1Kantor PF,Lucien A,Kozak R,et al. The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain3-ketoacyl coenzyme A thiolase[J]. Circ Res, 2000,86(5 ) : 580-588.
2Eugene B,Elliott M,John W,et al. ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction :executive summary and recommendtions [J]. Circulation, 2000,102 ( 5 ) : 1193 - 1209.
3[2]Dessideri A,Celegon L.Metabolic management of ischemic heart disease:clinical data with trimetazikdine.Am J Cardiol.1998,82(5A):50K～53K
4[3]Lopaschuk G D,Wambolt R B,barr R L.An imbalance between glycolysis and glucode oxidation is a possible explanation for the detrimental effects of high levels of fatty acids during aerobic perfusion of ischmic hearts.J Pharmacol Exp theer,1993,264:456
5[4]KAY L.Improvement of long-term preservation of the isolated arrested rat heart by trimetazidine:Effects on the energy state and mitochondrial function.Am J Cardiol,1995,76:456
6[5]Brottier L,Barat JL,Broussens B,et al.Therespeutic vdelue or a cardioprotaltive agent in patients with servere ischemic cardogo pathy.Eur Hear J.1990,11:207～212
7RiziR DG, Healy S, Margulis A, et al.A new clinical classification for hospital prgnosis of unstable angina pectoris[J].Am J Catdiol, 1995,75(15):993.
8EL Banani H, Bernard M, Beatz D, et al.Changes in intracellular sodium and pH during ischaemia - reperfusim are attenuated by trime tazidine.Comparison between low- and zero - flow ischaemia[J].cardiovasc Res,2000,47:688.
