IHU Liryc, Electrophysiology and Heart Modeling Institute, Fondation Bordeaux Université, France (M. Haïssaguerre, M. Hocini, G.C., J.D., F.S., S.P., H.C., M.T., A.D., R.M., N.D., P.B., P.R., S.P., T.P., N.K., G.M., X.P., C.D., L.L., R.C., P.J., D.B., E.V., M.P., R.W., O.B., R.D.).
Univ. Bordeaux (M. Haïssaguerre, M. Hocini, J.D., F.S., S.P., H.C., A.D., N.D., P.B., P.R., S.P., P.J., D.B., R.W., O.B., R.D.).
Circ Arrhythm Electrophysiol. 2018 Jul;11(7):e006120. doi: 10.1161/CIRCEP.117.006120.
Sudden cardiac death because of ventricular fibrillation (VF) is commonly unexplained in younger victims. Detailed electrophysiological mapping in such patients has not been reported.
We evaluated 24 patients (29±13 years) who survived idiopathic VF. First, we used multielectrode body surface recordings to identify the drivers maintaining VF. Then, we analyzed electrograms in the driver regions using endocardial and epicardial catheter mapping during sinus rhythm. Established electrogram criteria were used to identify the presence of structural alterations.
VF occurred spontaneously in 3 patients and was induced in 16, whereas VF was noninducible in 5. VF mapping demonstrated reentrant and focal activities (87% versus 13%, respectively) in all. The activities were dominant in one ventricle in 9 patients, whereas they had biventricular distribution in others. During sinus rhythm areas of abnormal electrograms were identified in 15/24 patients (62.5%) revealing localized structural alterations: in the right ventricle in 11, the left ventricle in 1, and both in 3. They covered a limited surface (13±6 cm) representing 5±3% of the total surface and were recorded predominantly on the epicardium. Seventy-six percent of these areas were colocated with VF drivers (<0.001). In the 9 patients without structural alteration, we observed a high incidence of Purkinje triggers (7/9 versus 4/15, =0.033). Catheter ablation resulted in arrhythmia-free outcome in 15/18 patients at 17±11 months follow-up.
This study shows that localized structural alterations underlie a significant subset of previously unexplained sudden cardiac death. In the other subset, Purkinje electrical pathology seems as a dominant mechanism.
心室颤动(VF)导致的心脏性猝死在年轻患者中通常原因不明。在这些患者中,尚未有详细的电生理标测的报道。
我们评估了 24 例(29±13 岁)存活的特发性 VF 患者。首先,我们使用多电极体表记录来识别维持 VF 的驱动区域。然后,我们在窦性心律期间使用心内膜和心外膜导管标测来分析驱动区域的心电信号。使用既定的电信号标准来识别是否存在结构改变。
3 例患者的 VF 自发性发生,16 例患者诱导发生,而 5 例患者的 VF 不可诱导。VF 标测显示所有患者均存在折返和局灶性活动(分别为 87%和 13%)。9 例患者的活动主要局限于一个心室,而其他患者则为双心室分布。在窦性心律时,15/24 例患者(62.5%)识别出异常电信号区域,显示出局部结构改变:右心室 11 例,左心室 1 例,双心室 3 例。它们覆盖了有限的表面(13±6cm),占总表面的 5±3%,主要记录在心外膜上。这些区域中的 76%与 VF 驱动区域重合(<0.001)。在 9 例无结构改变的患者中,我们观察到浦肯野纤维触发的高发生率(7/9 比 4/15,=0.033)。18 例患者中的 15 例在 17±11 个月的随访中无心律失常发生。
这项研究表明,局部结构改变是以前不明原因的心脏性猝死的一个重要亚组的基础。在另一亚组中,浦肯野纤维电病理似乎是主要机制。