Abstract 3330: Delayed Enhancement of Cardiac Magnetic Resonance Imaging Indicates Abnormality of Repolarization in Hypertrophic Cardiomyopathy with Ventricular Tachycardia
[Background]: In patients with idiopathic hypertrophic cardiomyopathy (HCM), site of delayed enhancement (DE) of cardiac magnetic resonance imaging (CMR) demonstrates a depolarization abnormality which may relate to the occurrence of ventricular tachycardia (VT). However, VT occurs in several HCM cases without showing depolarization abnormality represented by the late potential or slow conduction zone. Clinical significance of repolarization abnormality in occurrence of VT remains unclear in HCM.
[Purpose]: To elucidate whether repolarization abnormality is evident in HCM and whether it relates to the distribution of DE.
[Methods]: A Gadolinium-enhanced CMR and electrophysiologic study including left ventricular mapping were performed in 12 HCM patients with VT. An electrode catheter was put at 12 different sites of left ventricular endocardium (Basal - Middle - Apical × Anterior - Lateral - Posterior -Septal). In each site, effective refractory period (ERP) was measured by extrastimuli, and a monophasic action potential (MAP) was recorded. Area of DE on the CMR view was calculated for each of the 12 segments. ERP and MAP duration measured at 90% repolarization (APD90) were compared between groups of the sites with DE involvement (DE-positive) and without DE involvement (DE-negative). Correlations between the DE area and ERP or APD90 at the corresponding segment were also analyzed.
[Results]: Observed VTs were all originated from DE-positive segments. ERP on DE-positive sites (340±39 msec) was significantly longer than that on DE-negative sites (295±46 msec, p<0.001). APD90 at DE-positive sites (320±21 msec) was also significantly longer than that on DE-negative sites (284±28 msec, p<0.001). APD90 at the VT originating segment was especially longer (352±19 msec, p<0.001) compared with other segments. DE area showed significant positive correlations with ERP (r=0.51, p<0.001) and with APD90 (r=0.62, p<0.001), respectively.
[Conclusions]: Magnitude of localized DE significantly correlates with the corresponding myocardial refractoriness and prolongation of the repolarization phase. Dispersion of the repolarization among healthy and damaged myocardium accounts, at least in part, for the occurrence of VT in HCM.