FISH OIL AND ATORVASTATIN DECREASE SUSCEPTIBILITY OF HYPETRIGLYCEROLEMIC RAT HEARTS TO VENTRICULAR FIBRILLATIONRN

N-3 polyunsaturated fatty acids (PUFA) and lipid-lowering drugs were shown in human to possess an antiarhythmic potential, therefore, aim of this work was to examine their effects on VF threshold, cardiomyocyte ultrastructure and expression of gap junction protein Cx43 (ensuring electrical impulse propagation) in hypertryglycerolemic rats (HTG). HTG and control Wistar rats were feed with PUFA (40mg/100g of body weight) or Atorvastatin (0.05mg/100g of body weight) for 2 month. Isolated perfused heart model was used to test VF threshold starting with 1sec burst of electrical rectangular pulses at 100 pulses/sec, 1ms in duration at 15mA. When sustained VF was not induced after repetitive 5 stimuli, the stimulus intensity was increased in 5 mA steps. Ventricular tissues were taken for ultrastructure and Cx43 analysis. Results showed that VF threshold of HTG rat hearts was lower than in normal Wistar rats (15mA vs 25mA). PUFA and Atorvastatin treatment resulted in a significant increase of VF threshold to 40mA and 45mA in HTG rat hearts. Moreover, in three of eight PUFA fed HTG rats only transient VF could be induced using repetitive 45mA test stimulus. Immuno-labelling and electron microscopy of HTG rat heart ventricles revealed changes in distribution of Cx43-positive cell-to-cell gap junction, i.e. increased number of lateral gap junctions and internalisation of intercalated disc-related gap junctions. This pattern of distribution, known as highly arrhythmogenic, was not affected either by PUFA or Atorvastatin. However, structural integrity of the cardiomyocytes and gap junctions was better preserved upon treatment. It is concluded that PUFA and Atorvastatin exert significant anti-fibrillating effects in rats suffering of dyslipidemia despite arrhythmogenic gap junction Cx43 remodelling was not eliminated.