Acute cardiac disorder or pneumonia and concomitant presence of pulmonary embolism

Purpose To determine the frequency of apparent acute pulmonary embolism (PE) and of concomitant disease in computed tomography pulmonary angiography (CTPA); to compare the frequency of PE in patients with pneumonia or acute cardiac disorder (acute coronary syndrome, tachyarrhythmia, acute left ventricular heart failure or cardiogenic shock), with the frequency of PE in patients with none of these alternative chest pathologies (comparison group). Methods Retrospective analysis of all patients who received a CTPA at the emergency department (ED) within a period of four years and 5 months. Results Of 1275 patients with CTPA, 28 (2.2%) had PE and concomitant radiologic evidence of another chest disease; 3 more (0.2%) had PE and an acute cardiac disorder without radiological evidence of heart failure. PE was found in 11 of 113 patients (10%) with pneumonia, in 5 of 154 patients (3.3%) with an acute cardiac disorder and in 186 of 1008 patients (18%) in the comparison group. After adjustment for risk factors for thromboembolism and for other relevant patient’s characteristics, the proportion of CTPAs with evidence of PE in patients with an acute cardiac disorder or pneumonia was significantly lower than in the comparison group (OR 0.13, 95% CI 0.05–0.33, p<0.001 for patients with an acute cardiac disorder, and OR 0.45, 95% CI 0.23–0.89, p = 0.021 for patients with pneumonia). Conclusion The frequency of PE and a concomitant disease that can mimic PE was low. The presence of an acute cardiac disorder or pneumonia was associated with decreased odds of PE.

The Cultural Construction Of Posttraumatic Stress Disorder: Sociopolitical Responses To Psychological Trauma In American And Vie

In my thesis, I incorporate both psychological research and personal narratives in order to explain why, in the aftermath of the Vietnam War, the United States officially recognized Post-Traumatic Stress Disorder while the Vietnamese government did not. The absence of Vietnamese studies on the impact of PTSD on veterans, in comparison to the abundance of research collected on American soldiers, is reflective not of a disparity in the actual prevalence of the disorder, but of the influence of political policy on the scope of Vietnamese psychology. Personal narratives from Vietnamese civilians and soldiers thus reveal accounts of trauma otherwise hidden due to the absence of Vietnamese psychological research. Although these two nations conspicuously differed in their respective responses to the prevalence of psychological trauma in war veterans, these responses demonstrated that both the recognition and rejection of PTSD was a result of sociopolitical factors: political ideologies, rather than scientific reasons, dictated whether the postwar trajectory of psychological research focused on fully exploring the impact of PTSD on veteran populations. The association of military defeat with psychological trauma thus fixed attention on certain groups of veterans, including former American and South Vietnamese soldiers, while ignoring the impact of trauma on veterans of the Viet Cong and North Vietnamese Army. The correlation of a soldier¿s ideological background with psychological trauma, rather than exposure to actual traumatic experiences, demonstrates that cultural and sociopolitical factors are far more influential in the construction of PTSD than objective indicators of the disorder¿s prevalence. Culturally-constructed responses to disorders such as PTSD therefore account for the subjective treatment of mental illness. The American and Vietnamese responses to veterans suffering from PTSD both demonstrated that the evidence of mental health problems in an individual does not guarantee an immediate or appropriate diagnosis and treatment regimen. External authorities whose primary aims are not necessarily concerned with the objective treatment of all victims of mental illness subjectively dictate mental health care policy, and therefore risk ignoring or marginalizing the needs of individuals in need of proper treatment.

Evidence for low-grade systemic proinflammatory activity in patients with posttraumatic stress disorder

Posttraumatic stress disorder (PTSD) may increase cardiovascular risk but the psychophysiological mechanisms involved are elusive. We hypothesized that proinflammatory activity is elevated in patients with PTSD as diagnosed by the Clinician Administered PTSD Scale (CAPS) interview. Plasma levels of proinflammatory C-reactive protein (CRP), interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha, and of anti-inflammatory IL-4 and IL-10 were measured in 14 otherwise healthy PTSD patients and in 14 age- and gender-matched healthy non-PTSD controls. Levels of TNF-alpha (p=0.038; effect size Cohen's d=0.58) and of IL-1beta (p=0.075, d=0.68) were higher in patients than in controls. CRP (d=0.10), IL-6 (d=0.18), IL-4 (d=0.42), and IL-10 (d=0.37) were not significantly different between groups. Controlling for traditional cardiovascular risk factors, mood, and time since trauma revealed lower IL-4 in patients than in controls (p=0.029) and rendered group differences in TNF-alpha and IL-1beta insignificant. In all subjects, TNF-alpha correlated with total (frequency and intensity) PTSD symptom cluster of re-experiencing (r=0.49, p=0.008), avoidance (r=0.37, p=0.050), and hyperarousal (r=0.42, p=0.026), and with PTSD total symptom score (r=0.37, p=0.054). Controlling for time since trauma attenuated these associations. The correlation between IL-1beta and total avoidance symptoms (r=0.42, p=0.028) became insignificant when controlling for anxiety and depression. IL-4 correlated with total hyperarousal symptoms (r=-0.38, p=0.047), and after controlling for systolic blood pressure and smoking status, with PTSD total symptom score (r=-0.41, p=0.035). PTSD patients showed a low-grade systemic proinflammatory state, which, moreover, was related to PTSD symptom levels suggesting one mechanism by which PTSD could contribute to atherosclerotic disease.

Altered blood coagulation in patients with posttraumatic stress disorder

OBJECTIVE: Posttraumatic stress disorder (PTSD) has been associated with an increased cardiovascular risk, though the pathophysiologic mechanisms involved are elusive. A hypercoagulable state before occurrence of coronary thrombosis contributes to atherosclerosis development. We investigated whether PTSD would be associated with increased coagulation activity. METHODS: We measured resting plasma levels of clotting factor VII activity (FVII:C), FVIII:C, FXII:C, fibrinogen, and D-dimer in 14 otherwise healthy patients with PTSD and in 14 age- and gender-matched, trauma-exposed non-PTSD controls. Categorical and dimensional diagnoses of PTSD were made using the Clinician-Administered PTSD Scale (CAPS) interview. We also investigated to what extent the relationship between PTSD and coagulation measures would be confounded by demographics, cardiovascular risk factors, lifestyle variables, time since trauma, and mood. RESULTS: Coagulation factor levels did not significantly differ between patients with a categorical diagnosis of PTSD and controls while controlling for covariates. In all subjects, FVIII:C was predicted by hyperarousal severity (beta = 0.46, p = .014) independent of covariates and by overall PTSD symptom severity (beta = 0.38, p = .045); the latter association was of borderline significance when separately controlling for gender, smoking, exercise, and anxiety (p values <.07). In patients, fibrinogen was predicted by hyperarousal severity (beta = 0.70, p = .005) and by overall PTSD symptom severity (beta = 0.61, p = .020), with mood partially affecting these associations. FVII:C, fibrinogen, and D-dimer showed no independent association with PTSD symptoms. CONCLUSIONS: PTSD may elicit hypercoagulability, even at subthreshold levels, offering one psychobiological pathway by which posttraumatic stress might contribute to atherosclerosis progression and clinical cardiovascular disease.

Anger, hostility, and posttraumatic stress disorder in trauma-exposed adults: A meta-analysis

This meta-analysis synthesizes the available data on the strength of association between anger and posttraumatic stress disorder (PTSD) and between hostility and PTSD, covering 39 studies with trauma-exposed adults. Effect sizes did not differ for anger and hostility, which could therefore be combined; effect sizes for anger expression variables were analyzed separately. The analyses revealed large effects. The weighted mean effect size (r) was .48 for anger–hostility, .29 for anger out, .53 for anger in, and -.44 for anger control. Moderator analyses were conducted for anger–hostility, showing that effect sizes were substantially larger with increasing time since the event and that effect sizes were larger in samples with military war experience than in samples that had experienced other types of traumatic events.

Acute stress reactions in the first 3 weeks postpartum: A study of 219 parturients

OBJECTIVES: There is increasing research on posttraumatic stress (PS) 4-6 weeks and 3 months postpartum, but, there are no data on acute stress reactions (ASR) in the first 3 weeks postpartum, i.e. the potential precursors of PS. However, ASR may have long-term effects, e.g., on a subsequent pregnancy without having manifested as PS in the meantime. We propose: (i) to describe the patterns of ASR after childbirth, (ii) to explore differences between women with normal and traumatogenic ASR, and (iii) to provide data on the early detection of traumatogenic ASR 2 and 3 weeks postpartum. STUDY DESIGN: Intra-event variables (relationship with caregivers, overall birth experience, and dissociative experiences, as well as obstetric variables) were assessed 48-96h. postpartum, as were ASR (by means of the Impact-of-Event Scale IES) in weeks 1, 2, and 3 postpartum. According to research on PS the upper 33%-range of ASR in weeks 2 and 3 was defined as 'traumatogenic'. RESULTS: Normal ASR in week 1 are at a level which in non-obstetric trauma-situations is considered as the upper range of low stress or lower range of medium distress. ASR decline constantly from week 1 to week 3. However, high ASR in week 1 do not drop faster than do low ones, thus indicating a prolonged stress reaction in women with high ASR in week 1. Low ASR (IES-scores <10) and high ASR (IES-scores >20) in week 1 are highly predictive for normal ASR, and traumatogenic ASR in weeks 2 and 3, respectively. Medium ASR (IES-scores 10-20) in week 1 are of uncertain predictive value for stress reactions in weeks 2 and 3 and have to be re-assessed at that time. CONCLUSIONS: Clinical screening for ASR appears to be helpful in detecting women with a compromised ability to process childbirth-related stress. The association between ASR and long-term development should be further explored.

Posttraumatic stress disorder after implantation of a mechanical assist device followed by heart transplantation: evaluation of patients and partners

AIM: We sought to investigate the prevalence of posttraumatic stress disorder, anxiety, and depression in patients and their partners after implantation of a mechanical assist device as a bridge to heart transplantation. METHODS: This was a retrospective assessment of 41 patients (age 46.3 +/- 12.0 years; male-female ratio, 38:3; time since transplantation, 55.3 +/- 34.2 months [range, 7-122 months) and 27 partners (male-female ratio 2:25) by standardized instruments (Impact of Event Scale, Hospital Anxiety and Depression Scale), in 2 University Heart Transplant Centers (Vienna, Austria, Munster, Germany). The duration of the support systems (MicroMed DeBakey-VAD in 17 patients, Novacor in 10, Thoratec in 8, TCI HeartMate in 5, and Berlin Heart Incor in 1 patient) ranged from 28 to 711 (176 +/- 146) days. RESULTS: None of the patients, but 23% of the partners (n = 6), met the criteria for posttraumatic stress disorder (Maercker cutoff >0). The Impact of Event Scale (IES) sum scales differed significantly between the 2 groups (21.2 +/- 15.1, mean +/- SD) for the patients versus 38.1 +/- 27.8 for the partners, respectively; P = .001). Two percent of the patients, but 19% of the partners, showed mild to moderate depression; 4% of patients, but 23% of their partners, reported mild to moderate anxiety. None of the results were significantly influenced by the time since transplantation, patient age, diagnoses, type of assist device, or indication for heart transplantation. CONCLUSIONS: Despite patients being much closer to a life threat, their partners experience significantly more psychologic distress even in the long run. Our findings highlight the need for attention to the supporting persons.

INFLUENCE OF 24-HOUR SLEEP DEPRIVATION ON CARDIOVASCULAR AND NEURAL CONTROL AT REST AND DURING ACUTE STRESS IN HUMANS

Recent epidemiological studies report a consistent association between short sleep and incidence of hypertension, as well as short sleep and cardiovascular disease-related mortality. While the association between short sleep and hypertension appears to be stronger in women than men, the mechanisms underlying the relations between sleep deprivation, stress, risks of cardiovascular diseases, and sex remain unclear. We conducted two studies to investigate the underlying neural mechanisms of these relations. In study 1, we examined sympathetic neural and blood pressure responses to experimentally-induced sleep deprivation in men and women. We further investigated the influence of sleep deprivation on cardiovascular reactivity to acute stress. In study 2, we examined the neural and cardiovascular function throughout the ovarian cycle in sleep deprived women. Twenty-eight young healthy subjects (14men and 14 women) were tested twice in study 1, once after normal sleep (NS) and once after 24-h total sleep deprivation (TSD). We measured the blood pressure, heart rate (HR), muscle sympathetic nerve activity (MSNA) and forearm blood flow (FBF) during 10min baseline, 5min of mental stress (MS) and 2 min cold pressor test (CPT). We demonstrated that TSD increased resting arterial blood pressure to a similar extent in both men and women, but MSNA decreased only in men following TSD. This MSNA response was associated with altered baroreflex function in women and divergent testosterone responses to TSD between men and women. Regarding TSD and cardiovascular reactivity, TSD elicited augmented HR reactivity and delayed recovery during both MS and CPT in men and women, and responses between sexes were not statistically different. Fourteen young healthy women participated in study 2. Subjects were tested twice, once during their early follicular (EF) phase after TSD, once during their mid-luteal (ML) phase after TSD. Blood pressure, HR, MSNA, and FBF were recorded during 10min baseline, 5 min MS, and 2 min CPT. We observed an augmented resting supine blood pressure during EF compared to ML in sleep deprived women. In contrast, resting MSNA, as well as cardiovascular responses to stressors, were similar between EF and ML after TSD. In conclusion, we observed sex differences in MSNA responses to TSD that demonstrate reductions of MSNA in men, but not women. TSD elicited augmented HR reactivity and delayed HR recovery to acute stressors similarly in men and women. We also reported an augmented supine blood pressure during EF compared to ML in sleep deprived women. These novel findings provide new and valuable mechanistic insight regarding the complex and poorly understood relations among sleep deprivation, sex, stress, and risk of cardiovascular disease.

Measures of endothelial dysfunction in plasma of patients with posttraumatic stress disorder

Posttraumatic stress disorder (PTSD) confers an increased cardiovascular risk. In 14 otherwise healthy patients with PTSD and in 14 age- and gender-matched non-PTSD controls, we investigated whether the categorical diagnosis of PTSD and severity of PTSD symptom clusters (i.e. re-experiencing, avoidance, arousal, and overall score) would be associated with plasma concentrations of three markers of endothelial dysfunction [soluble tissue factor (sTF), von Willebrand factor (VWF), and soluble intercellular adhesion molecule (sICAM)-1]. Compared with controls, patients had significantly higher sTF; this difference became nonsignificant when controlling for psychological distress. VWF and sICAM-1 levels were not significantly different between patients and controls. In the entire sample virtually all PTSD symptom clusters correlated significantly and positively with sTF and VWF but not with sICAM-1. The correlation between symptoms of re-experiencing and sTF was significantly different between patients and controls. Controlling for symptoms of anxiety and depression (i.e. psychological distress) rendered most associations between PTSD symptom clusters and sTF nonsignificant, whereas controlling for age retained significance of associations with VWF. Posttraumatic stress showed a continuous relationship with sTF and VWF, with the former relationship being partly affected by psychological distress. This suggests one mechanism by which posttraumatic stress could contribute to atherosclerosis.

Aspirin, but not propranolol, attenuates the acute stress-induced increase in circulating levels of interleukin-6: a randomized, double-blind, placebo-controlled study

Psychosocial stress might increase the risk of atherothrombotic events by setting off an elevation in circulating levels of the proinflammatory cytokine interleukin (IL)-6. We investigated the effect of aspirin and propranolol on the responsiveness of plasma IL-6 levels to acute psychosocial stress. For 5 days, 64 healthy subjects were randomized, double-blind, to daily oral aspirin 100mg plus long-acting propranolol 80 mg, aspirin 100mg plus placebo, long-acting propranolol 80 mg plus placebo, or placebo plus placebo. Thereafter, all subjects underwent the 13-min Trier Social Stress Test, which combines a preparation phase, a job interview, and a mental arithmetic task. Plasma IL-6 levels were measured in blood samples collected immediately pre- and post-stress, and 45 min and 105 min thereafter. The change in IL-6 from pre-stress to 105 min post-stress differed between subjects with aspirin medication and those without (p =0.033; eta p2=0.059). IL-6 levels increased less from pre-stress to 105 min post-stress (p <0.027) and were lower (p =0.010) at 105 min post-stress in subjects with aspirin than in subjects without aspirin. The significance of these results was maintained when controlling for gender, age, waist-to-hip ratio, mean arterial blood pressure, and smoking status. Medication with propranolol was not significantly associated with the stress-induced change in IL-6 levels. Also, aspirin and propranolol did not significantly interact in determining the IL-6 stress response. Aspirin but not propranolol attenuated the stress-induced increase in plasma IL-6 levels. This suggests one mechanism by which aspirin treatment might reduce the risk of atherothrombotic events triggered by acute mental stress.

Clinical diagnosis of posttraumatic stress disorder after myocardial infarction

BACKGROUND: Clinician-rated large-scale studies estimating the prevalence of posttraumatic stress disorder (PTSD) related to myocardial infarction (MI) and identifying predictors of clinical PTSD are currently lacking. HYPOTHESES: We hypothesized that PTSD is prevalent in post-MI patients and that the subjective experience of the MI determines PTSD status. METHODS: We approached 951 post-MI patients with a questionnaire screening for PTSD symptoms related to their MI. Those responding and meeting a cutoff of PTSD symptom levels were invited to participate in a structured clinical interview to diagnose PTSD following Diagnostic and Statistical Manual of Mental Disorders (DSM-IV) criteria. Fear of dying, feelings of helplessness, and severity of pain perceived during the MI were also assessed by visual analog scales. RESULTS: The screening questionnaire was completed by 394 patients, whereby 77 met the cutoff for the interview (8 patients declined the interview). Forty of 394 patients (10.2%) had clinical PTSD (subsyndromal and syndromal forms combined). Younger age (OR 0.95, 95% CI 0.91-0.99), greater fear of dying (OR 2.77, 95% CI 1.28-5.97), and more intense feelings of helplessness (OR 2.97, 95% CI 1.42-6.21) were independent predictors of PTSD status. Perceived pain intensity during MI, sex, type of index MI, left ventricular ejection fraction, number of coronary occlusions, and highest level of total creatinine kinase were not significant predictors. CONCLUSIONS: Clinical PTSD is prevalent in post-MI patients. Demographic and particularly psychological variables related to the subjective experience of the event were stronger predictors of PTSD status than were objective measures of MI severity.

Trajectory of posttraumatic stress disorder caused by myocardial infarction: a two-year follow-up study

OBJECTIVE: A substantial proportion of patients develop posttraumatic stress disorder (PTSD) following myocardial infarction (MI). Previous research on the trajectory over time of PTSD in post-MI patients is scant and refers to self-rated posttraumatic symptoms. The aim of this study was to investigate the longitudinal course of an interviewer-rated diagnosis of PTSD and PTSD symptom severity following MI. METHODS: Study participants were 40 patients (78% men, mean age 54 +/- 8 years) who were diagnosed with PTSD using the Clinician-administered PTSD Scale (CAPS) after an average of 5 +/- 4 months (range 2-16 months) following an index MI. After a mean follow-up of 26 +/- 6 months (range 12-36 months), 24 patients underwent a second diagnostic interview. RESULTS: Two-thirds of patients (n = 16) still qualified for a diagnosis of PTSD at follow-up. In all 24 patients, total PTSD symptoms (p = 0.001), re-experiencing symptoms (p < 0.001), avoidance symptoms (p = 0.015), and, with borderline significance, hyperarousal symptoms (p < 0.06) had all decreased over time. However, in the subgroup of the 16 patients who had retained PTSD diagnostic status at follow-up, symptoms of avoidance (p = 0.23) and of hyperarousal (p = 0.48) showed no longitudinal decline. Longer duration of follow-up was associated with a greater decrease in avoidance symptoms (p = 0.029) and, with borderline significance, in re-experiencing symptoms (p < 0.07) across all patients. CONCLUSION: Although PTSD symptomatology waned over time and in relation to longer follow-up, two-thirds of patients still qualified for a diagnosis of PTSD 2 years after the initial diagnosis. In post-MI patients, clinical PTSD is a considerably persistent condition.