Reply to Sopek Merkaš, I.; Lakušić, N. Comment on “von Känel et al. Early Trauma-Focused Counseling for the Prevention of Acute Coronary Syndrome-Induced Posttraumatic Stress: Social and Health Care Resources Matter. J. Clin. Med. 2022, 11, 1993”

We thank Merkaš and Lakušić for commenting on our recently published paper; in the paper, we suggested that resources in a patient’s social environment may moderate the benefit of one single-session trauma-focused counseling in the prevention of acute coronary syndrome (ACS)-induced posttraumatic stress disorder (PTSD) symptoms [1]. Their comment gives a comprehensive summary on the topic of ACS-induced PTSD and its treatment [2]. We agree with the authors that guidelines and standards regarding the identification and treatment of patients at high risk for developing PTSD after ACS remain lacking. We designed the MI-SPRINT study to test whether trauma-focused psychological counseling is more effective than stress-focused counseling in preventing PTSD symptoms after acute ACS [3]. Our study showed no beneficial effect of trauma-focused counseling on PTSD symptoms; after 3 and 12 months, we found no difference in the severity of PTSD symptoms between patients with early trauma-focused counseling and those with stress-focused counseling in the total sample. However, our results suggested that psychological counseling in general might help distressed patients to prevent posttraumatic psychological responses compared with no intervention [4,5]. Importantly, PTSD symptoms that had developed after 3 months were shown to have been persistent up to 12 months after ACS, despite the delivery of one session of early psychological counseling [6]. Furthermore, as alluded to above, we showed that social support and cardiac rehabilitation act as moderators of the intervention; specifically, trauma-focused counseling was associated with fewer PTSD symptoms compared with stress-focused counseling in patients with high social support and with longer participation in cardiac rehabilitation [1]. Moreover, the data of MI-SPRINT showed that several factors contribute to identifying patients at risk for ACS-induced PTSD symptoms, such as high perceived distress during ACS [6], perception of higher harmful consequences of the illness [7], perception of a hectic hospital environment [8], sleep problems [9], and low trait resilience [10]. Screening for risk factors or specific symptoms—e.g., in the cardiac rehabilitation setting, as indicated by the Merkaš and Lakušić [1]—is important. However, we believe that screening alone may have little clinical benefit. It will be much more crucial to offer effective treatment to patients identified at high risk of developing PTSD or patients with established PTSD symptoms. In summary, further studies are needed to develop a standardized approach for the screening of patients at risk of clinically relevant, ACS-induced PTSD symptoms and to establish efficacious interventions that can be applied in a clinical setting. For instance, multisession early counseling could be elaborated and tested based on our findings to prevent the development of PTSD symptoms in patients at risk

Reply to Sopek Merkaš, I.; Lakušić, N. Comment on "von Känel et al. Early Trauma-Focused Counseling for the Prevention of Acute Coronary Syndrome-Induced Posttraumatic Stress: Social and Health Care Resources Matter. J. Clin. Med. 2022, 11, 1993".

We thank Merkaš and Lakušić for commenting on our recently published paper; in the paper, we suggested that resources in a patient's social environment may moderate the benefit of one single-session trauma-focused counseling in the prevention of acute coronary syndrome (ACS)-induced posttraumatic stress disorder (PTSD) symptoms [...]

Early Trauma-Focused Counseling for the Prevention of Acute Coronary Syndrome-Induced Posttraumatic Stress: Social and Health Care Resources Matter.

BACKGROUND A one-size-fits-all approach might explain why early psychological interventions are largely ineffective in preventing the development of posttraumatic stress disorder (PTSD) symptoms triggered by acute medical events. We examined the hypothesis that social and health care resources are moderators of an intervention effect. METHODS Within 48 h of hospital admission, 129 patients (mean age 58 years, 83% men) with acute coronary syndrome (ACS) self-rated their social support and were randomized to one single session of trauma-focused counseling (TFC) or stress-focused counseling (SFC) (active control intervention). Clinician-rated PTSD symptoms, use of cardiac rehabilitation (CR) and use of psychotherapy were assessed at 3 and 12 months. Random mixed regression multivariable models were used to analyze associations with PTSD symptoms over time. RESULTS TFC did not prevent ACS-induced PTSD symptom onset better than SFC; yet, there were significant and independent interactions between "intervention" (TFC or SFC) and social support (p = 0.013) and between "intervention" and duration of CR in weeks (p = 0.034). Patients with greater social support or longer participation in CR had fewer PTSD symptoms in the TFC group compared with the SFC group. The number of psychotherapy sessions did not moderate the intervention effect. CONCLUSIONS Early psychological intervention after ACS with a trauma-focused approach to prevent the development of PTSD symptoms may be beneficial for patients who perceive high social support or participate in CR for several weeks

Relationship between a Self-Reported History of Depression and Persistent Elevation in C-Reactive Protein after Myocardial Infarction.

BACKGROUND Elevated levels of C-reactive protein (CRP) are associated with both an increased risk of cardiovascular disease (CVD) and depression. We aimed to test the hypothesis that a self-report history of depression is associated with a smaller decrease in CRP levels from hospital admission to 3-month follow-up in patients with acute myocardial infarction (MI). METHODS We assessed 183 patients (median age 59 years; 84% men) with verified MI for a self-report history of lifetime depression and plasma CRP levels within 48 h of an acute coronary intervention and again for CRP levels at three months. CRP values were categorized according to their potential to predict CVD risk at hospital admission (acute inflammatory response: 0 to <5 mg/L, 5 to <10 mg/L, 10 to <20 mg/L, and ≥20 mg/L) and at 3 months (low-grade inflammation: 0 to <1 mg/L, 1 to <3 mg/L, and ≥3 mg/L). Additionally, in a subsample of 84 patients showing admission CRP levels below 20 mg/L, changes in continuous CRP values over time were also analyzed. RESULTS After adjustment for a range of potentially important covariates, depression history showed a significant association with a smaller decrease in both CRP risk categories (r = 0.261, p < 0.001) and log CRP levels (r = 0.340, p = 0.005) over time. CONCLUSIONS Self-reported history of depression may be associated with persistently elevated systemic inflammation three months after MI. This finding warrants studies to test whether lowering of inflammation in patients with an acute MI and a history of depression may improve prognosis

Relationship between a Self-Reported History of Depression and Persistent Elevation in C-Reactive Protein after Myocardial Infarction

Background: Elevated levels of C-reactive protein (CRP) are associated with both an increased risk of cardiovascular disease (CVD) and depression. We aimed to test the hypothesis that a self-report history of depression is associated with a smaller decrease in CRP levels from hospital admission to 3-month follow-up in patients with acute myocardial infarction (MI). Methods: We assessed 183 patients (median age 59 years; 84% men) with verified MI for a self-report history of lifetime depression and plasma CRP levels within 48 h of an acute coronary intervention and again for CRP levels at three months. CRP values were categorized according to their potential to predict CVD risk at hospital admission (acute inflammatory response: 0 to <5 mg/L, 5 to <10 mg/L, 10 to <20 mg/L, and ≥20 mg/L) and at 3 months (low-grade inflammation: 0 to <1 mg/L, 1 to <3 mg/L, and ≥3 mg/L). Additionally, in a subsample of 84 patients showing admission CRP levels below 20 mg/L, changes in continuous CRP values over time were also analyzed. Results: After adjustment for a range of potentially important covariates, depression history showed a significant association with a smaller decrease in both CRP risk categories (r = 0.261, p < 0.001) and log CRP levels (r = 0.340, p = 0.005) over time. Conclusions: Self-reported history of depression may be associated with persistently elevated systemic inflammation three months after MI. This finding warrants studies to test whether lowering of inflammation in patients with an acute MI and a history of depression may improve prognosis

Psychophysiological Stress Reactivity in Monozygotic Twins with and without Takotsubo Syndrome

Objective: Takotsubo syndrome (TTS) is characterized by transient left ventricular dysfunction, often elevated myocardial enzymes, and electrocardiographic changes. Previous studies suggested that an overstimulation of the sympathetic nervous system might cause TTS. However, the pathogenesis of TTS is largely unknown. Therefore, we investigated physiological stress reactivity with a standardized stress test in monozygotic twin sisters, only one of whom had experienced TTS. Methods: The 60-year-old Caucasian monozygotic twins, one with and one without a previous episode of TTS, were recruited in the Department of Cardiology at the University Hospital Zurich, Switzerland. We applied the Trier Social Stress Test (TSST) to investigate stress reactivity six weeks after the TTS. Hemodynamic measures (heart rate (HR), blood pressure (BP)), heart rate variability (HRV), plasma norepinephrine and epinephrine and salivary cortisol levels were collected immediately before and after the TSST, and 15, 45, and 90 min after TSST. The monozygotic twins differed in their hemodynamic stress response with the TTS twin showing blunted HR and BP reactivity and vagal withdrawal beyond the acute phase of stress. In contrast, the TTS twin showed a higher catecholamine and cortisol stress response with a steady increase in norepinephrine during the recovery period from stress compared to her non-TTS twin sister. Conclusion: Large studies applying a case-control design are needed to confirm blunted hemodynamic reactivity, increased catecholamine reactivity, vagal withdrawal, and increased cortisol reactivity to stress in TTS. This may advance the knowledge of psychophysiological mechanisms in TTS

Effect of Early Psychological Counseling for the Prevention of Posttraumatic Stress Induced by Acute Coronary Syndrome at Long-Term Follow-Up.

Objective Psychological consequences of myocardial infarction (MI) are substantial, as 4% of all MI patients develop posttraumatic stress disorder (PTSD) and 12% clinically relevant posttraumatic stress symptoms (PTSS). The study investigated the course and development within 12 months of MI-induced PTSS to gain novel insights in potentially delayed response to early trauma-focused counseling aimed at preventing the incidence of MI-induced PTSS. Methods In the MI-SPRINT two-group randomized controlled trial, 190 MI-patients were randomly allocated to receive a single-session intervention of either trauma-focused counseling or an active control intervention targeting the general role of stress in patients with heart disease. Blind interviewer-rated PTSS (primary outcome) and additional health outcomes were assessed at 12-month follow-up. Results 12-month follow-up of outcomes were available for 106 (55.8%) of 190 participants: In the entire sample, one patient (0·5%, 1/190) who received trauma-focused counseling developed full PTSD. There was no significant difference between trauma-focused counseling and stress counseling regarding total score of interviewer-rated PTSS (p > 0.05). The only group difference emerged in terms of more severe hyperarousal symptoms in the trauma-focused counseling group in the ITT analysis, but not in the completer analysis. Conclusions No benefits were found for trauma-focused counseling after 12 months when compared with an active control intervention. PTSD prevalence in the present study was low highlighting a potential beneficial effect of both interventions. Further studies are needed to determine the most accurate approach of counseling

Association Between Changes in Post-hospital Cardiac Symptoms and Changes in Acute Coronary Syndrome-Induced Symptoms of Post-traumatic Stress.

Background After acute coronary syndrome (ACS), one in eight patients develops clinically significant symptoms of Post-traumatic stress disorder (PTSD). We hypothesized that changes in cardiac symptoms from 3 to 12 months after ACS are associated with changes in ACS-induced PTSD symptoms. Methods At 3 (n = 154) and/or 12 months (n = 106) post-ACS, patients (n = 156, mean age 59 years, 85% men) completed a clinical interview assessing chest tightness/pain (at rest and/or during exertion), heartbeat symptoms (heart palpitations, racing of heart, heart stumbling or skipping a beat) and PTSD symptoms during the prior 4 weeks. Random mixed regression models examined the association between the onset (or remission) from 3 to 12 months in cardiac symptoms with changes in PTSD symptoms, adjusting for a range of potential predictors of ACS-induced PTSD symptoms. Results The onset of chest tightness/pain [estimate = 0.588, 95% confidence interval: 0.275, 0.090; p < 0.001] and of heartbeat symptoms [0.548 (0.165, 0.931); p = 0.005] from 3 to 12 months was independently associated with an increase in total PTSD symptoms. There were also independent associations between the onset of chest tightness/pain and heartbeat symptoms with an increase in PTSD symptom clusters. Specifically, the onset of chest tightness/pain showed associations with an increase in re-experiencing [0.450 (0.167, 0.733); p = 0.027] and avoidance/numbing [0.287 (0.001, 0.574); p = 0.049]. The onset of heartbeat symptoms showed associations with an increase in re-experiencing [0.392 (0.045, 0.739); p = 0.002], avoidance/numbing [0.513 (0.161, 0.864); p = 0.004] and hyperarousal [0.355 (0.051, 0.659); p = 0.022]. An increase in the total number of cardiac symptoms (score range 0-6) was also associated with an increase in total PTSD symptoms [0.343 (0.202, 0.484); p < 0.001]. Psychotherapy in the post-hospital period moderated the association between the change in heartbeat symptoms and the change in total PTSD symptoms [-0.813 (-1.553, -0.074); p = 0.031 for interaction]; the association between the onset of heart beat symptoms and an increase in total PTSD symptoms was weaker in patients who attended psychotherapy [0.437 (-0.178, 1.052); p = 0.16] than in those who did not [0.825 (0.341, 1.309); p < 0.001]. Conclusion Changes in cardiac symptoms between 3 and 12 months after hospitalization are associated with changes in ACS-induced PTSD symptoms. ClinicalTrials.gov #NCT01781247

Association Between Changes in Post-hospital Cardiac Symptoms and Changes in Acute Coronary Syndrome-Induced Symptoms of Post-traumatic Stress

Background: After acute coronary syndrome (ACS), one in eight patients develops clinically significant symptoms of Post-traumatic stress disorder (PTSD). We hypothesized that changes in cardiac symptoms from 3 to 12 months after ACS are associated with changes in ACS-induced PTSD symptoms. Methods: At 3 (n = 154) and/or 12 months (n = 106) post-ACS, patients (n = 156, mean age 59 years, 85% men) completed a clinical interview assessing chest tightness/pain (at rest and/or during exertion), heartbeat symptoms (heart palpitations, racing of heart, heart stumbling or skipping a beat) and PTSD symptoms during the prior 4 weeks. Random mixed regression models examined the association between the onset (or remission) from 3 to 12 months in cardiac symptoms with changes in PTSD symptoms, adjusting for a range of potential predictors of ACS-induced PTSD symptoms. Results: The onset of chest tightness/pain [estimate = 0.588, 95% confidence interval: 0.275, 0.090; p < 0.001] and of heartbeat symptoms [0.548 (0.165, 0.931); p = 0.005] from 3 to 12 months was independently associated with an increase in total PTSD symptoms. There were also independent associations between the onset of chest tightness/pain and heartbeat symptoms with an increase in PTSD symptom clusters. Specifically, the onset of chest tightness/pain showed associations with an increase in re-experiencing [0.450 (0.167, 0.733); p = 0.027] and avoidance/numbing [0.287 (0.001, 0.574); p = 0.049]. The onset of heartbeat symptoms showed associations with an increase in re-experiencing [0.392 (0.045, 0.739); p = 0.002], avoidance/numbing [0.513 (0.161, 0.864); p = 0.004] and hyperarousal [0.355 (0.051, 0.659); p = 0.022]. An increase in the total number of cardiac symptoms (score range 0–6) was also associated with an increase in total PTSD symptoms [0.343 (0.202, 0.484); p < 0.001]. Psychotherapy in the post-hospital period moderated the association between the change in heartbeat symptoms and the change in total PTSD symptoms [−0.813 (−1.553, −0.074); p = 0.031 for interaction]; the association between the onset of heart beat symptoms and an increase in total PTSD symptoms was weaker in patients who attended psychotherapy [0.437 (−0.178, 1.052); p = 0.16] than in those who did not [0.825 (0.341, 1.309); p < 0.001]. Conclusion: Changes in cardiac symptoms between 3 and 12 months after hospitalization are associated with changes in ACS-induced PTSD symptoms

The Influence of Personality Traits on Specific Coping Styles and the Development of Posttraumatic Stress Symptoms following Acute Coronary Syndrome: A Cluster Analytic Approach

Objective: A growing body of literature suggests a relationship between personality traits and posttraumatic stress disorder (PTSD) symptoms after acute coronary events (ACS). However, specific personality profiles have not been examined in patients after ACS. Thus, the aim of the present study was to examine personality profiles created from response patterns on the resilience, alexithymia and type D personality (TDP) scales and to examine associations with PTSD symptoms, symptom clusters and coping styles among a sample of ACS patients. Methods: A cluster analytic approach was utilized to identify risk profiles based on personality variables and a series of ANOVAs in 154 patients. Post hoc analyses were conducted to examine the relationship between each profile, and interviewer-rated PTSD symptoms and different coping styles. Results: The analyses indicated a three-cluster solution, including low- (high resilience, low alexithymia and non-TDP), medium- (average resilience, average alexithymia and non-TDP) and high-risk (low resilience, high alexithymia and TDP) profiles. Clusters differed significantly in all three coping subscales. At 3-month follow up, clusters differed significantly in all three PTSD subscales (re-experiencing, avoidance and hyperarousal). At 12-month follow up, the differences remained significant for the hyperarousal subscale only. Conclusions: The personality profiles identified and the respective associations to PTSD symptoms and coping strategies highlight the potential impact for the psychological adjustment following ACS