Intervening for exhaustion

Abstract

First paragraph: 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 b vital exhaustion Q (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 [2-5]. 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 [7,8], 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. Accordingly, the experimental evidence presented by Appels et al. [10] from the Exhaustion Intervention Trial (EXIT) in the paper published in this issue and its companion article published recently in Psychosomatic Medicine [11] is to be very much welcomed. Over 4000 CHD patients who had undergone successful angioplasty were approached. Refusal to participate and absence of VE reduced the sample to just over 700 who were randomized either to a 6-month exhaustion intervention comprising, among other things, group counseling, stress and anger management, and relaxation, or to a usual care control condition, largely involving routine checkups. The earlier publication focused on recurrent CHD events. Vital exhaustion measured at 6 months, i.e., immediately after the intervention, did not differ between intervention and control. By 18-month follow-up, however, fewer intervention patients reported feeling exhausted; they were also, following statistical adjustment for age, gender, and depression status at intake, less likely to be depressed at 18 months. Nevertheless, the intervention did not reduce the likelihood of patients having a recurrent CHD event, a result which is very much in line with findings from the recent ENRICHD trial that reductions in mortality and recurrent events did not follow from the successful treatment of depression in CHD patients [12]. Appels et al [11] concluded that, bThese negative outcomes do not refute the strong predictive power of depressive symptomatology or exhaustion observed in many studies, nor do they refute the biological plausibility of this association Q (p. 222). We would submit that they were being unduly modest and that their results and those from ENRICHD should cause us to pause, reconsider the issue of causality, and examine alternative, biologically plausible, explanations for the patterns of results that have emerged from observational studies. Although event-free survival will necessarily remain a key consideration in managing CHD, other outcomes, particularly quality of life, should not be disregarded. In an editorial in an earlier volume of Psychosomatic Medicine, Lesperance and Frasure-Smith [13] argued cogently that, b We should not lose sight of the fact that an intervention that improves well-being, but fails to change survival, is still a very valuable treatment Q (p. 20). It is to Appels and his colleagues' [10] credit that, in addition to recurrent CHD events, they measured such well-being outcomes in EXIT; these constitute the focus of their article in this issue. The outcomes reported, aside from depression which is mentioned above, are health-related quality of life, anxiety, anger, and anginal complaints. The intervention, despite including treatment for anger, failed to modify scores on the questionnaire measurement of anger. Effects are reported for the other outcomes, but they are not always easy to interpret. Intervention and control groups showed virtually identical mean health-related quality of life scores at both the 6-month and 18-month sampling points. However, the intervention group registered poorer quality of life at entry to the study and from multiple 0022-3999/06/$-see front matter D