Perioperative Endothelial Dysfunction

Status Completed

Clinical Trial Summary

More than one in 100 otherwise healthy patients undergoing non-cardiac surgery will die within 30 days post-operatively, and of these patients 45% will die from vascular causes such as myocardial infarction. The pathogenesis of perioperative myocardial infarction is complex and to date not fully elucidated. The physiological stress response associated with the surgical procedure is believed to be central in the development of perioperative cardiovascular complications. Surgery initiates systemic inflammation, hypercoagulability and increases the production of catecholamines and cortisol. These drastic systemic changes lead to a state of myocardial oxygen supply-demand mismatch, which added to acute endothelial dysfunction and ruptures of vulnerable plaques, may result in myocardial injury. The endothelium is a regulator of vascular homeostasis, vascular tone and structure and exerts anticoagulant, antiplatelet and fibrinolytic properties. Endothelial dysfunction is characterized by a decreased vascular bioavailability of nitric oxide probably due to an increased degradation of nitric oxide via its interaction with locally produced reactive oxygen species. No clinical studies have investigated whether peri- and postoperative endothelial dysfunction is associated with an increased risk of perioperative myocardial injury. Endothelial dysfunction may be a key element in the development of perioperative myocardial injury. The aim of this observational clinical study is to closely examine the endothelial function and its dynamics in the early postoperative period.

Clinical Trial Description

n/a

Study Design

Related Conditions & MeSH terms

Myocardial Injury

Clinical Trial Details

NCT number	NCT02344771
Study type	Observational
Source	Zealand University Hospital
Contact
Status	Completed
Phase
Start date	March 2015
Completion date	June 2015

View Details

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