John P. Kuhl

Hostility, Gender, and Cardiac Autonomic Control

Objective Although considerable evidence implicates hostility in the development of coronary artery disease (CAD), the pathogenic mechanisms remain poorly understood. We have developed a psychophysiological model that holds that altered autonomic nervous system function links psychological traits with CAD outcomes. In laboratory studies, stressors reduce high-frequency (HF) heart period variability, an index of cardiac vagal modulation. With ambulatory electrocardiographic recording, we demonstrated in a predominantly male sample that hostility was inversely associated with HF power, but only during waking hours. These findings are consistent with the hypothesis that hostile individuals experience multiple stressful interpersonal transactions each day, resulting in overall lower HF power during the day but not at night. Methods To further evaluate this hypothesis, we screened 96 subjects using the Cook-Medley Hostility Scale and selected 15 men and 15 women representing a wide distribution of hostility. These subjects were studied in a laboratory session assessing reactivity to psychological and orthostatic challenges with continuous electrocardiographic, blood pressure, and respiration monitoring. We predicted that for men and women, hostility would be inversely related to reductions in HF power in response to challenge. Results In response to mental stressors, all measures of heart period variability change were inversely related to hostility as predicted. No such relationships were found for responses to tilt. The data suggested a possible effect of gender on these relationships. Conclusions These data add to the growing body of evidence showing that hostility influences vagal modulation of the cardiovascular system and suggest that altered autonomic control is a pathogenic mechanism linking hostility and CAD.

On the absence of correlation between responses to noxious heat, cold, electrical and ischemie stimulation

&NA; Is a persons response to one noxious stimulus similar to his/her responses to other noxious stimuli? This long‐investigated topic in pain research has provided inconclusive results. In the present study, 2 samples were studied: one using 60 healthy volunteers and the other using 29 patients with coronary artery disease. Results showed near‐zero correlations between measures of heat, cold, ischemic, and electrical laboratory pains, as well as between these laboratory pains and an idiopathic pain, the latency to exercise‐induced angina in the patients. Power analyses showed that the sample sizes were sufficient to detect a correlation of 0.50 or greater at the 0.05 level 99% of the time in the healthy volunteers, and between 80 and 85% of the time in the patients. Reliability analyses indicated retest correlations on the order of 0.60 for these measures, indicating that the lack of correlation between modalities was not due to unreliability within a measure. These studies fail to demonstrate alternate‐forms reliability among these tests, and also fail to support the notion that a person can be characterized as generally stoical or generally complaining to any painful stimulus. In practice, this implies that a battery of tests should generally be used to assess pain sensitivity and also that assessments of one pain modality are not generally useful for making inferences about another.

Cerebral activation, hostility, and cardiovascular control during mental stress.

OBJECTIVE Hostility has been established as a risk factor for the development of coronary artery disease. Putatively pathogenic hemodynamic and neuroendocrine responses to psychological stressors are associated with hostility, but the cerebral effects of hostility and their relationship to these responses are unknown. This pilot study examined cardiovascular and cerebral blood flow responses to stress in subjects with high and low levels of trait hostility. METHODS Regional cerebral blood flow was measured by single-photon emission computed tomography (SPECT) during a control condition and in response to mental arithmetic stress. RESULTS The stressor was associated with reduced blood flow to the prefrontal cortex, and this reduction was greater in the high hostility subjects. CONCLUSION These preliminary findings support the hypothesis that mental arithmetic stress is associated with reduced blood flow to prefrontal cortex, and that trait hostility is associated with a stronger effect.

Pain sensitivity in silent myocardial ischemia.

&NA; Although, the cause of silent myocardial ischemia (SMI) is unknown, several theories have been advanced to explain the disorder. Most prominent among these are the suggestions that attribute the condition to generalized impaired pain sensitivity and/or enhanced endorphin activity. The present study examined both hypotheses. It was carried out in 33 patients with myocardial ischemia: 13 with silent myocardial ischemia (silents) and 20 with symptomatic: ischemia (symptomatics). Pain sensitivity was determined with thermal, electrical, and ischemic pain tests using signal detection theory (SDT) and conventional threshold procedures. To evaluate the significance of endorphin mechanisms naloxone (6 mg i.v.) and placebo were administered on alternate days in a double‐blind, cross‐over procedure before the pain tests and again before a treadmill exercise test (TET). Somatic pain sensitivity was found. not to be impaired in patients with SMI, and no evidence was found to support a causal role for endorphins in the disorder.