Relationship between catecholamines and major adverse cardiovascular events 公开

Manubolu, Sanjay (2017)

Permanent URL: https://etd.library.emory.edu/concern/etds/3r074v44h?locale=zh
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Abstract

Abstract

Background: Sympathetic nervous system hyperactivity has been reported as an important mechanism in ischemic heart disease. Some of the prior studies have indicated that higher catecholamine levels could be independent risk factor for cardiovascular events1, although the prognostic role of catecholamine changes to emotional provocation in patients with coronary artery disease (CAD) has not been previously explored.

Methods: We studied 695 patients with CAD enrolled between June 2011 and August 2014 from Emory University affiliated hospitals and clinics. Plasma catecholamines were assayed during a rest period prior to stress, and mid-way through a speech stressor task. Follow-up assessments performed regularly, for up to 3 years after enrollment. We used Cox proportional hazard models to determine the relationship between baseline noradrenaline/adrenaline levels, as well as their changes with stress, and major adverse cardiovascular events (MACE).

Results: No statistical significance was achieved for the hazard ratio of catecholamines in predicting MACE except for the change in adrenaline from baseline to stress, which, in multivariate analysis, predicted decreased MACE risk; CAD patients whose change in adrenaline from stress to rest were above the median had a hazard ratio of 0.48 (p=0.02) for MACE compared to those below the median.

Conclusion: We found a statistically significant negative association between increases in adrenaline, but not noradrenaline, from baseline to stress, and MACE. This suggests that blunted adrenaline reactivity is a negative prognostic finding in CAD patients.

Table of Contents


LITERATURE REVIEW.......................................................................................................... 1
ABSTRACT.............................................................................................................................. 3
INTRODUCTION.................................................................................................................... 4
METHODS.............................................................................................................................. 5
RESULTS................................................................................................................................ 9
DISCUSSION........................................................................................................................ 10
CONCLUSIONS.................................................................................................................... 11
PUBLIC HEALTH IMPLICATIONS....................................................................................... 12
REFERENCES...................................................................................................................... 13
FIGURES/ TABLES 14

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