BACKGROUND: Placental growth factor (PlGF), which is a member of the vascular endothelial growth factor family, stimulates angiogenesis and collateral growth in ischemic tissues. In addition, PlGF has been known to be a useful biomarker of vascular inflammation. This study was undertaken to examine whether plasma PlGF levels were increased in patients with congestive heart failure (CHF). METHODS: Ninety-eight patients with systolic heart failure (ejection fraction <40%) and twenty control subjects were enrolled. The patients were divided into four subgroups according to the criteria of NYHA functional class. Plasma PlGF, tumor necrosis factor (TNF)-alpha, brain natriuretic peptide (BNP), norepinephrine, high-sensitive C-reactive protein (hs-CRP) were determined. RESULTS: In analysis of all the subjects, there was no significant difference in plasma PlGF levels among the subgroups of NYHA classes and the controls. In the ischemic cardiomyopathy (ICM) patients, however, plasma PlGF levels were significantly increased according to the severity of NYHA class; control: 8.9+/-0.5; NYHA I: 9.4+/-1.1, NYHA II: 9.7+/-1.9, NYHA III: 14.6+/-1.2, NYHA IV: 17.9+/-1.9 pg/ml (p=0.0006). Plasma PlGF levels correlated positively with BNP (r=0.53, p=0.0003) and hs-CRP (r=0.23, p=0.02) in the ICM patients, whereas there was not any correlation between plasma PlGF levels and other variable values in the non-ICM patients. CONCLUSIONS: In the ICM patients, plasma PlGF levels are increased according to the severity of heart failure. These results may indicate that augmented release of PlGF is involved in the pathogenesis of cardiomyopathy derived from chronic myocardial ischemia.
BACKGROUND:Placental growth factor (PlGF), which is a member of the vascular endothelial growth factor family, stimulates angiogenesis and collateral growth in ischemic tissues. In addition, PlGF has been known to be a useful biomarker of vascular inflammation. This study was undertaken to examine whether plasma PlGF levels were increased in patients with congestive heart failure (CHF). METHODS: Ninety-eight patients with systolic heart failure (ejection fraction <40%) and twenty control subjects were enrolled. The patients were divided into four subgroups according to the criteria of NYHA functional class. Plasma PlGF, tumor necrosis factor (TNF)-alpha, brain natriuretic peptide (BNP), norepinephrine, high-sensitive C-reactive protein (hs-CRP) were determined. RESULTS: In analysis of all the subjects, there was no significant difference in plasma PlGF levels among the subgroups of NYHA classes and the controls. In the ischemic cardiomyopathy (ICM) patients, however, plasma PlGF levels were significantly increased according to the severity of NYHA class; control: 8.9+/-0.5; NYHA I: 9.4+/-1.1, NYHA II: 9.7+/-1.9, NYHA III: 14.6+/-1.2, NYHA IV: 17.9+/-1.9 pg/ml (p=0.0006). Plasma PlGF levels correlated positively with BNP (r=0.53, p=0.0003) and hs-CRP (r=0.23, p=0.02) in the ICM patients, whereas there was not any correlation between plasma PlGF levels and other variable values in the non-ICM patients. CONCLUSIONS: In the ICM patients, plasma PlGF levels are increased according to the severity of heart failure. These results may indicate that augmented release of PlGF is involved in the pathogenesis of cardiomyopathy derived from chronic myocardial ischemia.
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