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Langendorff-perfused Rabbit Hearts (Langendorff-perfuse + rabbit_heart)
Selected AbstractsSpatiotemporal Correlation Between Phase Singularities and Wavebreaks During Ventricular FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2003YEN-BIN LIU M.D. Introduction: Phase maps and the detection of phase singularities (PSs) have become a well-developed method for characterizing the organization of ventricular fibrillation (VF). How precisely PS colocalizes with wavebreak (WB) during VF, however, is unknown. Methods and Results: We performed optical mapping of 27 episodes of VF in nine Langendorff-perfused rabbit hearts. A WB is a point where the activation wavefront and the repolarization waveback meet. A PS is a site where its phase is ambiguous and its neighboring pixels exhibit a continuous phase progression from ,, to +,. The correlation coefficient between the number of WBs and PSs was 0.78 ± 0.09 for each heart and 0.81 for all VF episodes (P < 0.001), indicating a significant temporal correlation. We then superimposed the WBs and PSs for every 100 frames of each episode. These maps showed a high degree of spatial colocalization. To quantify spatial colocalization, the spatial shifts between the cumulative maps of WBs and PSs in corresponding frames were calculated by automatic alignment to obtain maximum overlap between these two maps. The spatial shifts were 0.04 ± 0.31 mm on the x-axis and 0.06 ± 0.27 mm on the y-axis over a 20 × 20 mm2 mapped field, indicating highly significant spatial correlation. Conclusion: Phase mapping provides a convenient and robust approach to quantitatively describe wave propagation and organization during VF. The close spatiotemporal correlation between PSs and WBs establishes that PSs are a valid alternate representation of WB during VF and further validated the use of phase mapping in the study of VF dynamics. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1103-1109, October 2003) [source] Mapping of Atrial Activation Patterns After Inducing Contiguous Radiofrequency Lesions: An Experimental StudyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2001FRANCISCO J. CHORRO CHORRO, F.J., et al.: Mapping of Atrial Activation Patterns After Inducing Contiguous Radiofrequency Lesions: An Experimental Study. High resolution mapping techniques are used to analyze the changes in atrial activation patterns produced by contiguous RF induced lesions. In 12 Langendorff-perfused rabbit hearts, left atrial activation maps were obtained before and after RF induction of epicardial lesions following a triple-phase sequential protocol: (phase 1) three separate lesions positioned vertically in the central zone of the left atrial wall; (phase 2) the addition of two lesions located between the central lesion and the upper and lower lesions; and (phase 3) the placement of four additional lesions between those induced in the previous phases. In six additional experiments a pathological analysis of the individual RF lesions was performed. In phase 1 (lesion diameter = 2.8 ± 0.2 mm, gap between lesions = 3 ± 0.8 mm), the activation process bordered the lesions line in two (2.0-ms cycles) and four experiments (1.0-ms cycles). In phase 2, activation bordered the lesions line in eight (2.0-ms cycles, P < 0.01 vs control) and nine experiments (1.0-ms cycles, P < 0.001), and in phase 3 this occurred in all experiments except one (both cycles, P < 0.001 vs control). In the experiments with conduction block, the increment of the interval between activation times proximal and distal to the lesions showed a significant correlation to the length of the lesions (r = 0.68, P < 0.05, 100-ms cycle). In two (17%) experiments, sustained regular tachycardias were induced with reentrant activation patterns around the lesions line. In conclusion, in this acute model, atrial RF lesions with intact tissue gaps of 3 mm between them interrupt conduction occasionally, and conduction block may be frequency dependent. Lesion overlap is required to achieve complete conduction block lines. Tachycardias with reentrant activation patterns around a lesions line may be induced. [source] Opposite Effects of Myocardial Stretch and Verapamil on the Complexity of the Ventricular Fibrillatory Pattern: An Experimental StudyPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2000FRANCISCO J. CHORRO CHORRO, F.J., et al.: Opposite Effects of Myocardial Stretch And Verapamil on The Complexity of The Ventricular Fibrillatory Pattern: An Experimental Study. An experimental model is used to analyze the effects of ventricular stretching and verapamil on the activation patterns during VF. Ten Langendorff-perfused rabbit hearts were used to record VF activity with an epicardial multiple electrode before, during, and after stretching with an intraventricular balloon, under both control conditions and during verapamil (Vp) infusion (0.4,0.8 ,mol). The analyzed parameters were dominant frequency (FrD) spectral analysis, the median (MN) of the VF intervals, and the type of activation maps during VF (I = one wavelet without block lines, II = two simultaneous wavelets with block lines, III = three or more wavelets with block lines). Stretch accelerates VF (FrD: 22.8 ± 6.4 vs 15.2 ± 1.0 Hz, P < 0.01; MN: 48 ± 13 vs 68 ± 6 ms, P < 0.01). On fitting the FrD time changes to an exponential model after applying and suppressing stretch, the time constants (stretch: 101.2 ± 19.6 s; stretch suppression: 97.8 ± 33.2 s) do not differ significantly. Stretching induces a significant variation in the complexity of the VF activation maps with type III increments and type I and II decrements (control: I = 17.5%, II = 50.5%, III = 32%; stretch: I = 7%, II = 36.5%, III = 56.5%, P < 0.001). Vp accelerates VF (FrD: 20.9 ± 1.9 Hz, P < 0.001 vs control; MN: 50 ± 5 ms, P < 0.001 vs control) and diminishes activation maps complexity (I = 25.5%, II = 60.5%, III = 14%, P < 0.001 vs control). On applying stretch during Vp perfusion, the fibrillatory process is not accelerated to any greater degree. However, type I and II map decrements and type III increments are recorded, though reaching percentages similar to control (I = 16.5%, II = 53%, III = 30.5%, NS vs control). The following conclusions were found: (1) myocardial stretching accelerates VF and increases the complexity of the VF activation pattern; (2) time changes in the FrD of VF during and upon suppressing stretch fit an exponential model with similar time constants; and (3) although stretching and verapamil accelerate the VF process, they exert opposite effects upon the complexity of the fibrillatory pattern. [source] Remodelling of action potential and intracellular calcium cycling dynamics during subacute myocardial infarction promotes ventricular arrhythmias in Langendorff-perfused rabbit heartsTHE JOURNAL OF PHYSIOLOGY, Issue 3 2007Chung-Chuan Chou We hypothesize that remodelling of action potential and intracellular calcium (Cai) dynamics in the peri-infarct zone contributes to ventricular arrhythmogenesis in the postmyocardial infarction setting. To test this hypothesis, we performed simultaneous optical mapping of Cai and membrane potential (Vm) in the left ventricle in 15 rabbit hearts with myocardial infarction for 1 week. Ventricular premature beats frequently originated from the peri-infarct zone, and 37% showed elevation of Cai prior to Vm depolarization, suggesting reverse excitation,contraction coupling as their aetiology. During electrically induced ventricular fibrillation, the highest dominant frequency was in the peri-infarct zone in 61 of 70 episodes. The site of highest dominant frequency had steeper action potential duration restitution and was more susceptible to pacing-induced Cai alternans than sites remote from infarct. Wavebreaks during ventricular fibrillation tended to occur at sites of persistently elevated Cai. Infusion of propranolol flattened action potential duration restitution, reduced wavebreaks and converted ventricular fibrillation to ventricular tachycardia. We conclude that in the subacute phase of myocardial infarction, the peri-infarct zone exhibits regions with steep action potential duration restitution slope and unstable Cai dynamics. These changes may promote ventricular extrasystoles and increase the incidence of wavebreaks during ventricular fibrillation. Whereas increased tissue heterogeneity after subacute myocardial infarction creates a highly arrhythmogenic substrate, dynamic action potential and Cai cycling remodelling also contribute to the initiation and maintenance of ventricular fibrillation in this setting. [source] | ||||||||||