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Circulating tumour necrosis factor-alpha (cachectin) in myocardial infarction
Journal of Internal Medicine
|May 1, 1989
Summary
Extensive myocardial infarction significantly elevates serum levels of tumour necrosis factor-alpha (TNF), a hormone linked to severe complications like hypotension and arrhythmia. This suggests TNF may play a role in the metabolic impact of heart attacks.
Area of Science:
- Cardiology
- Immunology
- Biochemistry
Background:
- Prolonged chest pain can indicate myocardial infarction (MI).
- Tumour necrosis factor-alpha (TNF), also known as cachectin, is a cytokine involved in inflammation and immune responses.
- The role of TNF in the systemic metabolic consequences of MI is not fully understood.
Purpose of the Study:
- To investigate the relationship between serum levels of tumour necrosis factor-alpha (TNF) and the severity of myocardial infarction (MI).
- To determine if elevated TNF is associated with complications following MI.
Main Methods:
- A prospective study monitored 22 patients with prolonged chest pain.
- Serial serum measurements of tumour necrosis factor-alpha (TNF) were performed.
- Patients were categorized based on infarct size, complications (hypotension, pulmonary edema, arrhythmia), and presence of angina without infarction.
Main Results:
- Five patients with large, complicated MIs showed markedly increased serum TNF levels (>145 ng/L).
- These severe cases were associated with hypotension, pulmonary edema, and/or arrhythmia, with two fatalities.
- Patients with smaller, uncomplicated MIs or angina without infarction had normal or only slightly elevated TNF levels.
Conclusions:
- Extensive myocardial infarction triggers the release of TNF into circulation.
- Elevated TNF levels correlate with severe MI complications and adverse outcomes.
- TNF may contribute to the systemic metabolic disturbances observed after myocardial infarction.