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Coronary microembolization: the role of TNF-alpha in contractile dysfunction
Hilmar Dörge1, Rainer Schulz, Sergej Belosjorow
1Abteilungen für Pathophysiologie, Universitätsklinikum Essen, Essen, Germany.
Journal of Molecular and Cellular Cardiology
|January 29, 2002
Summary
Coronary microembolization causes heart dysfunction. Tumor necrosis factor-alpha (TNF-alpha) drives this progressive contractile dysfunction, and blocking TNF-alpha prevents it.
Area of Science:
- Cardiovascular Biology
- Inflammation Research
Background:
- Coronary microembolization, a complication of acute coronary syndromes and interventions, leads to progressive contractile dysfunction and local inflammation.
- The precise mechanisms underlying this dysfunction require further elucidation.
Purpose of the Study:
- To investigate the causal role of tumor necrosis factor-alpha (TNF-alpha) in the contractile dysfunction induced by coronary microembolization.
Main Methods:
- Anesthetized dogs underwent coronary microembolization, intracoronary TNF-alpha infusion, or anti-TNF-alpha antibody treatment prior to microembolization.
- Posterior systolic wall thickening (PWT) was measured using sonomicrometry.
- Infarct size, apoptosis, TNF-alpha protein levels, and mRNA expression were assessed.
Main Results:
- Microembolization significantly reduced PWT, with minimal infarct size and apoptosis.
- Increased TNF-alpha protein and mRNA were detected, primarily from viable cardiomyocytes surrounding microinfarcts.
- Direct TNF-alpha infusion impaired PWT, while anti-TNF-alpha antibodies prevented microembolization-induced dysfunction.
Conclusions:
- Tumor necrosis factor-alpha (TNF-alpha) is the key mediator of progressive contractile dysfunction following coronary microembolization.
- Targeting TNF-alpha may represent a therapeutic strategy for managing microembolization-related cardiac dysfunction.