Considerable evidence indicates that depression is a risk factor for mortality following myocardial infarction. One potential mechanism is altered autonomic nervous system functioning. That is, depression may be associated with reduced parasympathetic nervous system activity and/or increased sympathetic nervous system activity, both of which are known to increase the risk of ventricular arrhythmias. This increased susceptibility to ventricular arrhythmia in patients with already damaged hearts may increase their risk of mortality. In cardiac patients, measures of autonomic nervous system have been related to depression. However, investigations with healthy samples have yielded unclear results. This study will investigate the hypothesized relationship between depression and parasympathetic nervous system activity in healthy young volunteers. Specifically, participants in this study will provide information concerning their mood, feelings, and personality, and will complete several tasks designed to alter autonomic nervous system activity. Measures of cardiovascular system responses, to include blood pressure, heart rate, pre-ejection period, high frequency heart rate variability, baroreflex sensitivity, and cholesterol will be taken before, during, and after each task. These data will be used to examine the hypothesis that depressed individuals differ from non-depressed individuals in their basal level of autonomic activity, and/or in their degree of autonomic response to laboratory stress tasks. In addition, the relationship between measures of autonomic nervous system functioning and cholesterol will be explored. These data may provide evidence that depression is related to parasympathetic nervous system activity, which would support the hypothesis that increased risk of post-myocardial infarction mortality among depressed individuals is due to alterations in parasympathetic nervous system activity.
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