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EDITORIAL COMMENT |
Distinguished Professor of Pathology Department of Pathology University of California, San Diego, School of Medicine La Jolla, California
"Oh, East is East, and West is West, and never the twain shall meet." These famous words of Rudyard Kipling typify the separation of thought that existed years ago between physician-scientists of different disciplines, for example, those investigators whose prime interest was in psychosomatic medicine and those whose prime interest was in pathology in the broadest sense. In recent years we have advanced in our thinking and understanding and have learned that perceived boundaries between various disciplines in medicine are too often artificial barriers that impede progress in medicine. In the past decade an increasing number and variety of studies have involved collaboration between investigators of different disciplines focusing on cardiovascular disease. In this issue the article by Appels et al. (1) clearly demonstrates the benefits of collaborative studies of this type. Although their study focused on a common cardiovascular disease, namely coronary artery disease, the approach used is one that can serve as a model for similar studies of other diseases.
In recent years studies have shown that atherosclerosis is a chronic inflammatory process (2). Plasma concentrations of markers of inflammation are increased in patients with atherosclerosis. Also, associations between Chlamydia pneumoniae and herpes simplex infections and coronary artery disease have been reported (3, 4). Appels et al. are the first to show the association between the mental status of patients with coronary artery disease and quantitative measurements of the degree of inflammation. To assess the extent of inflammation, they measured antibody titers against C. pneumoniae, cytomegalovirus, and the cytokines. The selection of these factors is very appropriate because recent studies have shown that cytomegalovirus and C. pneumoniae infections play a role in atherogenesis and can contribute to coronary artery disease (5, 6). Increased cytokine levels attest to the subsequent steps in the inflammatory process, including smooth muscle cell proliferation in vessels advancing to occlusive states and their role as a signal of tissue damage to the body.
Certainly a high incidence of depressive symptomatology in patients with coronary artery disease has been known for years (7). However, our ability to draw conclusions from those studies has been limited by the various criteria and diverse methods used to define the psychiatric morbidity and depressive symptoms. At times depression was considered a symptom of the coronary disease itself. At other times depression was considered a concomitant condition of coronary artery disease and was not recognized as an independent source of increased morbidity and mortality in these patients.
The study of Appels et al. shows that depressive symptomatology is associated with inflammation, a concept that has interesting therapeutic implications. A major question still remains and is identified by the authors. That question is which occurs first: Does the depressed state initiate the activation of latent organisms, inducing the inflammatory process, or is an ongoing inflammatory process initiated by other events causing the depressed state? Because the authors limited their study to patients with stable angina, their results may represent a restricted view because inclusion of patients with unstable angina could show larger measures of ongoing inflammation. Nevertheless, further exploration of these possibilities is very worthwhile because there are significant consequences for understanding pathogenetic mechanisms of acute coronary syndromes and in turn improved treatment of coronary artery disease.
Various social influences, including social support, occupational stress, and socioeconomic status, have been reported to significantly affect morbidity and mortality in individuals with coronary artery disease (7). Animal studies using models of stress and anger have shown a lower cardiac threshold for ventricular fibrillation in subjects with these characteristics as compared with calm controls (8, 9). Thus, behavioral states are able to induce functional-structural changes that are key parts of pathogenetic mechanisms. There are undoubtedly many other potential explorations to follow if creative investigators from different disciplines engage in more dialogue and in so doing discover that many accepted truths within one’s own field when viewed from afar may be early clues of more complex steps in unraveling the mysteries of disease. Thus, in reading the work by Appels et al., we should not only appreciate its unique contribution but also recognize its possibly more far-reaching value as a model for future investigations, not only in the cardiovascular field but also in other fields where increased dialogue between disciplines can provide crucial insights into specific mechanisms.
REFERENCES
This article has been cited by other articles:
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  M. Sala, M. Lazzaretti, G. De Vidovich, E. Caverzasi, F. Barale, G. d'Allio, and P. Brambilla Electrophysiological changes of cardiac function during antidepressant treatment Therapeutic Advances in Cardiovascular Disease, February 1, 2009; 3(1): 29 - 43. [Abstract] [PDF]
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 J. Macleod and D. Carroll Commentary: What should we make of associations between vital exhaustion and heart disease? Int. J. Epidemiol., December 1, 2003; 32(6): 997 - 999. [Full Text] [PDF]
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