© 2007 European Society of Cardiology
Post-infarction treatment with simvastatin reduces myocardial no-reflow by opening of the KATP channel
Department of Cardiology, Cardiovascular Institute and Fu-Wai Heart Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College Bei Li Shi Road 167, West City District, Beijing, 100037, China
* Corresponding author. Tel.: +86 13501076630. E-mail address: realplayone{at}yahoo.com.cn
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Abstract |
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Simvastatin can prevent cardiac remodelling after myocardial infarction, though the exact mechanisms are uncertain. Myocardial no-reflow is associated with progressive cardiac remodelling. However, it remains unknown whether post-infarction treatment with simvastatin can also reduce myocardial no-reflow for which suppression of adenosine triphosphate-sensitive K+ (KATP) channel opening is an important mechanism.
Methods: Area at risk and the area of no-reflow were determined by myocardial contrast echocardiography (MCE) and by pathology in 45 mini-swine randomised into 5 groups: 10 control, 9 simvastatin, 9 glibenclamide, 9 simvastatin plus glibenclamide and 8 sham-operated. A myocardial infarction and reperfusion model was created by 3-h occlusion of the coronary artery followed by 4 weeks of reperfusion.
Results: Compared with the control group, simvastatin significantly increased coronary blood volume (P<0.01) and decreased the area of no-reflow measured by MCE (78.5±4.5% to 43.7±4.3%) and pathological evaluation (82.3±1.9% to 45.2±3.8%) of area at risk (P<0.01). Simvastatin also increased the levels of KATP channel proteins (SUR2 and Kir6.2) (P<0.05), but had no effect on necrosis area. The combination of simvastatin and glibenclamide had no significant effect on the above parameters.
Conclusions: Post-infarction treatment with simvastatin can reduce myocardial no-reflow. This beneficial effect is due to activation of the KATP channel.
Key Words: Simvastatin • Acute myocardial infarction • No-reflow
Received January 5, 2006; Revised February 27, 2006; Accepted April 27, 2006
1 These authors contributed equally to this work.
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