Atorvastatin increases plasma soluble Fms-like tyrosine kinase-1 and decreases vascular endothelial growth factor and placental growth factor in association with …
Y Kodama, Y Kitta, T Nakamura, H Takano… - Journal of the American …, 2006 - jacc.org
Y Kodama, Y Kitta, T Nakamura, H Takano, K Umetani, D Fujioka, Y Saito, K Kawabata…
Journal of the American College of Cardiology, 2006•jacc.orgObjectives: This study examined whether atorvastatin increases plasma levels of soluble
Fms-like tyrosine kinase 1 (sFlt-1) and reciprocally decreases vascular endothelial growth
factor (VEGF) and placental growth factor (PlGF) levels in patients with acute myocardial
infarction (AMI). Background: Statins exert cardioprotective actions partly through anti-
inflammatory actions. By capturing VEGF and PlGF in plasma, sFlt-1 acts as a natural
inhibitor of VEGF and PlGF, which have proinflammatory properties. Methods: Left …
Fms-like tyrosine kinase 1 (sFlt-1) and reciprocally decreases vascular endothelial growth
factor (VEGF) and placental growth factor (PlGF) levels in patients with acute myocardial
infarction (AMI). Background: Statins exert cardioprotective actions partly through anti-
inflammatory actions. By capturing VEGF and PlGF in plasma, sFlt-1 acts as a natural
inhibitor of VEGF and PlGF, which have proinflammatory properties. Methods: Left …
Objectives
This study examined whether atorvastatin increases plasma levels of soluble Fms-like tyrosine kinase 1 (sFlt-1) and reciprocally decreases vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) levels in patients with acute myocardial infarction (AMI).
Background
Statins exert cardioprotective actions partly through anti-inflammatory actions. By capturing VEGF and PlGF in plasma, sFlt-1 acts as a natural inhibitor of VEGF and PlGF, which have proinflammatory properties.
Methods
Left ventriculography and enzyme-linked immunosorbent assay of plasma levels of sFlt-1, VEGF, and PlGF were repeated after AMI in 50 consecutive patients with a first AMI. Patients were randomized to treatment with atorvastatin (10 mg/day; n=25) or placebo (n=25) within 3 days after AMI, and therapy was continued for 6 months.
Results
The sFlt-1 levels were low in the acute phase, followed by an increase at 2 weeks after AMI, whereas free VEGF and PlGF levels were high in the acute phase, followed by a decrease at 2 weeks. Atorvastatin increased sFlt-1 levels and reciprocally decreased VEGF and PlGF levels at 6 months compared with placebo. The increase in sFlt-1 levels and the decrease in VEGF and PlGF levels were correlated with improvement of left ventricular ejection fraction during the follow-up period.
Conclusions
There was a reciprocal relationship between changes in sFlt-1 levels and changes in VEGF and PlGF levels after AMI; and atorvastatin increased sFlt-1 levels while decreasing VEGF and PlGF levels. These changes were associated with late improvement of post-MI ventricular function, and may represent an additional benefit of statin therapy.
jacc.org
