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Reduced high serum hepatocyte growth factor levels after successful cardioversion in patients with atrial
Harumi Katoh1, Toshio Shimada, Shin-Ichi Inoue
1Division of Cardiovascular Medicine, Department of Internal Medicine, Shimane University School of Medicine, Shimane, Japan.
Insights
Serum hepatocyte growth factor (HGF) levels are elevated in atrial fibrillation patients, indicating vascular endothelial injury. Successful direct current (DC) cardioversion reduces HGF levels, suggesting a link between atrial fibrillation, HGF, and vascular health.
Area of Science:
- Cardiology
- Vascular Biology
- Biomarkers
Background:
- Serum hepatocyte growth factor (HGF) is a recognized marker of vascular endothelial injury.
- Atrial fibrillation (AF) is a common arrhythmia with potential implications for vascular health.
Purpose of the Study:
- To investigate serum HGF levels in patients with atrial fibrillation.
- To assess changes in serum HGF levels following successful direct current (DC) cardioversion.
Main Methods:
- Serum HGF levels were measured in 39 AF patients and 30 controls.
- Measurements were taken before, 7 days, and 1 month after DC cardioversion.
- Forearm blood flow (FBF) response to acetylcholine was assessed in 10 patients.
Main Results:
- Serum HGF levels were significantly higher in AF patients compared to controls (0.16 vs 0.10 ng/mL).
- Successful DC cardioversion led to a significant decrease in HGF levels by 7 days and to control levels by 1 month.
- Improved FBF response to acetylcholine post-cardioversion correlated with decreased HGF levels.
Conclusions:
- Serum HGF levels are elevated in atrial fibrillation, suggesting vascular endothelial injury.
- Successful DC cardioversion normalizes elevated serum HGF levels.
- HGF may serve as a biomarker for vascular endothelial dysfunction in atrial fibrillation.
Abstract:
1. Serum hepatocyte growth factor (HGF) is considered to be a potent marker of vascular endothelial injury. The present study was designed to examine serum HGF levels in atrial fibrillation and after successful direct current (DC) cardioversion. 2. We measured serum HGF levels before and 7 days and 1 month after DC cardioversion in 39 patients with atrial fibrillation in whom sinus rhythm was maintained for at least 7 days after DC cardioversion and in 30 age- and sex-matched normal control subjects with sinus rhythm. We also measured acetylcholine-induced changes in forearm blood flow (FBF) using venous occlusive plethysmography in 10 patients. 3. Serum HGF levels were significantly higher in the atrial fibrillation patients (both lone atrial fibrillation and with underlying heart disease) than in the controls (0.16 +/- 0.07 vs 0.10 +/- 0.04 ng/mL; P < 0.001). Seven days after successful DC cardioversion, the patients' serum HGF levels had decreased significantly (0.16 +/- 0.07 vs 0.12 +/- 0.06 ng/mL; P < 0.05) and in the 24 patients maintaining sinus rhythm 1 month after DC cardioversion, serum HGF levels decreased to control values (0.10 +/- 0.08 ng/mL at 1 month). Serum HGF levels of the 15 patients who had relapsed into atrial fibrillation 1 month after DC cardioversion tended to decrease 7 days after DC cardioversion, but increased again 1 month after DC cardioversion. Percentage changes in FBF between baseline and the highest dose of acetylcholine before and after DC cardioversion were 180 +/- 98 and 323 +/- 196%, respectively (P = 0.0051). The rate of increase in FBF at the highest dose of acetylcholine between before and after DC cardioversion correlated negatively with the rate of decrease in serum HGF levels between before and after DC cardioversion (r = -0.837; P = 0.0025). 4. This study is the first to demonstrate that serum HGF levels increase in atrial fibrillation and decrease after successful DC cardioversion. This may reflect the fact that atrial fibrillation induces vascular endothelial injury.
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