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Am Heart J. 1999 Jun;137(6):1145-52.

Kinetics of tumor necrosis factor alpha in plasma and the cardioprotective effect of a monoclonal antibody to tumor necrosis factor alpha in acute myocardial infarction.

Author information

1
Department of Medicine, University of Florida and VA Medical Center, Gainesville, FL, USA.

Abstract

BACKGROUND:

Inflammation plays a critical role in acute myocardial infarction (AMI) and tumor necrosis factor alpha (TNF-alpha) is a potent inflammatory trigger. This study was designed to examine the kinetics of TNF-alpha in plasma in patients with AMI and the potential benefit of inhibition of TNF-alpha monoclonal antibody in AMI.

METHODS AND RESULTS:

TNF-alpha levels in plasma were measured in 42 patients with AMI. TNF-alpha levels were elevated at 4 hours after onset of chest pain and declined to control values at 48 hours. TNF-alpha levels were higher in patients with Killip III and IV than in those with Killip I and II (P <.01). To examine the pathogenic role of TNF-alpha, New Zealand White rabbits were treated with buffer or a TNF-alpha monoclonal antibody before left anterior descending artery (LAD) ligation. Treatment with the TNF-alpha monoclonal antibody decreased area of necrosis, number of circulating endothelial cells, and lipid peroxidation product malonaldehyde bis(dimethyl acetal). There was a significant correlation of TNF-alpha levels with peak CK-MB in AMI patients, and area of necrosis, MDA, and circulating endothelial cells in rabbits (all P <.05).

CONCLUSIONS:

TNF-alpha release early in the course of AMI contributes to myocardial injury and dysfunction. Treatment with the monoclonal antibody against TNF-alpha can be cardioprotective, particularly in the setting of heart failure in patients with AMI.

PMID:
10347344
DOI:
10.1016/s0002-8703(99)70375-3
[Indexed for MEDLINE]

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