Saumarez R C, Heald S, Gill J, Slade A K, de Belder M, Walczak F, Rowland E, Ward D E, Camm A J
Department of Cardiological Sciences, St. George's Hospital Medical School, London, UK.
Circulation. 1995 Nov 1;92(9):2565-71. doi: 10.1161/01.cir.92.9.2565.
The mechanisms of spontaneous ventricular fibrillation (primary VF) in patients without structural heart disease are obscure. A new technique has shown that in patients with hypertrophic cardiomyopathy conduction of fractionated ventricular paced beats, recorded at several right ventricular sites, is prolonged in individuals who have suffered a VF arrest, and this may reveal one component of a reentrant substrate. Patients with primary VF were studied with the same methods to determine whether similar abnormalities are present in this group.
Nine patients with primary VF were studied by pacing one right ventricular (RV) site by use of a constant drive train with an extrastimulus inserted every third beat and reducing the extrastimulus coupling interval (S1S2 interval) by 1 ms on each occasion while recording at three other sites. The delay of each fractionated potential in the high-pass-filtered electrograms in response to the extrastimulus was determined and used to form conduction curves of delay versus the S1S2 interval. These curves were repeated by pacing each RV site in turn and recording from the other three sites. The curves were characterized by determining the S1S2 interval at which electrogram components increased in delay by 0.75 ms/20 ms reduction in S1S2 interval and the increase in electrogram duration between a coupling interval of 350 ms and 1 ms above refractoriness. Seven control patients were studied using the same method. The mean increase in electrogram duration in VF patients was 13 ms (range, 3 to 23 ms) compared with 4 ms (range, -2 to 14 ms) in unaffected control patients. The extrastimulus coupling interval at which delay increased was 318 ms (range, 293 to 334 ms) in VF patients and 274 ms (range, 265 to 284 ms) in control patients (P < .01). There was no difference between the number of fractionated potentials in VF patients and control patients.
In primary VF patients, the individual potentials within fractionated electrograms have increased delays when compared with control patients. This may identify one component of a reentrant arrhythmic substrate.
无结构性心脏病患者发生自发性室颤（原发性室颤）的机制尚不清楚。一项新技术显示，在肥厚型心肌病患者中，在多个右心室部位记录的碎裂心室起搏搏动的传导，在发生过室颤骤停的个体中延长，这可能揭示了折返基质的一个组成部分。我们采用相同方法对原发性室颤患者进行研究，以确定该组患者是否存在类似异常。
对9例原发性室颤患者进行研究，通过使用恒定驱动序列起搏一个右心室（RV）部位，每隔三个搏动插入一个期外刺激，并在每次记录其他三个部位时将期外刺激的耦合间期（S1S2间期）每次缩短1毫秒。确定高通滤波心电图中每个碎裂电位对期外刺激的延迟，并用于形成延迟与S1S2间期的传导曲线。依次起搏每个RV部位并从其他三个部位记录，重复这些曲线。通过确定S1S2间期缩短20毫秒时心电图成分延迟增加0.75毫秒时的S1S2间期以及在350毫秒耦合间期和高于不应期1毫秒之间心电图持续时间的增加来表征这些曲线。使用相同方法对7例对照患者进行研究。室颤患者心电图持续时间的平均增加为13毫秒（范围3至23毫秒），而未受影响的对照患者为4毫秒（范围 -2至14毫秒）。室颤患者延迟增加时期外刺激的耦合间期为318毫秒（范围293至334毫秒），对照患者为274毫秒（范围265至284毫秒）（P <.01）。室颤患者和对照患者的碎裂电位数量没有差异。
与对照患者相比，原发性室颤患者碎裂心电图中的单个电位延迟增加。这可能识别出折返性心律失常基质的一个组成部分。
