Chemical ablation of the Purkinje system causes early termination and activation rate slowing of long-duration ventricular fibrillation in dogs (original) (raw)
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Circulation, 2007
Background— The roles of Purkinje fibers (PFs) and focal wave fronts, if any, in the maintenance of ventricular fibrillation (VF) are unknown. If PFs are involved in VF maintenance, it should be possible to map wave fronts propagating from PFs into the working ventricular myocardium during VF. If wave fronts ever arise focally during VF, it should be possible to map them appearing de novo. Methods and Results— Six canine hearts were isolated, and the left main coronary artery was cannulated and perfused. The left ventricular cavity was exposed, which allowed direct endocardial mapping of the anterior papillary muscle insertion. Nonperfused VF was induced, and 6 segments of data, each 5 seconds long, were analyzed during 10 minutes of VF. During 36 segments of data that were analyzed, 1018 PF or focal wave fronts of activation were identified. In 534 wave fronts, activation was mapped propagating from working ventricular myocardium to PF. In 142 wave fronts, activation was mapped pro...
The effect of chemical ablation of the endocardium on ventricular fibrillation threshold
Circulation, 1986
The purpose of this study was to examine the effects of ablation of the superficial endocardium and Purkinje network on left ventricular fibrillation threshold. Lugol's solution was applied through small ventriculotomies to the left and right ventricular endocardium of 10 dogs on cardiopulmonary bypass. Two control groups of five animals each underwent either endocardial application of saline or epicardial application of Lugol's solution. Ventricular fibrillation threshold was measured before and after each intervention by the single-stimulus technique. Application of Lugol's solution to the endocardium resulted in a 102 +/- 15% increase in ventricular fibrillation threshold from a control value of 26 +/- 2 to 53 +/- 6 mA (p less than .005). In two animals, ventricular fibrillation could not be initiated postoperatively. In the control groups, there were no significant changes in ventricular fibrillation threshold. Histologic examination revealed that Lugol's solutio...
American Journal of Physiology-Heart and Circulatory Physiology, 2010
Long-duration ventricular fibrillation (LDVF) in the globally ischemic heart is a common setting of cardiac arrest. Electrical heterogeneities during LDVF may affect outcomes of defibrillation and resuscitation. Previous studies in large mammalian hearts have investigated the role of Purkinje fibers and electrophysiological gradients between the endocardium (Endo) and epicardium (Epi). Much less is known about gradients between the right ventricle (RV) and left ventricle (LV) and within each chamber during LDVF. We studied the transmural distribution of the VF activation rate (VFR) in the RV and LV and at the junction of RV, LV, and septum (Sep) during LDVF using plunge needle electrodes in opened-chest dogs. We also used optical mapping to analyze the Epi distribution of VFR, action potential duration (APD), and diastolic interval (DI) during LDVF in the RV and LV of isolated hearts. Transmural VFR gradients developed in both the RV and LV, with a faster VFR in Endo. Concurrently, ...
Circulation Research, 1973
The cellular electrophysiological mechanisms underlying the ventricular arrhythmias that accompany myocardial infarction were studied in isolated, superfused infarcted myocardium excised from dogs previously subjected to a two-stage ligation of the anterior descending coronary artery. Ventricular arrhythmias frequently occurred in the intact heart 24 hours after coronary occlusion. Surviving subendocardial Purkinje fibers in infarcts excised at this time were highly arrhythmic when they were studied with intracellular microelectrodes in vitro. These arrhythmias consisted of rapid, repetitive depolarizations and occurred spontaneously or could be induced by premature electrical stimulation. Premature stimulation also resulted in single unstimulated responses. In such instances, premature impulses conducted extremely slowly through the infarcted region where surviving Purkinje fiber action potential durations were extraordinarily prolonged. Conduction block at some sites in the infarct caused phenomena which were interpreted as reentrant beats. Some surviving subendocardial Purkinje fibers in the infarct demonstrated spontaneous diastolic depolarization and appeared to function as pacemakers in the absence of electrical stimulation. In some instances, these fibers constituted typical parasystolic foci, demonstrating both entrance and exit block. These results suggest that subendocardial Purkinje fibers which survive in an infarct may be the site of origin of some of the ventricular arrhythmias that accompany myocardial infarction. KEY WORDS microelectrode spontaneous diastolic depolarization entrance block ventricular tachycardia reentry parasystole exit block From the Departments of Pharmacology and Anatomy,
Circulation, 2002
The combined effects of excitability and action potential duration (APD) restitution on wavefront dynamics remain unclear. We used optical mapping techniques to study Langendorff-perfused rabbit hearts. In protocol IA (n=10), D600 at increasing concentrations was infused during ventricular fibrillation (VF). With concentration increased to 0.5 mg/L, fast VF (dominant frequency, 19.1+/-1.8 Hz) was consistently converted to ventricular tachycardia (VT). However, increasing D600 further to 2.5 or 5.0 mg/L converted VT to slow VF (11.9+/-2.3 Hz, P=0.0011). In an additional 4 hearts (protocol IB), tetrodotoxin converted a preexisting VT to slow VF (11.0+/-1.4 Hz). Optical maps show wandering wavelets in fast VF, organized reentry in VT, and spatiotemporal periodicity in slow VF. In protocol II, we determined APD and conduction time(-1) (CT(-1)) restitutions during D600 infusion. CT(-1) was used as an estimate of excitability. At 0.1 mg/L, APD and CT(-1) restitutions were steep and flat, ...
Journal of Cardiovascular Electrophysiology, 1999
Ischemic Ventricular Fibrillation. Introduction: Although premature heats originating in areas of ischemia have been shown to he important in initiating ventricular fibrillation (VF), the participation of the ischemic zone in maintenance of VF has not been investigated.Methods and Results: Ten normal dogs underwent induction of two separate episodes of VF, before and 10 minutes after left anterior descending coronary artery ligation. Ischemic VF was allowed to occur spontaneously or was induced by burst pacing after 10 minutes of ischemia. Unipolar epicardial electrograms were recorded using an 8 × 14 plaque electrode array (interelectrode distance 2.5 mm) placed over the anterior wall. Activation during VF was characterized by VF cycle length (CL) and wavefront organization based on linking analysis of epicardial activation directions at adjacent sites. Individual plaque sites were separated into regions based on electrogram morphology during ischemia: R1 = no ischemia; R2 = mild-to-moderate ischemia (minor ST elevation and QRS widening); and R3 = severe ischemia (marked ST elevation and QRS widening). Percent conduction block was calculated based on the percent of cycles during which sites were not activated during VF. There were no significant differences noted in mean CL or mean percent conduction block in the peri-ischemic region R1 compared to the same region under nonischemic (control) conditions. During ischemia, the mean CL was noted to increase in R2 from 111 ± 14 msec (control) to 128 ± 29 msec (ischemia) and in R3 from 113 ± 14 msec (control) to 150 ± 42 msec (ischemia) (P < 0.05). The percentage conduction block in R2 increased from 6%± 11% (control) to 14%± 16% (ischemia) and in R3 from 4%± 6% (control) to 44%± 21% (ischemia) (P < 0.05). Linking analysis revealed no significant changes in VF organization at distances of 2.5 mm in regions R1 and R2 under both control and ischemic conditions. Premature heats initiating fibrillation originated at the border between the normal and mildly ischemic zones.Conclusions: (1) Some VF characteristics are altered in ischemic regions including a longer VFCL and greater percentage of functional block. (2) VF characteristics are unchanged in immediately adjacent nonischemic myocardium. (3) Although the ischemic zone may he involved in the initiation of VF and has unique activation characteristics during VF, it does not affect VF characteristics in the adjacent nonischemic zone, suggesting that it may not play a major role in VF maintenance.
Heart Rhythm, 2010
Background-While reentry within the ventricular myocardium (VM) is responsible for the maintenance of short duration ventricular fibrillation (SDVF, VF duration < 1 min), Purkinje fibers (PFs) are important in the maintenance of long duration ventricular fibrillation (LDVF, VF duration > 1 min). Objective-We hypothesized that the mechanisms of defibrillation may also be different for SDVF and LDVF. Methods-A multielectrode basket catheter was deployed in the left ventricle of 8 beagles. External defibrillation shocks were delivered with a ramp-up protocol following SDVF (20 s) and LDVF (150 s). Earliest VM and PF activations were identified following the highest energy shock that failed to terminate VF and the successful shock. Results-Defibrillation was successful after 36±12 s and 181±14 s for SDVF and LDVF, respectively. The time after shock delivery until earliest activation was detected for failed shocks and was significantly longer following LDVF (138.7±24.1 ms) than SDVF (75.6±8.7 ms). Earliest postshock activation following SDVF typically initiated in the VM (14 of 16 episodes) while it always initiated in the PF (16 of 16 episodes) following LDVF. Sites of earliest activity during sinus rhythm correlated with sites of earliest postshock activation for PF-led cycles but not VM-led cycles. Conclusion-Earliest recorded postshock activation is in the Purkinje system following LDVF but not SDVF. This difference raises the possibility that the optimal defibrillation strategy is different for SDVF and LDVF.
Virchows Archiv A Pathological Anatomy and Histopathology, 1991
During open heart surgery, reperfusion-induced arrhythmias arising after short periods of ischaemia may originate from subendocardial Purkinje fibres. We investigated the ultrastructure of these fibres during 30 min of global ischaemia at 25 ~ C. The effects both with myocardial protection (HTK cardioplegia) and without it (pure ischaemia) were compared qualitatively and morphometrically. After 30 min pure ischaemia overcontraction of sarcomeres, hypercontraction and contraction bands, together with considerable changes in organelles, predominate over cellular oedema. In Purkinje fibres, both cellular and mitochondrial swelling were significantly increased within this 30-min time period from the onset of pure ischaemia. In contrast, following HTK cardioplegia and 30 min ischaemia, cellular and mitochondrial swelling remain moderate and overcontractions are almost entirely lacking. This means that despite remarkable differences between pure ischaemia and HTK cardioplegia in the degree of protection attained it is clear that, compared with the working myocardium, subendocardial Purkinje fibres do not display a higher resistance to early global ischaemia. Further investigations of this sensitivity of Purkinje fibres to global ischaemia and certain drugs may bring about new insights into myocardial protection and pharmacotherapy of arrhythmias.
Induction and maintenance of in vivo ventricular fibrillation in rabbits
Resuscitation, 2009
Aim: To provide new sustainable in vivo models of ventricular fibrillation in rabbits. Methods: New Zealand rabbits were submitted to anaesthesia and mechanical ventilation, after which ventricular fibrillation was induced through electrical stimulation (for 2 min at 100 Hz, with 2-ms pulses, 10 mA, and 10 V) directly to the heart. To that end, the animals were divided into two groups: right ventricle (n = 11) and left ventricle (n = 11). In group right ventricle, the thoracic cavity was exposed, and a catheter was introduced into the right ventricle via the right jugular vein. In group left ventricle, the thorax remained closed, and the catheter was introduced into the left ventricle via the left common carotid artery (cervical access). Results: Sustained ventricular fibrillation was achieved in 100% of group right ventricle rabbits (n = 11) and in 82% of group left ventricle rabbits (n = 9). Conclusion: Both models proved appropriate for achieving sustained ventricular fibrillation. However, in view of the invasiveness of the procedure adopted in group right ventricle, the experimental conditions used in group left ventricle seemed more physiological and more effective in inducing sustained ventricular fibrillation.