Behavioral-neuroendocrine-immunologic interactions in myocardial infarction.
An enduring state of exhaustion as opposed to chronic hostility-a long-term risk factor-has been found to be a more proximal precursor of myocardial infarction. The strength of the association with exhaustion suggests that this behavioral factor reflects not only a breakdown in adaptation to chronic stressors but also the disease process itself. Recent research on the pathogenesis of myocardial infarction lends credence to a role for immunological factors. herein, we outline a two-stage theoretical model, postulating a feedback relationship between behavior, associated neuroendocrine changes, immunological responses, and the pathogenesis of this disease. We propose a long-term first stage consisting of chronic hostility, prolonged occupational over-exertion, and exposure to other life stressors, terminating eventually in a much shorter second stage of 'vital exhaustion'. Stressor-associated neuroendocrine changes result in immunosuppression leading to reactivation of latent, systemic infections (such as cytomegalovirus) and potentially to autoimmune reactions as well. The consequent release of pro-inflammatory cytokines exacerbates fatigue and induces a stimulus for cytokine production in brain. This cytokine production stimulates a chronically activated, over-compensated limbic-hypothalamic-pituitary-adrenal axis, resulting in a dampened response, continued exhaustion, and a potential 'reverberating circuit' between behavior, neuroendocrine change, cytokine release and coronary artery occlusion, culminating in myocardial infarction.
Goodkin
K
K
Department of Psychiatry, University of Miami School of Medicine, FL 33136, USA. kgoodkin@mednet.med.miami.edu
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D000900:Anti-Bacterial Agents / Q000627:therapeutic use; D000998:Antiviral Agents / Q000627:therapeutic use; D001521:Behavior Therapy; D003141:Communicable Diseases / Q000453:epidemiology / Q000503:physiopathology; D016207:Cytokines / Q000037:antagonists & inhibitors; D004032:Diet; D006791:Hostility; D006801:Humans; D007107:Immune System / Q000502:physiology* / Q000503:physiopathology; D007165:Immunosuppression Therapy; D008954:Models, Biological; D008960:Models, Psychological; D009203:Myocardial Infarction / Q000453:epidemiology / Q000503:physiopathology* / Q000523:psychology*; D009490:Neurosecretory Systems / Q000502:physiology* / Q000503:physiopathology; D012307:Risk Factors; D017367:Selective Serotonin Reuptake Inhibitors / Q000627:therapeutic use
D000900:Anti-Bacterial Agents; D000998:Antiviral Agents; D016207:Cytokines; D017367:Selective Serotonin Reuptake Inhibitors