Pravastatin attenuates cardiac dysfunction induced by lysophosphatidylcholine in isolated rat hearts

Lysophosphatidylcholine (LPC), which accumulates in the ischemic myocardium, is responsible for mechanical and metabolic derangements of hearts, and also contributes to the development of ventricular arrhythmias. We examined the effects of pravastatin on the LPC-induced cardiac dysfunction in isolated rat hearts. Rat hearts were randomly divided into four groups. The groups comprised a control group ( n = 10), a group treated with LPC (5 μM) ( n = 20), a group treated with pravastatin (400 ng/ml) ( n = 10) and a group treated with both LPC and pravastatin ( n = 20). Our data suggest that, pravastatin possesses some protective profiles against LPC, as manifested by better recovery of cardiac function (improvement in heart rate, left ventricular developed pressure, maximal and minimal first derivatives of left ventricular developed pressure, coronary flow and coronary resistance, less release of biomarkers of cardiac injury (lactate dehydrogenase, creatine kinase–MB and endothelin-1), and attenuation of ventricular arrhythmias (ventricular tachyarrhythmia and ventricular fibrillation).