The preponderance of evidence links depressive disorder and coronary heart disease (CHD). Despite this evidence, multiple clinical trials have failed to show that effective treatment of depression favorably modifies the development, clinical course, or outcome of comorbid CHD. Possible reasons for these failures include the heterogeneity of depression, limitations of assessment instruments, limited understanding of the biology of depressive disorders, lack of biological markers, and the observation that depression may be more a product of CHD than a true risk factor for it. In this commentary, to better address the effects of externally provoked stress on physical health, we examine evidence about 2 specific examples of stress and subsequent heart disease: earthquake-induced adverse cardiac events among individuals with coronary artery disease, and stress-induced Takotsubo cardiomyopathy. In the former case, existing studies suggest that the stress and distress of earthquakes accelerate the development of poor cardiac outcomes for individuals with established coronary artery disease. In the latter example, existing case studies indicate that the profound left ventricular dysfunction of Takotsubo cardiomyopathy tends to quickly normalize once the acute stress is relieved. Together, these examples indicate that the presence or absence of prestress medical illness and its severity may better determine the outcome of the medical illness than the nature and severity of the stress, including depression. That is, any effort to look at depression among individuals with medical illness must look carefully at the medical illness itself and consider depression a possible nonspecific stress. In patients with comorbid depression and CHD, we propose using the more firmly established CHD outcome measurements to better understand how depression or other stressors and their associated treatments influence the prognosis and outcome of this medical illness.
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