A new mechanism linking stress to coronary pathophysiology?

For generations, physicians have been struck by the powerful impact of stressors on the heart. Who has not seen cases of angina, myocardial infarction, arrhythmia, or sudden death in settings of emotional travail? Such phenomena are difficult to study, and it is so easy to find stress post hoc. After all, most of us could relate numerous significant stressors per week (and perhaps per day). How often or under what circumstances do stressors relate to cardiac disease? Investigators are still grappling with this problem of defining stress consistently. In the 1960s and 1970s, research flourished, generating a glossary of life events that could be reliably rated (for a recent review, see Reference 2). Unfortunately, it may be inadequate to define stress without considering the subjective impact, for there is nothing either good or bad, but thinking makes it so."3 Sometimes even the most stark stressors affect people differently; loss of a spouse may be an occasion for one person's bereavement and another's relief. Because of this, in evaluating stressfulness, investigators are increasingly considering both the stressful event and the subjective assessment of the patient.4 Aside from these basic issues in defining stressors, it is important to recognize that there are substantial differences in host vulnerabilities to stressors. Activation of the sympathetic nervous system may produce little more than an increase in heart rate, blood pressure, and free fatty acids in normal subjects; whereas, in those with serious coronary atherosclerosis, it can precipitate angina, cardiac arrhythmia, or pulmonary edema.5-'0 Certain psychosocial factors