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Depression and Social Support in Recovery From Myocardial Infarction: Confounding and Confusion

Rush Institute for Health Aging and, the Department of Preventive Medicine, Rush-Presbyterian-St. Luke’s Medical Center, 1645 W. Jackson Blvd, Suite 675, Chicago, IL 60612, Email: cmendes@rush.edu

Given the rapid growth of the aging population, prevention of adulthood chronic conditions and their disabling consequences will no doubt be one of the major public health challenges of the early 21st century. Most of these conditions are the result of underlying disease processes whose clinical manifestations alternate between periods of little or no symptoms and acute disease episodes that require immediate medical attention. These acute events often pose the greatest threat to life and future health, and much of our health care resources are directed at preventing death and enhancing recovery from such acute disease episodes. It is becoming increasingly clear that adverse psychosocial characteristics play an important, if still poorly understood, role in the recovery from acute disease events, such as myocardial infarction (MI), the acute manifestation of coronary artery disease (CAD).

In recent years, two themes have dominated the search for the specific psychosocial features that affect recovery from MI: depression and lack of social support. With few exceptions (1, 2), there has been little investigation of the combined effect of depression and lack of social support on prognosis after MI. Does each factor play an independent role, or does the primary benefit of social support exist in mitigating the adverse effect of depression? It is these important questions that are subject of the article by Irvine and colleagues in this issue of Psychosomatic Medicine (3). The results indicate that depression was associated with an increased risk for sudden cardiac death (SCD) only among patients randomized to the control group, with no evidence of this excess risk being alleviated by the presence of social support. Social support itself was not related to the risk of SCD, but other indicators of social interaction showed significant, albeit contradictory, associations with SCD: social participation reduced risk, while having a large social network increased risk.

So far, progress in our understanding of the role of depression and social support in recovery from acute MI has been hampered by some nagging questions. One of the main issues regarding the role of depression is the potential confounding with severity of disease. One source of potential confounding has to do with assessment of depression in cardiac patients: are depressed MI patients really depressed, or do they only seem so because (some) depressive symptoms mimic cardiac symptoms? The second source of confounding is related to establishing causal relationships: do depressed MI patients have a poorer prognosis primarily because they have more severe disease, or because of the depression? One major contribution of this article is that it attempts to address both these sources of confounding.

We need to recognize, however, what implicit assumptions we make when we control for confounding. One assumption in this analysis is that cardiac symptoms are an unbiased marker of severity of underlying disease, regardless of depression status. But what if depressed patients report more cardiac symptoms, regardless of disease severity? Given that disease severity was assessed by self-evaluations of fatigue and dyspnea, this possibility should be considered, and, to the extent this is the case, adjustment for these symptoms may lead to an artificial underestimation of the true effect of depression.

The second implicit assumption is that more severe disease causes depression, rather than the other way around. This is perhaps the more conservative assumption, but the actual interrelationship is likely to be complex, and we should not prematurely ascribe the adverse effect of depression to disease severity before we have a better understanding of this interrelationship.

In many ways, there still is a considerable degree of confusion about the role of social support in recovery from MI. Various studies have suggested an important role for social support (1, 4–6), but these studies have used widely varying and often imprecise definitions of social support. Adding to the confusion is a tendency to use all sorts of definitions and terms for various aspects and dimensions of social relationships interchangeably. Social support, social networks, social contacts, social isolation or integration, social participation: do all these terms really capture the same underlying idea? Is every aspect of our social relationships supposed to be supportive, and to provide a clear and unambiguous health benefit to a person?

In the end, what we probably mean most by social support is an exchange of resources between two persons, designed to fulfill particular needs of the support recipient. In the context of acute and life-threatening disease events, we typically think of these needs as emotional, but there are obviously other types of needs. Social contacts and social participation may provide opportunities for such exchanges to take place, but they remain only indirect measures of social support. Furthermore, social contacts or social participation may affect recovery from acute disease events in ways that have little to do with social support. For example, having many social ties harbor the possibility of excessive social demands and interpersonal conflict, which may undermine health (7). Social participation, on the other hand, may confer a powerful general survival benefit through a variety of physiologic and psychosocial pathways (8).

What is needed to clear up this confusion is to formulate more precise hypotheses about the role of social support, or any other aspect of our social relationships for that matter, during recovery from acute MI. We might find more consistent relationships if we move away from treating social support as a stable person-specific characteristic, and start considering the particular social context in which it is enacted. Who is providing the support, when should it be provided, and how does it affect the relationship between provider and recipient are but a few of the critical questions. Once we have a better understanding of these issues, we can start exploring how social support acts jointly or interactively with other psychosocial risk factors, such as depression.

Finally, how can we take these results to the next step of developing effective interventions aimed specifically at alleviating some of the adverse psychosocial characteristics in MI patients? First, we need to recognize that depression may only be one of a series of negative emotions that increase risk in patients with CAD (9–11). Moreover, many of these harmful emotional and interpersonal characteristics often coexist, or mutually influence one another (12, 13). Thus, at this stage, we probably should adopt an inclusive approach in our interventions, targeting negative emotions and psychosocial conditions generally, rather than trying to isolate and focus on a single "risk" emotion or condition. Second, we are still uncertain about the most effective way and time to modify psychosocial risk in MI patients, and interventions are likely to be relatively imprecise. Nevertheless, the overall approach seems to have sufficient merit (14), even if not all of our efforts may prove to be successful. Third, the preponderance of these acute disease events will shift more and more to the elderly, for whom quality of life and limiting disability may be as important, if not more important, than prolonging survival. It is perhaps toward that goal that psychosocial interventions can make their greatest and most effective contribution.

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