- Email: [email protected]
Reentrant wavefronts anchoring to the papillary muscle during ventricular fibrillation in open chest swine and dogs
Session 44 differences in the transmural distribution of VV. These findings raise the possibility that Purkinje fibers may be the origin of earliest postshock activation following shocks of near DFT strength. AB43-4 REENTRANT WAVEFRONTS ANCHORING TO THE PAPILLARY MUSCLE DURING VENTRICULAR FIBRILLATION IN OPEN CHEST SWINE AND DOGS Hui-Nam Pak, MD, PhD, Hong Euy Lim, MD, ChungChuang Chou, MD, Yasushi Miyauchi, MD, Young Ho Bang, MD, Kyung Sun, MD, PhD, Hwang Chun, MD, Young-Hoon Kim, MD, PhD and Peng-Sheng Chen, MD. Korea University Cardiovascular Center, Seoul, Republic of Korea, CedarsSinai Medical Center and David Geffen School of Medicine at UCLA, Los Angeles, CA and Utah Vally Medical Center, Provo, UT. Background: We previously demonstrated that propranolol converts multiple wavelet ventricular fibrillation (VF) into VF with a focal source anchored to the papillary muscle (PM) in Langendorff-perfused rabbit hearts. Ablation of this focal source may terminate VF. It is unclear if this finding can be reproduced in large animals in vivo. Methods and Results: We mapped left ventricles (LV) during VF by non-contact endocardial mapping (2 dogs, 10 pigs) or epicardial mapping (896 channels, 1 mm resolution, 6 pigs). Simultaneous epi- and endocardial mappings were done in 2 pigs. Posterior PM (PPM) was localized by 2D-echocardiography and ablated with radiofrequency (RF) energy in 2 dogs and 6 pigs. VF inducibility (pacing cycle length 100 ms with 5 mA strength for 5 s at right ventricular apex) was measured before and after PPM ablation. Results: 1) We mapped VF repeatedly for 12 min after induction (n⫽5). As global ischemia progressed, dominant frequency (DF) was reduced from 10.4⫾1.8 Hz to 4.3⫾1.2 Hz at 12 min (p⬍0.001). The maximum DF mostly (76.3%) localized at the PPM area. 2) Propranolol (0.05 mg/Kg bolus ⫹ 0.02 mg/Kg/min IV, n⫽9) increased VF cycle length from 82.0⫾29.3 ms to 109.2⫾29.3 ms (p⬍0.0001), the number of reentrant wavefronts (RWFs) from 0.40⫾0.53/s to 0.86⫾0.25/s (p⬍0.01) and increased the life-span of RWFs from 0.06⫾0.10 s to 0.18⫾0.23 s (p⫽0.001). Propranolol also facilitated the anchoring of RWFs to the PM. When the epicardial map showed repetitive breakthrough patterns at the PPM area, simultaneous endocardial map demonstrated reentry around PPM and mitral valve annulus (MVA). 3) VF inducibility was reduced remarkably (100⫾0% to post-ablation 5⫾7%, p⬍0.01) by RF ablation at PPM with linear extension of ablation line from PPM to MVA and LV apex in 2 dogs. However, RF application near PPM frequently initiated VF in pigs (n⫽6). Conclusion: PPM frequently served as an anchor to the RWFs during VF in swine and dogs with acute global ischemia or during propranolol infusion. RF ablation targeted at the PPM may prevent anchoring of RWFs and reduce the inducibility of VF in dogs. Further studies will be required for clinical catheter-based therapy of VF.
AB43-5 MECHANISMS OF VENTRICULAR FIBRILLATION IN CANINE MODELS OF CONGESTIVE HEART FAILURE AND ISCHEMIA ASSESSED BY IN VIVO HIGH-DENSITY MAPPING Thomas H. Everett, IV, PhD, Emily E. Wilson, BS, Scott Foreman, BS and Jeffrey E. Olgin, MD. University of California San Francisco, San Francisco, CA. Much of the research performed studying the mechanism of ventricular fibrillation (VF) has been in normal ventricles rather than under a pathological condition predisposing to VF. We hypothesized that different ventricular substrates would alter the mechanism and characteristics of VF.
S87 Methods: Three groups of dogs (n⫽20) were studied: 1) control; 2) congestive heart failure (CHF); and 3) acute ischemia (Isch) produced by 30 minutes of mid LAD ligation. A non-contact mapping catheter (Ensite 3000 TM, ESI) was placed via transseptal into the left ventricle (LV) along with an electrophysiology (EP) catheter. A multi-electrode basket catheter (EP Technologies) was placed in the right ventricle (RV) along with an EP catheter. Several episodes of VF were recorded in each animal. In addition to constructing isopotential and isochronal maps of the VF episodes, signals underwent frequency domain analysis as a fast-Fourier transform (FFT) was performed over a 2 sec window every 1 sec. From the FFT, the dominant frequency (DF) was determined, and the organization (OI) was calculated. Results: In control dogs meandering, reentrant spiral wave activity was the main feature of the VF. The CHF group showed evidence of either a stable rotor (n⫽3), a stable focal source (n⫽3), or no evidence of a driver in the LV (n⫽1). The Isch group showed evidence of an initial focal mechanism that transitioned into reentry. In the CHF and Isch groups the focus or reentrant wavefront was stable and if it extinguished, it would reappear in the same location. In the Control and Isch groups, the LV always had higher DFs than the RV. LV isochrones are shown below. Conclusion: Different ventricular substrates produced by the different animal models altered the characteristics of the VF. Both rotors and focal drivers may be present in the LV as mechanisms of VF.
AB43-6 VENTRICULAR MAZE CRYO-ABLATION RAISES THE VENTRICULAR FIBRILLATION INDUCTION THRESHOLD Saman Nazarian, MD, Menekhem M. Zviman, PhD, Venku B. Jayanti, PhD, Henry R. Halperin, MD and Ronald Berger, MD, PhD. Johns Hopkins Hospital, Baltimore, MD. Background: Ventricular fibrillation is the leading cause of sudden death. The mechanism of ventricular fibrillation is thought to involve multiple reentrant wavelets similar to that for atrial fibrillation. The surgical maze approach for treatment of atrial fibrillation has achieved 90% success in selected cases. We tested the hypothesis that “ventricular maze” ablation increases the ventricular fibrillation induction threshold (VFIT). Methods: Six healthy dogs were anesthetized and underwent implantable cardioverter defibrillator implantation and a standard thoracotomy. The VFIT was measured as the lowest energy shock delivered at the T-wave peak capable of producing sustained ventricular fibrillation. Five longitudinal ablation lines starting from the atrio-ventricular groove and intersecting at the apex were produced by epicardial cryo-ablation (-160 °C, SurgiFrost, CryoCath Inc). The VFIT was re-measured 1 hour following ablation. Results: Transmural lines of conduction block were produced in 3 animals by 3-minute right ventricular and 5-minute left ventricular cryo-ablations (Figure). To serve as controls, 3 animals underwent non-transmural ablation by 1-minute right ventricular and 3-minute left ventricular cryoablations. There was no significant change in the VFIT within control animals (0.23⫾0.12J to 0.30⫾0.00J, P⫽0.423). In contrast, transmural ventricular maze ablation increased the mean VFIT from a baseline of 0.53⫾0.40J to 1.60⫾0.46J (P⫽0.001). Conclusion: Ventricular maze cryo-ablation acutely increases the ventricular fibrillation induction threshold in the normal canine heart. We speculate that a ventricular maze strategy may render the ventricular substrate less susceptible to fibrillation.
AB43-5 MECHANISMS OF VENTRICULAR FIBRILLATION IN CANINE MODELS OF CONGESTIVE HEART FAILURE AND ISCHEMIA ASSESSED BY IN VIVO HIGH-DENSITY MAPPING Thomas H. Everett, IV, PhD, Emily E. Wilson, BS, Scott Foreman, BS and Jeffrey E. Olgin, MD. University of California San Francisco, San Francisco, CA. Much of the research performed studying the mechanism of ventricular fibrillation (VF) has been in normal ventricles rather than under a pathological condition predisposing to VF. We hypothesized that different ventricular substrates would alter the mechanism and characteristics of VF.
S87 Methods: Three groups of dogs (n⫽20) were studied: 1) control; 2) congestive heart failure (CHF); and 3) acute ischemia (Isch) produced by 30 minutes of mid LAD ligation. A non-contact mapping catheter (Ensite 3000 TM, ESI) was placed via transseptal into the left ventricle (LV) along with an electrophysiology (EP) catheter. A multi-electrode basket catheter (EP Technologies) was placed in the right ventricle (RV) along with an EP catheter. Several episodes of VF were recorded in each animal. In addition to constructing isopotential and isochronal maps of the VF episodes, signals underwent frequency domain analysis as a fast-Fourier transform (FFT) was performed over a 2 sec window every 1 sec. From the FFT, the dominant frequency (DF) was determined, and the organization (OI) was calculated. Results: In control dogs meandering, reentrant spiral wave activity was the main feature of the VF. The CHF group showed evidence of either a stable rotor (n⫽3), a stable focal source (n⫽3), or no evidence of a driver in the LV (n⫽1). The Isch group showed evidence of an initial focal mechanism that transitioned into reentry. In the CHF and Isch groups the focus or reentrant wavefront was stable and if it extinguished, it would reappear in the same location. In the Control and Isch groups, the LV always had higher DFs than the RV. LV isochrones are shown below. Conclusion: Different ventricular substrates produced by the different animal models altered the characteristics of the VF. Both rotors and focal drivers may be present in the LV as mechanisms of VF.
AB43-6 VENTRICULAR MAZE CRYO-ABLATION RAISES THE VENTRICULAR FIBRILLATION INDUCTION THRESHOLD Saman Nazarian, MD, Menekhem M. Zviman, PhD, Venku B. Jayanti, PhD, Henry R. Halperin, MD and Ronald Berger, MD, PhD. Johns Hopkins Hospital, Baltimore, MD. Background: Ventricular fibrillation is the leading cause of sudden death. The mechanism of ventricular fibrillation is thought to involve multiple reentrant wavelets similar to that for atrial fibrillation. The surgical maze approach for treatment of atrial fibrillation has achieved 90% success in selected cases. We tested the hypothesis that “ventricular maze” ablation increases the ventricular fibrillation induction threshold (VFIT). Methods: Six healthy dogs were anesthetized and underwent implantable cardioverter defibrillator implantation and a standard thoracotomy. The VFIT was measured as the lowest energy shock delivered at the T-wave peak capable of producing sustained ventricular fibrillation. Five longitudinal ablation lines starting from the atrio-ventricular groove and intersecting at the apex were produced by epicardial cryo-ablation (-160 °C, SurgiFrost, CryoCath Inc). The VFIT was re-measured 1 hour following ablation. Results: Transmural lines of conduction block were produced in 3 animals by 3-minute right ventricular and 5-minute left ventricular cryo-ablations (Figure). To serve as controls, 3 animals underwent non-transmural ablation by 1-minute right ventricular and 3-minute left ventricular cryoablations. There was no significant change in the VFIT within control animals (0.23⫾0.12J to 0.30⫾0.00J, P⫽0.423). In contrast, transmural ventricular maze ablation increased the mean VFIT from a baseline of 0.53⫾0.40J to 1.60⫾0.46J (P⫽0.001). Conclusion: Ventricular maze cryo-ablation acutely increases the ventricular fibrillation induction threshold in the normal canine heart. We speculate that a ventricular maze strategy may render the ventricular substrate less susceptible to fibrillation.