Coghlan J G, Flitter W D, Paul V E, Mitchell A G, Slater T F, Ilsley C D
Department of Cardiology, Harefield Hospital, UK.
Coron Artery Dis. 1994 Dec;5(12):961-70. doi: 10.1097/00019501-199412000-00002.
Recent studies have shown that free radical activity is increased in humans during percutaneous transluminal coronary angioplasty. These studies, however, have failed to localize the site of free radical activity or to demonstrate a relationship between ischaemic burden and free radical production.
The relationship between ischaemic burden and subsequent lipid peroxidation was studied during 16 inflations in eight patients undergoing angioplasty to anterior descending artery lesions. Two inflations 15 min apart were studied in each patient, one using a conventional (occlusive) balloon and one using the ACS Rx 'perfusion' balloon. The severity of the ischaemic insult associated with each inflation was assessed by contrast ventriculography, change in left ventricular end-diastolic pressure and myocardial lactate release 30 s after balloon deflation. Plasma levels of lipid peroxidation products were assessed by analysis of thiobarbituric-acid-reactive substances.
A direct relationship was observed between the ischaemic burden and the myocardial release of lipid peroxidation products over the first 4 min after balloon deflation (F = 5.6; P < 0.006). In each patient, one of the inflations was associated with a greater degree of ischaemia. Left ventricular ejection fraction was lower (P < 0.001) and left ventricular end-diastolic pressure was higher (P < 0.002) during the 'ischaemic' inflations. Myocardial release of lipid peroxidation products was significantly higher after the 'ischaemic' balloon inflation (F = 7.65; P < 0.009).
Brief periods of human myocardial ischaemia result in myocardial release of lipid peroxidation products in direct proportion to the severity of the preceding ischaemic insult.
最近的研究表明,在经皮腔内冠状动脉成形术期间,人体自由基活性会增加。然而,这些研究未能确定自由基活性的部位,也未能证明缺血负荷与自由基产生之间的关系。
对8例接受前降支动脉病变血管成形术的患者进行16次球囊扩张,研究缺血负荷与随后脂质过氧化之间的关系。每位患者相隔15分钟进行两次球囊扩张,一次使用传统(闭塞)球囊,另一次使用ACS Rx“灌注”球囊。通过对比心室造影、球囊放气后30秒左心室舒张末期压力变化和心肌乳酸释放来评估每次扩张相关的缺血损伤严重程度。通过分析硫代巴比妥酸反应性物质来评估血浆脂质过氧化产物水平。
在球囊放气后的前4分钟内,观察到缺血负荷与脂质过氧化产物的心肌释放之间存在直接关系(F = 5.6;P < 0.006)。在每位患者中,其中一次扩张与更严重的缺血相关。在“缺血性”扩张期间,左心室射血分数较低(P < 0.001),左心室舒张末期压力较高(P < 0.002)。“缺血性”球囊扩张后,脂质过氧化产物的心肌释放明显更高(F = 7.65;P < 0.009)。
短暂的人体心肌缺血会导致脂质过氧化产物的心肌释放,且与先前缺血损伤的严重程度成正比。