Restivo M, Gough W B, el-Sherif N
Cardiology Section, Veterans Administration Medical Center, Brooklyn, NY 11209.
Circulation. 1988 Feb;77(2):429-44. doi: 10.1161/01.cir.77.2.429.
Stimulation at two ventricular sites during basic rhythm as a means of preventing the induction of ventricular arrhythmias in the postinfarction heart was investigated. Isochronal maps of ventricular epicardial activation from dogs were analyzed 4 days after ligation of the left anterior descending coronary artery. Activation patterns were obtained by use of a computerized data acquisition system recording from 62 sites. Effective refractoriness and conduction time during basic paced rhythm (S1) for each site were summed to construct isochronal maps of recovery time. The patterns of recovery time on the heart were eccentrically layered, with a narrow zone of differentially prolonged recovery time along one border of the infarct. The formation of an arc of functional conduction block after premature stimulation (S2) was correlated with regions of differentially prolonged recovery time (59 +/- 30 msec, mean +/- SD) between recording sites spaced 5 to 10 mm apart. The recovery time difference between sites that did not block (17 +/- 14 msec) was significantly shorter. The spatial distribution of recovery time on the heart could be modified by application of stimuli at two sites during the basic rhythm. Reentry was prevented by appropriate placement of the secondary site in the ischemic zone and the temporal sequencing of the paired stimuli. Stimulation at the secondary site "peeled back" refractoriness in the ischemic zone. Prevention of reentry was a result of either: (1) a shift in the arc of conduction block toward the ischemic zone, (2) a reduction in the extent of the continuous arc, (3) early activation of regions distal to the arc, or (4) a combination of the above. In two dogs, the arc of block was abolished entirely after dual stimulation. This report illustrates the criteria for effective prevention of reentry, applied to a well-described verifiable model of reentrant activation.
研究了在基础节律期间对两个心室部位进行刺激,以此作为预防心肌梗死后心脏室性心律失常诱发的一种方法。在结扎左前降支冠状动脉4天后,对犬的心外膜心室激动进行等时图分析。通过使用从62个部位记录的计算机化数据采集系统获得激动模式。将每个部位在基础起搏节律(S1)期间的有效不应期和传导时间相加,构建恢复时间等时图。心脏上恢复时间的模式呈偏心分层,在梗死灶的一条边界处有一个恢复时间差异延长的狭窄区域。过早刺激(S2)后功能性传导阻滞弧的形成与相距5至10毫米的记录部位之间恢复时间差异延长的区域(59±30毫秒,平均值±标准差)相关。未发生阻滞的部位之间的恢复时间差异(17±14毫秒)明显较短。在基础节律期间对两个部位施加刺激可改变心脏上恢复时间的空间分布。通过将第二个刺激部位适当地置于缺血区并对成对刺激进行时间排序,可预防折返。在缺血区,第二个刺激部位的刺激“剥脱”了不应期。预防折返是以下原因之一:(1)传导阻滞弧向缺血区移位,(2)连续弧的范围缩小,(3)弧远端区域的早期激动,或(4)上述情况的组合。在两只犬中,双重刺激后阻滞弧完全消失。本报告阐述了有效预防折返的标准,该标准应用于一个描述详尽且可验证的折返激动模型。