EFFECT OF PACING RATE ON THE HUMAN ATRIAL STRENGTH-DURATION CURVE
EFFECT OF PACING RATE ON THE HUMAN ATRIAL STRENGTH-DURATION CURVE
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DOI：
10.1016/0735-1097(90)92835-p
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发表时间：
1990-06-01
影响因子：
24
通讯作者：
PLUMB, VJ
中科院分区：
文献类型：
--
作者：
KAY, GN;MULHOLLAND, DH;PLUMB, VJ
快速起搏对人类心房恒压刺激阈值的影响尚未定义为适用于抗心动过速起搏的频率。为探讨永久性抗心动过速起搏频率范围内的兴奋性，测定了10例患者在125~300次/分起搏频率范围内的起搏频率对心房强度-时程关系的影响。在每个起搏速率下测量了定义强度-持续时间曲线的两个点：流基电压-导致在2ms的脉冲持续时间下捕获的最低刺激电压；以及时轴脉冲持续时间-在两倍流基电压下的阈值脉冲持续时间。在右心耳放置高电流密度、低极化电极的J形永久起搏电极，用于阴极刺激。用于刺激的是一个恒定电压输出，其中包含一个旨在最小化电极极化的快速充电脉冲。当起搏频率为225次/分时，血流基础电压(p=0.009)、时轴脉冲持续时间(p=0.001)和最小阈值刺激进入(p=0.001)均显著增加。3例患者在起搏频率下出现了5V的流变基电压。275次/分钟。在300次/分钟的起搏频率下，10名患者中有8名患者的血流底电压升高。在舒张期末期阈值的1.5倍、起搏周期为500ms时，心房有效不应期与起搏频率225次/分时的血流底电压有一定的相关性(r=0.8)，而在250次/分时则不相关(r=0.36)。在任何起搏频率下，以3倍舒张期晚期阈值测定的心房有效不应期与心动基波电压或时轴脉搏持续时间之间均无相关性。这些数据表明，在适用于抗心动过速起搏的起搏速率下，人的心房强度-持续时间曲线上移并右移，这对永久抗心动过速起搏系统的设计和编程具有重要意义。
The effect of rapid pacing on the atrial constant voltage stimulation threshold in humans has not been defined at rates applicable to those of antitachycardia pacing. The effect of pacing rate on the atrial stength-duration relation was determined in 10 patients at pacing rates between 125 and 300 beats/min to explore excitability over the range of rates used for permanent antitachycardia pacing systems. Two points that define the strength-duration curve were measured at each pacing rate: rheobase voltage-the lowest stimulus voltage that results in capture at a pulse duration of 2 ms; and chronaxie pulse duration-the threshold pulse duration at twice rheobase voltage. A permanent, tined, J-shaped pacing lead with a high current density and low polarization electrode was positioned in the right atrial appendage for cathodal stimulation. A constant voltage output, incorporating a fast recharge pulse designed to minimize electrode polarization, was used for stimulation. There was a significant increase in rheobase voltage (p = 0.009), chronaxie pulse duration (p = 0.001) and minimal threshold stimulus entery (p = 0.05) at pacing rates > 225 beats/min. A rheobase voltage > 5 V occurred in three patients at pacing rates .gtoreq. 275 beats/min. At a pacing rate of 300 beats/min, rheobase voltage had increased in 8 of 10 patients. The atrial effective refractory period determined at 1.5 times late diastolic threshold and a cycle length of 500 ms demonstrated a modest correlation with rheobase voltage at pacing rates .ltoreq.225 beats/min (r = 0.8), but not at .ltoreq.250 beats/min (r = 0.36). There were no correlation between either rheobase voltage or chronaxie pulse duration and atrial effective refractory periods determined at three times late diastolic threshold at any pacing rate. These data demonstrate that the human atrial strength-duration curve is shifted upward and to the right at pacing rates applicable to antitachycardia pacing, and have important implications for the design and programming of permanent antitachycardia pacing systems.