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[Changes of serum hepatocyte growth factor in coronary artery disease]
H Suzuki1, M Murakami, T Kondo
1Third Department of Internal Medicine, Showa University School of Medicine, Tokyo.
Insights
Hepatocyte growth factor (HGF) is elevated in acute coronary syndromes, suggesting significant endothelial cell damage. HGF may serve as a biomarker for endothelial injury in patients with acute myocardial infarction.
Area of Science:
- Cardiology
- Biochemistry
Context:
- Hepatocyte growth factor (HGF) is an endothelial cell-specific growth factor.
- Its role in coronary artery disease (CAD) pathogenesis is not fully understood.
- HGF is involved in endothelial repair and collateral formation.
Purpose:
- To investigate the clinical significance of serum HGF levels in various coronary artery diseases.
- To examine the relationship between HGF levels and acute myocardial infarction (AMI).
Summary:
- Serum HGF levels were measured in patients with stable angina, old myocardial infarction, unstable angina pectoris (UAP), and AMI using ELISA.
- HGF levels were significantly higher in UAP and AMI groups compared to controls.
- In AMI patients, HGF peaked 48 hours post-reperfusion, with higher levels in the coronary sinus than peripheral veins.
- No correlation was found between peak HGF and cardiac damage markers (CK, CK-MB, ejection fraction, cardiac index).
Impact:
- Elevated serum HGF in acute coronary syndrome indicates advanced endothelial cell damage.
- HGF is produced, at least partially, in the heart during AMI.
- Serum HGF may be a valuable biomarker for detecting endothelial cell damage in AMI, rather than myocardial damage.
Abstract:
Hepatocyte growth factor (HGF) is an endothelial cell specific growth factor involved in the repair of endothelial cells and collateral formation, however, the role for coronary artery disease is still unknown. We measured serum HGF level in various coronary artery diseases to examine the clinical significance. Serum HGF level was measured using the enzyme-linked immunosorbent assay method in patients with stable effort angina pectoris (n = 26), old myocardial infarction (n = 18), unstable angina pectoris (UAP; n = 10) and acute myocardial infarction (AMI; n = 21). As a control group, we selected 11 patients with neurocirculatory asthenia. Blood samples from peripheral veins were collected at cardiac catheterization before heparin administration. In the AMI group, blood samples were also collected at 48, 72 hr, 1, 2, 3 and 4 weeks from the peripheral veins and 48 and 72 hr after reperfusion from the coronary sinus. Serum HGF level was significantly higher in the UAP (0.41 +/- 0.12 ng/ml, p < 0.001) and AMI groups (0.38 +/- 0.26 ng/ml, p < 0.05) compared to the control group (0.19 +/- 0.09 ng/ml). Serum HGF level peaked 48 hr after reperfusion in both the peripheral veins (0.42 +/- 0.16 ng/ml) and coronary sinus (0.58 +/- 0.23 ng/ml) in the AMI group, with a significantly higher level in the coronary sinus than the peripheral veins (p < 0.05). No significant correlation between peak HGF level in the peripheral veins and peak creatine kinase (CK), CK-MB, ejection fraction and cardiac index was observed. Serum HGF was elevated in acute coronary syndrome, indicating advanced endothelial cell damage. HGF is produced, at least partially, in the heart in patients with AMI. Serum HGF level may be useful to detect endothelial cell damage rather than myocardial cell damage.