Miljoen Hielko, State Simona, de Chillou Christian, Magnin-Poull Isabelle, Dotto Pierre, Andronache Marius, Abdelaal Ahmed, Aliot Etienne
Département de Cardiologie, CHU Brabois, Rue Morvan, 54511 Vandoeuvre-les-Nancy, France.
Europace. 2005 Nov;7(6):516-24. doi: 10.1016/j.eupc.2005.07.004. Epub 2005 Sep 22.
Ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) has been previously explored using entrainment mapping techniques but little is know about VT mechanisms and the characteristics of their circuits using an electroanatomical mapping system.
Three-dimensional electroanatomical mapping was performed in 11 patients with well tolerated sustained VT and ARVD. Sinus rhythm mapping of the right ventricle was performed in eight patients showing areas of low bipolar electrogram voltage (<1.2 mV). In total 12 tachycardias (mean cycle length 382+/-62 ms) were induced and mapped. Complete maps demonstrated a reentry mechanism in eight VTs and a focal activation pattern in four VTs. The reentrant circuits were localized around the tricuspid annulus (five VTs), around the right ventricular outflow tract (one VT) and on the RV free lateral wall (two VTs). The critical isthmus of each peritricuspid circuit was bounded by the tricuspid annulus with a low voltage area close to it. The isthmus of tachycardia originating from the right ventricular outflow tract (RVOT) was delineated by the tricuspid annulus with a low voltage area localized on the posterior wall of the RVOT. Each right ventricular free wall circuit showed an isthmus delineated by two parallel lines of block. Focal tachycardias originated on the right ventricular free wall. Linear radiofrequency ablation performed across the critical isthmus was successful in seven of eight reentrant tachycardias. The focal VTs were successfully ablated in 50% of cases. During a follow-up of 9-50 months VT recurred in four of eight initially successfully ablated VTs.
Peritricuspid ventricular reentry is a frequent mechanism of VT in patients with ARVD which can be identified by detailed 3D electroanatomical mapping. This novel form of mapping is valuable in identifying VT mechanisms and in guiding RF ablation in patients with ARVD.
此前曾使用拖带标测技术对致心律失常性右室心肌病/发育异常(ARVD)中的室性心动过速(VT)进行研究,但对于使用电解剖标测系统了解VT机制及其折返环特征的研究较少。
对11例耐受性良好的持续性VT和ARVD患者进行三维电解剖标测。对8例右室双极电图电压低(<1.2 mV)区域的患者进行右室窦性心律标测。共诱发并标测了12次心动过速(平均周长382±62 ms)。完整的标测显示8次VT为折返机制,4次VT为局灶性激动模式。折返环定位于三尖瓣环周围(5次VT)、右室流出道周围(1次VT)和右室游离侧壁(2次VT)。每个三尖瓣周围环的关键峡部由三尖瓣环界定,其附近有低电压区域。起源于右室流出道(RVOT)的心动过速峡部由三尖瓣环界定,低电压区域位于RVOT后壁。每个右室游离壁环显示峡部由两条平行阻滞线界定。局灶性心动过速起源于右室游离壁。在8次折返性心动过速中的7次中,跨越关键峡部进行的线性射频消融成功。50%的局灶性VT消融成功。在9至50个月的随访期间,8例最初成功消融的VT中有4例复发。
三尖瓣周围室性折返是ARVD患者VT的常见机制,可通过详细的三维电解剖标测识别。这种新型标测形式对于识别ARVD患者的VT机制和指导射频消融具有重要价值。