Hostility and Coronary Risk--Role of Weak Vagal Function

Last updated: February 17, 2016
Sponsor: National Heart, Lung, and Blood Institute (NHLBI)
Overall Status: Completed

Phase

N/A

Condition

Chest Pain

Cardiovascular Disease

Coronary Artery Disease

Treatment

N/A

Clinical Study ID

NCT00005337
4196
R01HL044998
  • Ages < 100
  • Male

Study Summary

To determine whether deficient vagal antagonism of sympathetic nervous system (SNS) actions on the heart contributed to increased coronary heart disease risk in hostile persons.

Eligibility Criteria

Inclusion

No eligibility criteria

Study Design

Study Start date:
April 01, 1991
Estimated Completion Date:
March 31, 1995

Study Description

DESIGN NARRATIVE:

Sophisticated electrophysiologic monitoring approaches were used to: 1) show greater sensitivity in nonhostile young men to T-wave attenuation effects of isoproterenol infusion following vagal blockade; 2) show that vagal enhancement reduced and shortened the T-wave attenuation effects of isoproterenol infusion more in hostile young men; 3) evaluate these effects of vagal blockage and enhancement in middle-aged men and in young and middle-aged women; and 4) relate the T-wave effects in these studies to other measures of vagal tone and other biobehavioral mechanisms of coronary-prone behavior.

Four studies were conducted in normal young and middle-aged men and women selected as high and low on hostility, evaluating vagal tone measures and effects of isoproterenol infusion on EKG T-wave and ST response after pretreatment with saline, neostigmine, and atropine. Demonstration that hostility was associated with deficient vagal anatagonism of SNS effects on the heart, especially in middle-aged as compared to younger persons, suggested that diminished vagal tone was one pathway whereby high hostility contributed to increased CHD risk. Clinical studies were then conducted to determine whether weaker vagal tone predicted increased myocardial ischemia and/or poorer outcomes in coronary heart disease patients.

The study completion date listed in this record was obtained from the "End Date" entered in the Protocol Registration and Results System (PRS) record.