Pop G, Serruys P W, Piscione F, de Feyter P J, van den Brand M, Huizer T, de Jong J W, Hugenholtz P G
Int J Cardiol. 1987 Jul;16(1):27-41. doi: 10.1016/0167-5273(87)90267-1.
Twelve patients with proximal stenosis of the left anterior descending artery, normal myocardial wall motion but without angiographically demonstrable collateral circulation, were studied during transluminal occlusion. Prior to the first transluminal occlusion before crossing the lesion with the balloon, patients were randomly given 0.2 mg nifedipine or its solvent in the left mainstem. The same dose was repeated via the balloon catheter, positioned across the lesion, immediately prior to the second transluminal occlusion. In all patients great cardiac venous flow and ST-elevation were monitored during and after each transluminal occlusion. The lactate extraction ratio A-GCV/A (A = arterial, GCV = great cardiac vein) was determined prior to the angioplasty procedure, 10-15 seconds after each transluminal occlusion and 10 minutes after the third transluminal occlusion. Great cardiac venous flow rose significantly to an average of 160% of basal flow when nifedipine was administered into the mainstem before the angioplasty procedure while its solvent had no effect. During each transluminal occlusion, great cardiac venous flow diminished on average by 30% in those who received nifedipine and by 28% in those who received only its solvent. This difference was statistically not significant. After angioplasty great cardiac venous flow was slightly, but not significantly, increased in both groups with respect to basal flow (104% resp. 120% of control). Patients who received nifedipine in the post-stenotic area just before the second transluminal occlusion, had significantly lower lactate production, measured immediately after the transluminal occlusion compared with the patients who received only its solvent (P less than 0.01). The ST-elevation during the second transluminal occlusion was significantly lower in the nifedipine group (0.1 mm in nifedipine group versus 1.4 mm in solvent group; P less than 0.05, unpaired t-test). Nifedipine given intracoronary in the post-stenotic area just before coronary angioplasty reduces lactate release and electrocardiographic signs of myocardial ischemic injury. This regional cardioprotective effect seems not due to an enhanced collateral flow, but to a regional cardioplegic effect, which precedes the ischemic event.
对12例左前降支近端狭窄、心肌壁运动正常但血管造影未显示侧支循环的患者在经腔闭塞期间进行了研究。在首次经腔闭塞、球囊穿过病变之前,患者被随机给予0.2毫克硝苯地平或其溶剂于左主干。在第二次经腔闭塞之前,通过置于病变处的球囊导管重复给予相同剂量。在每次经腔闭塞期间及之后,对所有患者的心大静脉血流和ST段抬高进行监测。在血管成形术之前、每次经腔闭塞后10 - 15秒以及第三次经腔闭塞后10分钟测定乳酸提取率A - GCV/A(A = 动脉,GCV = 心大静脉)。在血管成形术之前将硝苯地平注入主干时,心大静脉血流显著增加至平均基础血流的160%,而其溶剂则无此作用。在每次经腔闭塞期间,接受硝苯地平的患者心大静脉血流平均减少30%,接受溶剂的患者平均减少28%。这种差异无统计学意义。血管成形术后,两组的心大静脉血流相对于基础血流均略有增加,但无统计学意义(分别为对照的104%和120%)。在第二次经腔闭塞之前,在狭窄后区域接受硝苯地平的患者,与仅接受溶剂的患者相比,经腔闭塞后立即测量的乳酸生成显著降低(P小于0.01)。硝苯地平组在第二次经腔闭塞期间的ST段抬高显著低于溶剂组(硝苯地平组为0.1毫米,溶剂组为1.4毫米;P小于0.05,成组t检验)。在冠状动脉成形术之前,在狭窄后区域冠状动脉内给予硝苯地平可减少乳酸释放和心肌缺血损伤的心电图表现。这种局部心脏保护作用似乎不是由于侧支血流增加,而是由于在缺血事件之前的局部心脏停搏作用。