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Research article summary (published 30 Jul 2009):

The inflammatory response as a target to reduce myocardial ischaemia and reperfusion injury.

Full Abstract

Acute myocardial infarction is the leading cause of morbidity and mortality in the adult population of developed and developing nations. Although the prompt restoration of antegrade blood flow in the infarct-related coronary artery is the mean therapy for improving survival, reperfusion itself may cause damage to ischaemic myocardial tissue. This event is well known as "reperfusion injury". Crucial mediators for cardiac damage in the reperfusion phases are oxidative stress, inflammation and leukocyte infiltration. Already approved and novel therapies might directly reduce these inflammatory processes. Treatments modulating chemokine secretion and activity should be considered as very promising approaches to reduce myocardial reperfusion injury.

 

Author information

Author/s: Steffens, Sabine (S); Montecucco, Fabrizio (F); Mach, François (F);

Affiliation: Department of Medicine, Geneva University Hospital, Foundation for Medical Researches, 1211 Geneva, Switzerland.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't; Review

Journal: Thrombosis and haemostasis (Thromb Haemost), published in Germany. (Language: eng)

Reference: 2009-Aug; vol 102 (issue 2) : pp 240-7

Dates: Created 2009/08/04; Completed 2009/10/21;

PMID: 19652874, status: MEDLINE (last retrieval date: 10/21/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Associated Chemicals: Adrenergic beta-Antagonists (0) ; Angiotensin-Converting Enzyme Inhibitors (0) ; Anti-Inflammatory Agents (0) ; Anticoagulants (0) ; Hydroxymethylglutaryl-CoA Reductase Inhibitors (0) ; Immunosuppressive Agents (0) ; Inflammation Mediators (0) ; Platelet Aggregation Inhibitors (0)

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