scholarly journals Spatiotemporal Heterogeneity in the Induction of Ventricular Fibrillation by Rapid Pacing

1999 ◽  
Vol 84 (11) ◽  
pp. 1318-1331 ◽  
Author(s):  
Ji-Min Cao ◽  
Zhilin Qu ◽  
Young-Hoon Kim ◽  
Tsu-Juey Wu ◽  
Alan Garfinkel ◽  
...  
Author(s):  
David E. Krummen ◽  
Gordon Ho ◽  
Kurt S. Hoffmayer ◽  
Franz Schweis ◽  
Tina Baykaner ◽  
...  

Background - Refractory ventricular fibrillation (VF) is a challenging clinical entity, for which ablation of triggering premature ventricular complexes (PVCs) is described. When PVCs are infrequent and multifocal, the optimal treatment strategy is uncertain. Methods - We prospectively enrolled consecutive patients presenting with multiple ICD shocks for VF refractory to antiarrhythmic drug therapy, exhibiting infrequent (≤3%), multifocal PVCs (≥3 morphologies). Procedurally, VF was induced with rapid pacing and mapped, identifying sites of conduction slowing and rotation or rapid focal activation. VF electrical substrate ablation (VESA) was then performed. Outcomes were compared against reference patients with VF who were unable or unwilling to undergo catheter ablation. The primary outcome was a composite of ICD shock, electrical storm, or all-cause mortality. Results - VF was induced and mapped in 6 patients (60±10 y, LVEF 46±19%) with ischemic (n=3) and nonischemic cardiomyopathy. An average of 3.3±0.5 sites of localized reentry during VF were targeted for radiofrequency ablation (38.3±10.9 minutes) during sinus rhythm, rendering VF non-inducible with pacing. Freedom from the primary outcome was 83% in the VF ablation group versus 17% in 6 non-ablation reference patients at a median of 1.0 years (IQR 0.5-1.5 years, p=0.046) follow-up. Conclusions - VESA is associated with a reduction in the combined endpoint compared with the non-ablation reference group. Additional work is required to understand the precise pathophysiologic changes which promote VF in order to improve preventative and therapeutic strategies.


2012 ◽  
Vol 302 (6) ◽  
pp. H1294-H1305 ◽  
Author(s):  
Wei Kong ◽  
Raymond E. Ideker ◽  
Vladimir G. Fast

Intramural gradients of intracellular Ca2+ (Cai2+) Cai2+ handling, Cai2+ oscillations, and Cai2+ transient (CaT) alternans may be important in long-duration ventricular fibrillation (LDVF). However, previous studies of Cai2+ handling have been limited to recordings from the heart surface during short-duration ventricular fibrillation. To examine whether abnormalities of intramural Cai2+ handling contribute to LDVF, we measured membrane voltage ( Vm) and Cai2+ during pacing and LDVF in six perfused canine hearts using five eight-fiber optrodes. Measurements were grouped into epicardial, midwall, and endocardial layers. We found that during pacing at 350-ms cycle length, CaT duration was slightly longer (by ≃10%) in endocardial layers than in epicardial layers, whereas action potential duration (APD) exhibited no difference. Rapid pacing at 150-ms cycle length caused alternans in both APD (APD-ALT) and CaT amplitude (CaA-ALT) without significant transmural differences. For 93% of optrode recordings, CaA-ALT was transmurally concordant, whereas APD-ALT was either concordant (36%) or discordant (54%), suggesting that APD-ALT was not caused by CaA-ALT. During LDVF, Vm and Cai2+ progressively desynchronized when not every action potential was followed by a CaT. Such desynchronization developed faster in the epicardium than in the other layers. In addition, CaT duration strongly increased (by ∼240% at 5 min of LDVF), whereas APD shortened (by ∼17%). CaT rises always followed Vm upstrokes during pacing and LDVF. In conclusion, the fact that Vm upstrokes always preceded CaTs indicates that spontaneous Cai2+ oscillations in the working myocardium were not likely the reason for LDVF maintenance. Strong Vm-Cai2+ desynchronization and the occurrence of long CaTs during LDVF indicate severely impaired Cai2+ handling and may potentially contribute to LDVF maintenance.


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