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Hepatocyte growth factor and vascular endothelial growth factor in ischaemic heart disease
Hiroshi Suzuki1, Mikitaka Murakami, Makoto Shoji
1The Third Department of Internal Medicine, Showa University, School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan. hrsuzuki@med.showa-u.ac.jp
Insights
Serum levels of hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) increase after acute myocardial infarction (AMI) and angina pectoris (AP). VEGF may predict left ventricular remodeling post-AMI.
Area of Science:
- Cardiology
- Biomarkers
- Myocardial Infarction Research
Background:
- Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are key growth factors, with known production in cardiomyocytes.
- Previous research has not extensively detailed the dynamic changes of HGF and VEGF serum levels following coronary interventions in patients with angina pectoris (AP) and acute myocardial infarction (AMI).
Purpose of the Study:
- To investigate the time-course changes in serum HGF and VEGF levels in patients diagnosed with AP and AMI.
- To compare these levels against a control group and explore potential correlations with cardiac remodeling.
Main Methods:
- Serum HGF and VEGF levels were measured in 60 AP patients, 62 AMI patients, and 56 controls at various time points post-intervention.
- Specific sampling times included pre-heparin and multiple follow-ups up to four weeks for AMI patients.
- Left ventricular remodeling was defined by an increase in left ventricular end-diastolic volume index (LVEDVI) in the sub-acute phase of AMI.
Main Results:
- HGF levels were significantly elevated in both AP and AMI patients compared to controls, with higher levels in AMI.
- HGF peaked at 48 hours in both AP and AMI groups.
- VEGF levels were significantly higher in AMI patients than in controls and AP patients, peaking at two weeks post-AMI.
- A positive correlation was observed between peak VEGF levels and LVEDVI in the sub-acute phase of AMI.
- Patients with remodeling post-AMI exhibited significantly higher peak VEGF levels.
Conclusions:
- Elevated HGF levels are associated with both myocardial and vascular damage, whereas VEGF increases are not solely linked to vascular damage.
- VEGF may play a role in left ventricular remodeling during the sub-acute phase of myocardial infarction.
- The distinct temporal profiles of HGF and VEGF suggest different roles in the cardiac response to injury.
Background:
Hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are endothelial cell-specific growth factors, but the production of these growth factors in cardiomyocytes has also been demonstrated. However, there have been no reports focusing their attention on the changes in these growth factors after coronary intervention. We investigated the time-course changes of the serum VEGF and HGF levels in angina pectoris (AP) and acute myocardial infarction (AMI).
Methods:
The serum HGF and VEGF levels were measured in 60 patients with AP, in 62 patients with AMI (AP, before heparin administration, and at 24 and 48 hours, and one week after intervention; AMI, before heparin, and at 48 and 72 hours, and one, two, three and four weeks) and in 56 patients with neurocirculatory asthenia as controls. We defined the patients with remodelling who showed an increase in left ventricular end-diastolic volume index (LVEDVI) in the sub-acute phase of AMI.
Results:
Hepatocyte growth factor levels in the AP and AMI were significantly higher than that in the control (p<0.0001). The AMI level was also significantly higher than AP (p<0.001). In the AMI and AP, HGF peaked at 48 hours. Vascular endothelial growth factor level in the AMI was significantly higher than that in the control and AP (p<0.0001). In the AMI, VEGF peaked at two weeks. There was a significant positive correlation between the peak VEGF and LVEDVI in the sub-acute phase of AMI (p=0.0089, r=0.436). Peak VEGF in the remodelling (+) group was significantly higher than that in the remodelling (-) group (p<0.001). In the AP, VEGF was unchanged.
Conclusion:
While both myocardial and vascular damage contribute to an increase in HGF level, vascular damage is not associated with the increase in VEGF. Vascular endothelial growth factor might be related to left ventricular remodelling in the sub-acute phase of myocardial infarction.