Saumarez R C, Camm A J, Panagos A, Gill J S, Stewart J T, de Belder M A, Simpson I A, McKenna W J
Department of Cardiological Sciences, St. George's Hospital Medical School, London, UK.
Circulation. 1992 Aug;86(2):467-74. doi: 10.1161/01.cir.86.2.467.
Intraventricular conduction in hypertrophic cardiomyopathy (HCM) has been characterized to test the hypothesis that myofibrillar disarray will cause dispersion of activation throughout the ventricular myocardium.
Of 37 patients with HCM, four had spontaneous ventricular fibrillation (VF), five had nonsustained ventricular tachycardia (VT), 13 had no risk factors, and 15 had a family history of sudden death. These patients and four controls were studied by pacing one site in the right ventricle and recording electrograms from three other right ventricular sites. These electrograms were high-pass filtered to emphasize small deflections due to activation of small bundles of myocytes close to the electrode. Intraventricular conduction curves were obtained with S1S2 coupling intervals decreasing in 1-msec steps from 479 msec to ventricular effective refractory period (VERP). These curves were repeated by pacing each RV site in turn and were characterized by two parameters: the point at which latency increased by 0.75 msec/20 msec reduction of the S1S2 coupling interval and an increase in electrogram duration between an S1S2 of 350 msec and VERP. Patients with VF, VT, and family history of sudden death had a mean increase in electrogram duration of 12.8 (2.9-32.3) msec versus 4.6 (-4.2 to 14.0) msec in low-risk patients and controls. Electrogram latency increased at an S1S2 of 363 msec in the VF group (342-386), 269 msec in the controls (266-279), and 326 msec in the non-VF group (260-399). Discriminant analysis separated VF patients from the remainder (p less than 0.0001) and VF, VT, and family history of sudden death patients from the low-risk and control groups (p less than 10(-6)).
Patients with HCM who are at risk of sudden death have increased dispersion and inhomogeneity of intraventricular conduction, and this may create the conditions for reentry and arrhythmogenesis.
肥厚型心肌病（HCM）患者的室内传导情况已得到研究，以检验肌原纤维排列紊乱会导致整个心室肌激活离散这一假说。
37例HCM患者中，4例发生过自发性心室颤动（VF），5例有非持续性室性心动过速（VT），13例无危险因素，15例有猝死家族史。对这些患者及4名对照者进行研究，在右心室的一个部位起搏，同时记录右心室其他三个部位的电图。对这些电图进行高通滤波，以突出因靠近电极的小束心肌细胞激活而产生的小偏转。以S1S2耦合间期从479毫秒以1毫秒步长递减至心室有效不应期（VERP）来获得室内传导曲线。依次对每个右心室部位进行起搏，重复这些曲线，并通过两个参数进行表征：S1S2耦合间期每减少20毫秒潜伏期增加0.75毫秒的点，以及S1S2为350毫秒至VERP之间电图持续时间的增加。VF、VT及有猝死家族史的患者电图持续时间平均增加12.8（2.9 - 32.3）毫秒，而低风险患者及对照者为4.6（-4.2至14.0）毫秒。VF组在S1S2为363毫秒（342 - 386）时电图潜伏期增加，对照组在269毫秒（266 - 279）时增加，非VF组在326毫秒（260 - 399）时增加。判别分析将VF患者与其余患者区分开（p < 0.0001），并将VF、VT及有猝死家族史的患者与低风险和对照组区分开（p < 10⁻⁶）。
有猝死风险的HCM患者室内传导的离散和不均匀性增加，这可能为折返和心律失常的发生创造条件。
