It has long been recognized that severe or sudden emotional stress could result in a heart attack or sudden death. Walter Cannon at Harvard first delineated the mechanisms responsible for this in the early part of the last century. (Cannon 1914) Cannon's studies demonstrated that responses to the stress of acute fear resulted in a marked increase in sympathetic nervous system activity and an outpouring of sympathin (adrenaline) that prepared the animal for lifesaving "fight or flight." His later studies of the mechanism of "bone pointing" or "voodoo" death also implicated excess secretion of hormones from the adrenal medulla into the blood stream as the most likely cause of fatal arrhythmia. (Cannon 1942) Hans Selye's formulation of the stress concept in the late 1940’s provided further insight into the role of pituitary and adrenal cortical hormones in mediating damaging cardiovascular responses to stress.
His subsequent research included the experimental production of "metabolic cardiac necroses," in which direct biochemical injury to heart muscle rather than occlusion of the coronary vessels was the causative factor. (Selye 1958) Since then, it has been observed that stress can cause accelerated atherosclerosis and coronary occlusion that is associated with elevated cholesterol, triglycerides, and free fatty acids, increased fibrinogen, haptoglobin, plasma seromucoids, platelet aggregation and adhesiveness, polycythemia, and accelerated blood clotting. We have also become increasingly aware of the important role of stress-induced coronary vasospasm in the production of clinical symptoms and disease.
Even more significant has been the identification of myocardial infarction in the absence of significant coronary occlusion due to excessive release of norepinephrine at myocardial nerve endings. This has been shown to produce a specific type of microscopic myocardial damage that appears to be identical in laboratory animals as well as humans who have succumbed to sudden cardiac death as a result of an acutely stressful situation. (Cebelin, Hirsch 1981) There is also abundant evidence that severe and acute emotional stress following an earthquake or other natural disaster or the loss of a loved one can result in hypertension, a heart attack or sudden death.
In 1982, the disappointing results of the seven-year, $115 million MRFIT study were published in the Journal of the American Medical Association. MRFIT is an acronym for Multiple Risk Factor Intervention Trail, which was designed to show the beneficial effect of stopping smoking and lowering cholesterol and blood pressure. (Multiple Risk Factor Intervention Trial Group 1982)
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