CESIUM CHLORIDE-INDUCED LONG QT SYNDROME - DEMONSTRATION OF AFTERDEPOLARIZATIONS AND TRIGGERED ACTIVITY INVIVO

CESIUM CHLORIDE-INDUCED LONG QT SYNDROME - DEMONSTRATION OF AFTERDEPOLARIZATIONS AND TRIGGERED ACTIVITY INVIVO
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DOI:
10.1161/01.cir.72.5.1092
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发表时间:
1985-01-01
期刊:
影响因子:
37.8
通讯作者:
MOORE, EN
MOORE, EN
中科院分区:
医学1区
文献类型:
--
作者:
LEVINE, JH;SPEAR, JF;MOORE, EN

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目前尚不能确定体内后去极化及其与心律失常的关系。进行实验,以确定是否可以检测到后去极化在单相动作电位(MAP)记录在体内,以及它们是否与心律失常在一个完整的犬制备的长QT综合征。对6只犬的离体心脏组织进行了研究,以验证该技术。在同时MAP和跨膜记录,后去极化诱导钡(早期)或乙酰毒毛旋花子苷(延迟)被检测到MAP时,存在于微电极记录。然后在8只患有氯化铯诱导的长QT综合征伴室性心律失常的狗中原位记录MAP。在每只犬中识别出后除极,与体外识别出的早期后除极相似;它们发生在第3阶段,并在起搏期间减弱。后除极与心律失常密切相关:(1)后除极总是先于室性心律失常;(2)后除极(AD)和室性早搏(VPB)的耦合间期(CI)基本一致(VPB CI = 1.06 AD CI-10.24; r2 = 0.87),(3)室性早搏的起始电位与后除极的振幅基本一致(起飞电位= 0.98后除极振幅+0.46,r2 = 0.87);(4)后除极和室性心律失常在双相起搏期间随时间同时消退。因此,一种新的导管技术已得到验证,并已被用于直接识别后去极化和体内触发活动。
The identification of afterdepolarizations and their relationship to arrhythmias in vivo is not available. Experiments were undertaken to determine whether afterdepolarizations could be detected in monophasic action potentials (MAPs) recorded in vivo and whether they were related to arrhythmias in an intact canine preparation of the long QT syndrome. Isolated cardiac tissues from six dogs were studied to validate the technique. In simultaneous MAP and transmembrane recordings, afterdepolarizations induced with barium (early) or acetylstrophanthidin (delayed) were detected in MAPs when present in microelectrode recordings. MAPs were then recorded in situ in eight dogs with cesium chloride-induced long QT syndrome associated with ventricular arrhythmias. Afterdepolarizations were identified in each of the dogs and were similar to early afterdepolarizations identified in vitro; they occurred during phase 3 and were attenuated during overdrive pacing. The afterdepolarizations were closely related to arrhythmias: (1) afterdepolarizations always preceded ventricular arrhythmias, (2) the coupling intervals (CI) of the afterdepolarizations (AD) and the ventricular premature beats (VPB) were nearly identical (VPB CI = 1.06 AD CI -10.24; r2 = .87), (3) the take-off potentials of the ventricular premature beats were nearly identical to the amplitude of the afterdepolarizations (take-off potential = 0.98 afterdepolarization amplitude + 0.46, r2 = .87), and (4) afterdepolarizations and ventricular arrhythmias resolved concurrently during overdrive pacing and with time. Thus, a new catheter technique has been validated and has been used to directly identify afterdepolarizations and triggered activity in vivo.