Intervening for exhaustion

"The search for psychosocial factors that contribute to the aetiology and course of coronary heart disease (CHD) has been an energetic, although not always fruitful, pursuit for more than half a century. Around 20 years ago, Appels [1] identified a prodromal constellation of symptoms, including physical exhaustion and feelings of hopelessness, that preceded major CHD events. It was hypothesized that this syndrome of “vital exhaustion” (VE) was a causal risk factor for CHD events, and several observational studies demonstrating prospective associations between VE and subsequent events have been adduced as supporting the hypothesis [2], [3], [4] and [5]. In a recent commentary, however, we discussed the difficulties inherent in drawing causal conclusions from observational evidence [6]. Applying general arguments that are by now very well rehearsed [7] and [8], we suggested that considerations such as confounding by common antecedents of both VE and CHD and reverse causation could not be readily dismissed and resolution was likely only following experimental studies. For example, an explanation of these prospective associations that regards CHD events as the result of inflammatory processes involved in the progress of atherosclerosis and VE as a consequence of such processes is just as parsimonious as one that regards VE as a causal risk. It is also equally, if not more, plausible biologically; there is now substantial evidence that inflammatory cytokines communicate with the central nervous system contributing to illness behaviour and experience and fostering feelings of depression and fatigue [9]. We also posed the question of what implications do the results of observational studies of VE hold for treatment [6]. Again, we would argue that in the absence of experimental evidence, the implications are extremely limited."\ud \u

Invited Commentary: Stress and Mortality

In this issue of the Journal, Nielsen et al. (Am J Epidemiol 2008;168:481−91) use data from a large Danish study to provide evidence that self-reported stress is associated with increased all-cause mortality over the next 20 years. The finding is remarkable. In this commentary, the authors explore what is really meant by stress; they argue that it would be naïve to view stress as reported in this way, with some external exposure. It has to be seen through the lens of the participant's personal experience, and this lens is likely to be clouded by personality, coping styles, and the common mental disorders—depression and anxiety. The authors discuss a wider literature concerning similar findings associating depression with mortality, suggesting three broad reasons for the association. First, the findings might be explained by the impact of stress or distress on well-established risk factors for cardiovascular disease and cancer. Second, there might be direct, underlying psychosomatic pathways by which stress or distress can affect immune or autonomic function. Third, there might be common causal pathways—shared genes or early adversities that predict both stress and mortality from other causes independently. The authors suggest that life course epidemiologic research is required to test these competing hypotheses

Psychological interventions for coronary heart disease

A meta-analysis was conducted on 35 trials involving 10,703 individuals who had experienced a myocardial infarction and were randomised to an intervention involving some form of psychological therapy. Ten of these studies involved individuals with confirmed psychiatric diagnoses. Moderate quality evidence found no reduction of risk for total mortality or revascularisation procedures in comparison to usual care. Low quality evidence found no risk reduction for non-fatal MI although there was a 21% reduction in cardiac mortality. There was also some evidence of benefit on measures of psychological morbidity including anxiety, depression, and stress. It is concluded that psychological interventions may reduce cardiac mortality, although stronger evidence is required before this can be definitively concluded. It is also not clear who benefits most from psychological interventions

Coronary heart disease and depression : getting evidence into clinical practice

Clinical guidelines based on systematic reviews of the evidence recommend identification and treatment of patients with coronary heart disease and depression. The evidence shows that depression is an independent risk factor for heart disease, and when present after an acute coronary event, is a predictor of poor prognosis. This paper will describe our experience of getting that evidence into practice using change management based on mapping the processes of the patient's journey through the healthcare system. This allowed identification of the points in the journey where screening and intervention could take place. Cardiac rehabilitation is the intervention point for acute presentation, and primary care has the role in long term follow up of risk factors including depression. Overall, comorbid depression is best managed within a system of collaborative care based on chronic disease management principles. Copyright © 2008 John Wiley & Sons, Ltd