer from depression [
61,
62]. The prevalence of anxiety was 20.5% in the entire patient cohort, which is more than two times higher than that in the general population [
63]. However, the anxiety prevalence did not differ between the groups. Consistent with the literature [
5,
64‐
66], concurrent depression was common in patients with anxiety, which again confirmed the need to treat depression in people with anxiety after MI, TIA and stroke. Half of our PTSD-positive patients had anxiety symptoms. This is not surprising, as PTSD appears to be a common comorbidity of anxiety disorder [
58,
67]. Our three patient groups developed adaptive and maladaptive coping after MI, TIA and stroke equally. Multiple comparisons of the three patient groups did not show any significant differences between the coping strategies. In the literature, most negative life events appear to elicit both types of coping strategies [
68]. The maladaptive coping style did not predict the development of PTSD, which is in contradiction to the few results in other studies [
69]. In our patients, we observed significant differences in adaptive coping only between those who additionally had anxiety, depression or PTSD and patients who did not develop these symptoms. Consistent with other studies [
45,
70], we found that the more our patients used adaptive coping strategies, the higher the mental HRQoL they were able to achieve, and this association was significant. In addition, patients with a higher depression score showed both significantly less adaptive coping ability and significantly more maladaptive coping ability. This finding is supported by numerous studies [
71‐
73]. Nevertheless, regulatory and coping strategies are not consistently beneficial or maladaptive in response to stressful events [
74]. There is evidence that some of the coping strategies can be both adaptive and maladaptive [
75,
76]. In patients with chronic life stressors Waugh et al. found that positive distraction was related to higher well-being and positive emotions, and fewer depressive symptoms especially when controlling for avoidance. Thus, positive distraction can be an adaptive disengagement coping strategy for chronic stressors [
75]. Wolgast and Lundh suggest that distraction may be either adaptive or maladaptive, depending on whether it is combined with an attitude of acceptance or avoidance [
76].
Our findings need to be interpreted cautiously due to the overall small sample size. Particularly the low number of TIA patients makes it difficult to make inferences about the minority of patients in this small group who have elevated PTSD symptoms. Our findings should be further evaluated in larger prospective studies. Thus, the comparison of three different patient groups up to five years after ictus can only provide limited findings. Due to the study design severe cases of stroke and MI might be underrepresented. Moreover, the cross-sectional design is a limitation of our study. A prospective rather than a cross-sectional study design would require to assess changes in coping styles and PTSD symptoms over time. Additionally, there are differences in DSM-IV and DSM-5 regarding medical events that may be considered traumatic. These differences have to be taken into account when interpreting our findings on PTSD. Another limitation of our study is that the exact time between the health event (i.e., stroke, TIA, MI) and the time of the survey was not recorded. The length of time between ictus and interview could have an influence on the results. Still, we were able to examine an unselected outpatient population with a comprehensive clinical and neuropsychological assessment.