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Introduction: Acute myocardial infarction (MI) is a potentially fatal condition, leading to high psychological distress and possibly resulting in the development of depressive symptoms and posttraumatic stress symptoms (PTSS). The aim of this study was to investigate the association of clusters of positive psychosocial factors (resilience, task-oriented coping, positive affect and social support) with both MI-induced depressive symptoms and PTSS, independent of demographic factors. Methods: We investigated 154 consecutive patients with MI, 3 and 12 months after hospital discharge. All patients completed the short version of the German Resilience Scale, the Coping Inventory for Stressful Situations (CISS), the Enriched Social Support Inventory (ESSI) and the Global Mood Scale (GMS). The level of interviewer-rated MI-induced posttraumatic stress disorder (PTSD) symptoms at 3- and 12-months follow-up was evaluated through the Clinician-Administered PTSD Scale (CAPS). Depressive symptoms were assessed at 3- and 12-month follow-up with the Beck Depression Inventory (BDI-II). Results: Three different clusters were revealed: (1) lonely cluster: lowest social support, resilience and average task-oriented coping and positive affect; (2) low risk cluster: highest resilience, task-oriented coping, positive affect and social support; (3) avoidant cluster: lowest task-oriented coping, positive affect, average resilience and social support. The clusters differed in depressive symptoms at 3 months (F = 5.10; p < 0.01) and 12 months follow-up (F = 7.56; p < 0.01). Cluster differences in PTSS were significant at 3 months (F = 4.78, p < 0.05) and 12 months (F = 5.57, p < 0.01) follow-up. Differences in PTSS subscales were found for avoidance (F = 4.8, p < 0.05) and hyperarousal (F = 5.63, p < 0.05), but not re-experiencing, at 3 months follow-up. At 12 months follow-up, cluster differences were significant for re-experiencing (F = 6.44, p < 0.01) and avoidance (F = 4.02, p < 0.05) but not hyperarousal. Discussion: The present study contributes to a better understanding of the relationships among different positive psychosocial factors, depressive symptoms and PTSS following acute MI. Future interventions may benefit from taking into account positive psychosocial factors to potentially reduce patients' depressive symptoms and PTSS after MI.
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OBJECTIVE: Unfavorable blood lipid profiles are robust risk factors in predicting atherosclerotic disease. Studies have shown that positive affect (PA) is associated with a favorable lipid profile. However, longitudinal studies regarding the course of PA and lipid profiles in myocardial infarction (MI) patients are lacking. Therefore, the aim of this study was to prospectively explore the association between PA and blood lipid levels across three inv estigations over 12 months following acute MI. METHODS: Patients following an acute MI were examined at hospital admission (n = 190), and at 3 months (n = 154) and 12 months (n = 106) thereafter. Linear mixed effect regression models were used to evaluate the relation between PA, assessed with the Global Mood Scale, and blood lipid levels. Potential confounding variables were controlled for in the analysis. RESULTS: Higher PA was significantly associated with higher high-density lipoprotein cholesterol (HDL-C) levels and a lower total cholesterol (TC)/HDL-C ratio over time, independent of demographic factors, indices of cardiac disease severity, comorbidity, medication use, health behaviors, serum cortisol and negative affect (p≤0.040). No association was found between PA and the two blood lipids low-density lipoprotein-cholesterol (LDL-C) and triglycerides (TG). CONCLUSIONS: Positive affect was independently associated with HDL-C levels and the TC/HDL-C ratio in patients up to 1 year after MI. The findings support a potential role of PA for cardiovascular health through an association with a favorable blood lipid profile.
Subject(s)
Lipids , Myocardial Infarction , Humans , Cholesterol, HDL , Myocardial Infarction/etiology , Triglycerides , Risk FactorsABSTRACT
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.
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Background: Takotsubo syndrome (TTS) is an acute heart failure syndrome characterized by transient left ventricular dysfunction, increased myocardial biomarkers, and electrocardiographic changes. Symptoms of TTS are similar to those of acute coronary syndromes, but there is often no significant coronary stenosis. Although emotional and physical stressors are often reported as having triggered TTS, the pathogenesis is largely unknown. To address this issue, we comprehensively characterized a monozygous pair of twin sisters, one of whom experienced TTS. Case summary: The 60-year-old Caucasian monozygotic female twins with and without TTS were examined at the University Hospital Zurich in Switzerland. The twins completed questionnaires and clinical interviews assessing several sociopsychological factors. The twin sister with TTS exhibited higher levels of anxiety, vital exhaustion, social inhibition, and alexithymia, and lower levels of quality of and meaning in life. She was given the diagnoses of social phobia, adjustment disorder, specific anxiety disorder, obsessive-compulsive personality disorder, and an accentuated anxiety-avoidant personality disorder. Additionally, the twin with TTS experienced more-and also more severe-stressors involving life-threatening and dangerous situations over the life course. Discussion: These monozygous female twins with and without TTS differed in several notable aspects of their psychological functioning, psychiatric status, personality, and lifetime stressor exposure. The results thus highlight several factors, besides genetic components, that may play an important role in the pathogenesis of TTS. Looking forward, larger studies using experimental and longitudinal designs are needed to elucidate the role that psychosocial factors play in TTS.
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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.
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Flavanol-rich dark chocolate consumption relates to lower risk of cardiovascular mortality, but underlying mechanisms are elusive. We investigated the effect of acute dark chocolate consumption on inflammatory measures before and after stress. Healthy men, aged 20-50years, were randomly assigned to a single intake of either 50g of flavanol-rich dark chocolate (n=31) or 50g of optically identical flavanol-free placebo-chocolate (n=34). Two hours after chocolate intake, both groups underwent the 15-min Trier Social Stress Test. We measured DNA-binding-activity of the pro-inflammatory transcription factor NF-κB (NF-κB-BA) in peripheral blood mononuclear cells, as well as plasma and whole blood mRNA levels of the pro-inflammatory cytokines IL-1ß and IL-6, and the anti-inflammatory cytokine IL-10, prior to chocolate intake as well as before and several times after stress. We also repeatedly measured the flavanol epicatechin and the stress hormones epinephrine and cortisol in plasma and saliva, respectively. Compared to the placebo-chocolate-group, the dark-chocolate-group revealed a marginal increase in IL-10 mRNA prior to stress (p=0.065), and a significantly blunted stress reactivity of NF-κB-BA, IL-1ß mRNA, and IL-6 mRNA (p's⩽0.036) with higher epicatechin levels relating to lower pro-inflammatory stress reactivity (p's⩽0.033). Stress hormone changes to stress were controlled. None of the other measures showed a significant chocolate effect (p's⩾0.19). Our findings indicate that acute flavanol-rich dark chocolate exerts anti-inflammatory effects both by increasing mRNA expression of the anti-inflammatory cytokine IL-10 and by attenuating the intracellular pro-inflammatory stress response. This mechanism may add to beneficial effects of dark chocolate on cardiovascular health.
Subject(s)
Anti-Inflammatory Agents/pharmacology , Chocolate , Flavonols/pharmacology , Inflammation/metabolism , Interleukin-1beta/blood , Interleukin-6/blood , NF-kappa B/blood , Stress, Psychological/metabolism , Adult , Anti-Inflammatory Agents/administration & dosage , Catechin/blood , Epinephrine/metabolism , Flavonols/administration & dosage , Humans , Hydrocortisone/metabolism , Inflammation/drug therapy , Male , Middle Aged , Stress, Psychological/drug therapy , Young AdultABSTRACT
OBJECTIVES: Myocardial infarction (MI) may be experienced as a traumatic event causing acute stress disorder (ASD). This mental disorder has an impact on the daily life of patients and is associated with the development of post-traumatic stress disorder. Trait resilience has been shown to be a protective factor for post-traumatic stress disorder, but its association with ASD in patients with MI is elusive and was examined in this study. METHODS: We investigated 71 consecutive patients with acute MI within 48â h of having stable haemodynamic conditions established and for 3â months thereafter. All patients completed the Acute Stress Disorder Scale and the Resilience Scale to self-rate the severity of ASD symptoms and trait resilience, respectively. RESULTS: Hierarchical regression analysis showed that greater resilience was associated with lower symptoms of ASD independent of covariates (b=-0.22, p<0.05). Post hoc analysis revealed resilience level to be inversely associated with the ASD symptom clusters of re-experiencing (b=-0.05, p<0.05) and arousal (b=-0.09, p<0.05), but not with dissociation and avoidance. CONCLUSIONS: The findings suggest that patients with acute MI with higher trait resilience experience relatively fewer symptoms of ASD during MI. Resilience was particularly associated with re-experiencing and arousal symptoms. Our findings contribute to a better understanding of resilience as a potentially important correlate of ASD in the context of traumatic situations such as acute MI. These results emphasise the importance of identifying patients with low resilience in medical settings and to offer them adequate support.
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The aim of this study was to examine whether heart drawings of patients with acute myocardial infarction reflect acute distress symptoms and negative illness beliefs and predict posttraumatic stress symptoms 3 months post-myocardial infarction. In total, 84 patients aged over 18 years drew pictures of their heart. The larger the area drawn as damaged, the greater were the levels of acute distress (r = 0.36; p < 0.05), negative illness perceptions (r = 0.42, p < 0.05), and posttraumatic stress symptoms (r = 0.54, p < 0.01). Pain drawings may offer a tool to identify maladaptive cognitions and thus patients at risk of posttraumatic stress disorder.
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Anticipatory cognitive stress appraisal (ACSA) can affect the stress-induced release of stress hormones, which, in turn, can modulate microbicidal potential of macrophages. This study examines whether ACSA modulates wound-induced activation of macrophage microbicidal potential in 22 acutely stressed compared to 17 nonstressed healthy men. After catheter-induced wound infliction and completing the ACSA questionnaire, the stress group underwent an acute mental stress task, while the nonstressed group did not. Macrophage microbicidal potential and stress hormones were repeatedly measured. In acutely stressed men, but not in nonstressed men, higher scores in ACSA related to lower macrophage microbicidal potential. This association was statistically mediated by the norepinephrine (NE) stress response. Our data suggest that ACSA modulates stress-induced suppression of wound-induced macrophage activation and that the NE stress response underlies this effect.