Background: The 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhi-bitors (statins) have revolutionized the treatment of hypercholesterolemia. Some evide-nce indicated the role of nodal refractoriness and concealed conduction in anticipating the ventricular rate during atrial fibrillation. Recent evidence has indicated that statins can reduce the incidence of both supraventricular and ventricular arrhythmias. The aim of the present study is to investigate adenosine A1 receptor role on simvastatin protecti-ve effects on atrioventricular nodal properties in isolated atrial fibrillation model of rabbit heart.
Methods: The present study was performed in cardiovascular research center of Golestan University of Medical Sciences in 2012. Recovery and atrial fibrillation protoc-ols were used to study electrophysiological properties of atrioventricular node in 5 groups of male Newsland rabbits (n=40). Extracellular recording was carried out from transitional cells of posterior and anterior extension of AV-node and upper part of atrium and its bundle. All stimuli protocols repeated in the presence of adenosine A1 receptor agonist and antagonist (dipridamole and CPX) alone or with simvastatin on isolated perfused atrio-nodal preparation. Extracellular field potential recording was sampled during specific stimulation protocols.
Results: Significant inhibition was observed in basic node properties such as wencke-bach prolongation, functional refractory period, effective refractory period and atriove-ntricular node conduction time with simvastatin (P<0.05). Simvastatin prolonged His-His interval and increased number of concealed beat in atrial fibrillation protocol (P<0.05). The simvastatin protective effects on atrioventricular nodal properties were intensified by dipridamole as an adenosine A1 receptor agonist (P<0.05), but CPX as an adenosine A1 receptor antagonist could only dampen them (P>0.05).
Conclusion: Our results showed that the use of adenosine agonist increased simvastatin effects on electrophysiological properties of atrioventricular node, but its antagonist could not prevent these effects. This may indicate simvastatin protective mechanism on atrioventricular node electrophysiological properties without adenosine direct involve-ment.