Revista Cubana de Cardiologia y Cirugia Cardiovascular vol:19 issue:1 pages:13-16
Introduction Despite its degradation by ectonucleotidases, interstitial adenosine triphosphate concentration ([ATP]out) increases after an acute myocardial
infarction (AMI) and correlates with the occurrence of ventricular premature beats and ventricular tachycardia. It has been recently shown
that extracellular ATP activates a depolarizing arrhythmogenic current carried by the transient receptor potential (TRP) channels TRPC3/7. A
decrease in [ATP]out could be a strategy to prevent arrhythmias during an acute ischemic episode. Previous results from our laboratories in a
rat model of AMI suggest that this could be the case.
Objective To study whether extracellular creatine would serve as a buffer for the sudden increase of [ATP]out and decrease arrhythmic events in an
isolated rat heart model of AMI.
Method Electrical and contractile activities were recorded on isolated Langendorff perfused rat hearts. The left coronary artery was occluded to induce
a myocardial infarction.
Results Under control condition, creatine (1-3 mmol/L) had no major effects on QRS and QT durations nor on RR interval or force of contraction. The
ligature of the left coronary artery markedly decreased the ventricular fibrillation threshold (VFT). However, when hearts were previously
treated with creatine (1-3 mmol/L) the VFT was significantly higher after the AMI compared to untreated hearts. Moreover, in hearts perfused
with creatine after coronary ligature, VFT was also increased but to a lesser extent.
Conclusion Our results suggest that creatine, at a relatively high concentration, would serve as a buffer for the sudden release of ATP during the early
phase of ischemia thus having an antiarrhythmic effect.