Posttraumatic stress disorder and soluble cellular adhesion molecules at rest and in response to a trauma-specific interview in patients after myocardial infarction.

Posttraumatic stress disorder (PTSD) and circulating cellular adhesion molecules (CAMs) predict cardiovascular risk. We hypothesized a positive relationship between PTSD caused by myocardial infarction (MI) and soluble CAMs. We enrolled 22 post-MI patients with interviewer-rated PTSD and 22 post-MI patients with no PTSD. At 32±6months after index MI, all patients were re-scheduled to undergo the Clinician-Administered PTSD Scale (CAPS) interview and had blood collected to assess soluble CAMs at rest and after the CAPS interview. Relative to patients with no PTSD, those with PTSD had significantly higher levels of soluble vascular cellular adhesion molecule (sVCAM)-1 and intercellular adhesion molecule (sICAM)-1 at rest and, controlling for resting CAM levels, significantly higher sVCAM-1 and sICAM-1 after the interview. Greater severity of PTSD predicted significantly higher resting levels of sVCAM-1 and soluble P-selectin in patients with PTSD. At follow-up, patients with persistent PTSD (n=15) and those who had remitted (n=7) did not significantly differ in CAM levels at rest and after the interview; however, both these groups had significantly higher sVCAM-1 and sICAM-1 at rest and also after the interview compared to patients with no PTSD. Elevated levels of circulating CAMs might help explain the psychophysiologic link of PTSD with cardiovascular risk.

Momentary stress moderates procoagulant reactivity to a trauma-specific interview in patients with posttraumatic stress disorder caused by myocardial infarction.

Hypercoagulability of the blood might partially explain the increased cardiovascular disease risk in posttraumatic stress disorder (PTSD) and is also triggered by anticipatory stress. We hypothesized exaggerated procoagulant reactivity in patients with PTSD in response to a trauma-specific interview that would be moderated by momentary stress levels. We examined 23 patients with interviewer-diagnosed PTSD caused by myocardial infarction (MI) and 21 post-MI patients without PTSD. A second diagnostic (i.e., trauma-specific) interview to assess posttraumatic stress severity was performed after a median follow-up of 26 months (range 12-36). Before that interview patients rated levels of momentary stress (Likert scale 0-10) and had blood collected before and after the interview. The interaction between PTSD diagnostic status at study entry and level of momentary stress before the follow-up interview predicted reactivity of fibrinogen (P=0.036) and d-dimer (P=0.002) to the PTSD interview. Among patients with high momentary stress levels, PTSD patients had greater fibrinogen (P=0.023) and d-dimer (P=0.035) reactivity than non-PTSD patients. Among patients with low momentary stress levels, PTSD patients had less d-dimer reactivity than non-PTSD patients (P=0.024); fibrinogen reactivity did not significantly differ between groups. Momentary stress levels, but not severity of posttraumatic stress, correlated with d-dimer reactivity in PTSD patients (r=0.46, P=0.029). We conclude that momentary stress levels moderated the relationship between PTSD and procoagulant reactivity to a trauma-specific interview. Procoagulant reactivity in post-MI patients with PTSD confronted with their traumatically experienced MI was observed if patients perceived high levels of momentary stress before the interview.

Posttraumatic stress disorder and dyslipidemia: previous research and novel findings from patients with PTSD caused by myocardial infarction.

OBJECTIVES: Based on a brief systematic review suggesting dyslipidemia in posttraumatic stress disorder (PTSD), we studied, for the first time, levels of blood lipids in patients with a DSM-IV diagnosis of PTSD caused by myocardial infarction (MI). METHODS: Study participants were eight patients with full PTSD, eight patients with subsyndromal PTSD, and 31 patients with no PTSD who were diagnosed using the Clinician-Administered PTSD Scale (CAPS) interview after a mean of 32+/-8 months after MI. Levels of total cholesterol, low-density lipoprotein-cholesterol, triglycerides, and high-density lipoprotein-cholesterol (HDL-C) were determined in plasma. RESULTS: Patients with full PTSD had lower HDL-C than patients with subsyndromal PTSD (P = 0.044) and those with no PTSD (P = 0.014) controlling for sex, body mass index, and statin equivalent dosage. Moreover, HDL-C levels were inversely associated with PTSD total symptoms (r = -0.33, P = 0.027), re-experiencing symptoms (r = -0.32, P = 0.036), and avoidance symptoms (r = -0.34, P = 0.025). There were no significant associations of PTSD diagnostic status and symptomatology with the three other lipid measures. CONCLUSION: Chronic PTSD caused by MI was associated with lower plasma levels of HDL-C. The finding concurs with the notion of dyslipidemia partially underlying the atherosclerotic risk in individuals with PTSD caused by different types of trauma.

Stress hormones in patients with posttraumatic stress disorder caused by myocardial infarction and role of comorbid depression.

BACKGROUND: Chronic posttraumatic stress disorder (PTSD) has been associated with perturbed hypothalamic-pituitary-adrenal (HPA) axis function and a hyperadrenergic state. We hypothesized that patients with PTSD attributable to myocardial infarction (MI) would show peripheral hypocortisolemia and increased norepinephrine levels, whereby taking into account that depressive symptoms would affect this relationship. METHODS: We investigated 15 patients with interviewer-rated PTSD caused by myocardial infarction (MI) and 29 post-MI patients with no PTSD. Patients also completed the depression subscale of the Hospital Anxiety and Depression Scale and had blood collected to determine plasma cortisol and norepinephrine levels. RESULTS: In bivariate correlation analysis PTSD and depressive symptoms were not significantly associated with cortisol levels. However, patients with PTSD had lower mean+/-SEM cortisol levels than patients with no PTSD when controlling for depressive symptoms (77+/-11 vs. 110+/-7 ng/ml, p=.035). In turn, depressive symptoms correlated with cortisol levels when taking PTSD into account (r=.36, p=.019). In all patients cortisol levels correlated with total PTSD symptoms (r=-.43, p=.005) and hyperarousal symptoms (r=-.45, p=.002) after controlling for depressive symptoms. Depression correlated with cortisol levels after controlling for total PTSD symptoms (r=.45, p=.002). Posttraumatic stress disorder and depressive symptoms were not significantly associated with norepinephrine levels. CONCLUSIONS: In post-MI patients we found peripheral hypocortisolemia related to PTSD, respectively hypercortisolemia related to depressive symptoms, when taking joint effects of PTSD and depression into account. No evidence was found for a hyperadrenergic state. Comorbid depressive symptoms ought to be considered to disentangle the unique associations of PTSD with HPA axis dysfunction in cardiac patients.

Inflammatory biomarkers in patients with posttraumatic stress disorder caused by myocardial infarction and the role of depressive symptoms.

OBJECTIVE: Inflammation might link posttraumatic stress disorder (PTSD) with an increased risk of cardiovascular events. We explored the association between PTSD and inflammatory biomarkers related to cardiovascular morbidity and the role of co-morbid depressive symptoms in this relationship. METHODS: We investigated 15 patients with interviewer-rated PTSD caused by myocardial infarction (MI) and 29 post-MI patients with no PTSD. All patients completed the depression subscale of the Hospital Anxiety and Depression Scale and had blood collected to determine inflammatory markers of increased cardiovascular risk. RESULTS: Controlling for demographic and medical covariates, patients with PTSD had higher leptin levels than patients with no PTSD (p = 0.038, explained variance 10.4%); this difference became nonsignificant when controlling for depressive symptoms. After controlling for depressive symptoms, PTSD patients had higher interleukin-6 (p = 0.041; explained variance 10%), lower C-reactive protein (p = 0.022, explained variance 12.1%), and lower soluble CD40 ligand (p = 0.016, explained variance 13.4%) than patients without PTSD. After controlling for PTSD status, depressive symptoms correlated with soluble CD40 ligand (r = 0.45, p = 0.002) and with C-reactive protein (r = 0.29, p < 0.07). CONCLUSIONS: The findings provide further evidence for altered inflammation in PTSD. Comorbid depressive symptoms ought to be considered to disentangle the unique associations of PTSD caused by MI and systemic inflammation.

Association between posttraumatic stress disorder following myocardial infarction and liver enzyme levels: a prospective study.

BACKGROUND: Research in rodents demonstrated that psychological stress increases circulating levels of alanine transaminase, aspartate transaminase, and alkaline phosphatase reflecting liver injury. Moreover, chronic posttraumatic stress disorder and transaminases predicted coronary heart disease. AIMS: To investigate the hypothesis that severity of posttraumatic stress disorder following myocardial infarction would prospectively relate to liver enzymes. METHODS: Study participants were 24 patients (mean 59+/-7 years, 79% men) with an interviewer-rated diagnosis of posttraumatic stress disorder caused by an index myocardial infarction 3+/-3 months before. After a mean follow-up of 26+/-6 months, patients had a clinical interview to reassess posttraumatic stress disorder severity, a medical history, and blood collected to determine liver enzymes. RESULTS: Total posttraumatic stress disorder symptoms assessed at study entry prospectively predicted plasma levels of alanine transaminase (r=.47, p=.031) and alkaline phosphatase (r=.57, p=.004), but not of aspartate transaminase (p=.15), controlling for follow-up duration and antidepressant use. Total posttraumatic stress disorder symptoms assessed at follow-up were associated with alanine transaminase (r=.72, p=.004), aspartate transaminase (r=.60, p=.018), and alkaline phosphatase (r=.64, p=.001) in the 16 patients who had maintained diagnostic posttraumatic stress disorder, but not in all 24 patients. CONCLUSIONS: The severity of posttraumatic stress disorder following myocardial infarction was associated with mild increase in liver enzyme levels, suggesting that chronic psychological stress relates to hepatic damage in humans. This might help to explain the previously observed increased cardiovascular risk in chronically traumatized individuals.

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.