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±7years, 79% men) with an interviewer-rated diagnosis of posttraumatic stress disorder caused by an index myocardial infarction 3±3months before. After a mean follow-up of 26±6months, 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 individual

Mind-Body Practices in Integrative Medicine

Mind-Body practices have become increasingly popular as components of psychotherapeutic and behavior medicine interventions. They comprise an array of different methods and techniques that use some sort of mental-behavioral training and involve the modulation of states of consciousness in order to influence bodily processes towards greater health, well-being and better functioning. Mind-body practices may thus be interpreted as the salutogenetic mirror image of psychosomatic medicine, where psychophysiological and health consequences of specific psychological states are studied, such as stress arousal, psychological trauma or depression. This contribution examines the empirical evidence of the most common mind-body techniques with regard to their salutogenetic potential. We concisely discuss some aspects of the mind-body problem, before we consider some historical aspects and achievements of psychosomatic medicine. We then turn to some prominent mind-body practices and their application, as well as the empirical database for them

Association Between Posttraumatic Stress Disorder Following Myocardial Infarction and Liver Enzyme Levels: A Prospective Study

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

Algometry with a clothes peg compared to an electronic pressure algometer: a randomized cross-sectional study in pain patients

<p>Abstract</p> <p>Background</p> <p>Hypersensitivity of the central nervous system is widely present in pain patients and recognized as one of the determinants of chronic pain and disability. Electronic pressure algometry is often used to explore aspects of central hypersensitivity. We hypothesized that a simple pain provocation test with a clothes peg provides information on pain sensitivity that compares meaningfully to that obtained by a well-established electronic pressure algometer. "Clinically meaningful" was defined as a medium (r = 0.3-0.5) or high (r > 0.5) correlation coefficient according to Cohen's conventions.</p> <p>Methods</p> <p>We tested 157 in-patients with different pain types. A calibrated clothes peg was applied for 10 seconds and patients rated the pain intensity on a 0 to 10 numerical rating scale. Pressure pain detection threshold (PPdt) and pressure pain tolerance threshold (PPtt) were measured with a standard electronic algometer. Both methods were performed on both middle fingers and ear lobes. In a subgroup of 47 patients repeatability (test-retest reliability) was calculated.</p> <p>Results</p> <p>Clothes peg values correlated with PPdt values for finger testing with r = -0.54 and for earlobe testing with r = -0.55 (all p-values < 0.001). Clothes peg values also correlated with PPtt values for finger testing with r = -0.55 (p < 0.001). Test-retest reliability (repeatability) showed equally stable results for clothes peg algometry and the electronic algometer (all r-values > 0.89, all p-values < 0.001).</p> <p>Conclusions</p> <p>Information on pain sensitivity provided by a calibrated clothes peg and an established algometer correlate at a clinically meaningful level.</p

Myocardial infarction and post-traumatic stress disorder: frequency, outcome, and atherosclerotic mechanisms

BACKGROUND: Post-traumatic stress disorder (PTSD) may develop in the aftermath of an acute myocardial infarction (MI). Whether PTSD is a risk factor for cardiovascular disease (CVD) is elusive. The biological mechanisms linking PTSD with atherosclerosis are unclear. DESIGN: A critical review of 31 studies in the English language pursuing three aims: (i) to estimate the prevalence of PTSD in post-MI patients; (ii) to investigate the association of PTSD with cardiovascular endpoints; and (iii) to search for low-grade systemic inflammatory changes in PTSD pertinent to atherosclerosis. METHODS: We located studies by PubMed electronic library search and through checking the bibliographies of these sources. RESULTS: The weighted prevalence of PTSD after MI was 14.7% (range 0-25%; a total of 13 studies and 827 post-MI patients). Two studies reported a prospective association between PTSD and an increased risk of cardiovascular readmission in post-MI patients and of cardiovascular mortality in combat veterans, respectively. In a total of 11 studies, patients with PTSD had increased rates of physician-rated and self-reported cardiovascular diseases. Various cytokines and C-reactive protein were investigated in a total of seven studies suggesting that PTSD confers a pro-inflammatory state. CONCLUSIONS: Increasing evidence suggests that PTSD specifically related to MI develops considerably frequently in post-MI patients. More research is needed in larger cohorts applying a population design to substantiate findings suggesting PTSD is an atherogenic risk factor and to understand better the suspected behavioural and biological mechanisms involved