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Canine Hearts (canine + heart)
Selected AbstractsRelationship of Specific Electrogram Characteristics During Sinus Rhythm and Ventricular Pacing Determined by Adaptive Template Matching to the Location of Functional Reentrant Circuits that Cause Ventricular Tachycardia in the Infarcted Canine HeartJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2000EDWARD J. CIACCIO Ph.D. Localization of Reentrant Circuits. Introduction: It would be advantageous, for ablation therapy, to localize reentrant circuits causing ventricular tachycardia by quantifying electrograms obtained during sinus rhythm (SR) or ventricular pacing (VP). In this study, adaptive template matching (ATM) was used to localize reentrant circuits by measuring dynamic electrogram shape using SR and VP data. Methods and Results: Four days after coronary occlusion, reentrant ventricular tachycardia was induced in the epicardial border zone of canine hearts by programmed electrical stimulation. Activation maps of circuits were constructed using electrograms recorded from a multichannel array to ascertain block line location. Electrogram recordings obtained during SR/AP then were used for ATM analysis. A template electrogram was matched with electrograms on subsequent cycles by weighting amplitude, vertical shift, duration, and phase lag for optimal overlap. Sites of largest cycle-to-cycle variance in the optimal ATM weights were found to be adjacent to block lines bounding the central isthmus during reentry (mean 61.1% during SR; 63.9% during VP). The distance between the mean center of mass of the ten highest ATM variance peaks and the narrowest isthmus width was determined. For all VP data, the center of mass resided in the isthmus region ocurring during reentry. Conclusion: ATM high variance measured from SR/AP data localizes functional block lines forming during reentry. The center of mass of the high variance peaks localizes the narrowest width of the isthmus. Therefore, ATM methodology may guide ablation catheter position without resorting to reentry induction. [source] Ionic Basis for Action Potential Prolongation by Phenylephrine in Canine Epicardial MyocytesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2000RICHARD B. ROBINSON Ph.D. Phenylephrine Action on Repolarization. Introduction: In canine ventricle, ,-adrenergic agonists prolong action potential duration (APD) without any effect on the action potential notch, suggesting that, in this species, the effect on repolarization might he independent of inhibition of Ito. The present study investigated the action of the ,-adrenergic agonist phenylephrine on the action potential and the repolarizing currents Ito and IK in isolated canine epicardial myocytes. Methods and Results: Isolated cells from canine epicardial tissue, and Purkinje fibers, were studied with the whole cell, voltage clamp method. Phenylephrine 0.1 ,M increased APD by 13%± 4% at 90% repolarization without affecting the notch or amplitude. Under voltage clamp, concentrations of phenylephrine as high as 10 ,M had no effect on Itp in canine epicardial myocytes. However, Ito of isolated canine Purkinje myocytes was reduced to 69%± 7% of control by 1 ,M phenylephrine. Further studies in canine epicardial myocytes revealed an action of phenylephrine to inhibit Ik, and in particular IKs Using a voltage protocol that included a two-step repolarization to separate IKs and IKr tail components, the largely 1Ke, component was not significantly affected by 1 ,M phenylephrine, whereas the largely IKs component was reduced to 81%± 5% of control value. Conclusion: ,-Adrenergic prolongation of repolarization in canine epicardium does not result from inhibition of Ito. Rather, it appears that reduction of IKs contributes to the action of phenylephrine. The unresponsiveness of epicardial Ito is not a general characteristic of the canine heart, because Purkinje myocyte Ito was inhibited, suggesting regional differences in the molecular basis of lto, and/or a-adrenergic signaling in the canine heart. [source] Arrhythmogenesis of T Wave Alternans Associated with Surface QRS Complex Alternans and the Role of Ventricular Prematurity: Observations from a Canine Model of LQT3 SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2002MASAOMI CHINUSHI M.D. Intramural TWA and Its Arrhythmogenesis.Introduction: T wave alternans (TWA) is characterized by cycle-to-cycle changes in the QT interval and/or T wave morphology. It is believed to amplify the underlying dispersion of ventricular repolarization. The aim of this study was to examine the mechanisms and arrhythmogenesis of TWA accompanied by QRS complex and/or blood pressure (BP) waveform alternans, using transmural ventricular electrogram recordings in an anthopleurin-A model of long QT syndrome. Methods and Results: The cardiac cycle length was gradually shortened by interruption of vagal stimulation, and TWA was induced in six canine hearts. Transmural unipolar electrograms were recorded with plunge needle electrodes from endocardial (Endo), mid-myocardial (Mid), and epicardial (Epi) sites, along with the surface ECG and BP. The activation-recovery interval (ARI) was measured to estimate local refractoriness. During TWA, ARI alternans was greater at the Mid than the Epi/Endo sites, and it was associated with the development of marked spatial dispersion of ventricular repolarization. As TWA increased, ventricular activation of the cycles associated with shorter QT intervals displayed delayed conduction at the Mid sites as a result of a critically longer ARI of the preceding cycle and longer QT interval, while normal conduction was preserved at the Epi site. Delayed conduction at the Mid sites manifested as surface ECG QRS and BP waveform alternans, and spontaneous ventricular tachyarrhythmias developed in absence of ventricular prematurity. In other instances, in absence of delayed conduction during TWA, ventricular premature complexes infringed on a prominent spatial dispersion of ventricular repolarization of cycles with long QT intervals and initiated ventricular tachyarrhythmia. Conclusion: TWA accompanied by QRS alternans may signal a greater ventricular electrical instability, since it is associated with intramural delayed conduction, which can initiate ventricular tachyarrhythmia without ventricular premature complexes. [source] Relationship of Specific Electrogram Characteristics During Sinus Rhythm and Ventricular Pacing Determined by Adaptive Template Matching to the Location of Functional Reentrant Circuits that Cause Ventricular Tachycardia in the Infarcted Canine HeartJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2000EDWARD J. CIACCIO Ph.D. Localization of Reentrant Circuits. Introduction: It would be advantageous, for ablation therapy, to localize reentrant circuits causing ventricular tachycardia by quantifying electrograms obtained during sinus rhythm (SR) or ventricular pacing (VP). In this study, adaptive template matching (ATM) was used to localize reentrant circuits by measuring dynamic electrogram shape using SR and VP data. Methods and Results: Four days after coronary occlusion, reentrant ventricular tachycardia was induced in the epicardial border zone of canine hearts by programmed electrical stimulation. Activation maps of circuits were constructed using electrograms recorded from a multichannel array to ascertain block line location. Electrogram recordings obtained during SR/AP then were used for ATM analysis. A template electrogram was matched with electrograms on subsequent cycles by weighting amplitude, vertical shift, duration, and phase lag for optimal overlap. Sites of largest cycle-to-cycle variance in the optimal ATM weights were found to be adjacent to block lines bounding the central isthmus during reentry (mean 61.1% during SR; 63.9% during VP). The distance between the mean center of mass of the ten highest ATM variance peaks and the narrowest isthmus width was determined. For all VP data, the center of mass resided in the isthmus region ocurring during reentry. Conclusion: ATM high variance measured from SR/AP data localizes functional block lines forming during reentry. The center of mass of the high variance peaks localizes the narrowest width of the isthmus. Therefore, ATM methodology may guide ablation catheter position without resorting to reentry induction. [source] Relation Between the Pacing Induced Sequence of Activation and Left Ventricular Pump Function in AnimalsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2002FRITS W. PRINZEN PRINZEN, F.W., et al.: Relation Between the Pacing Induced Sequence of Activation and Left Ventricu-lar Pump Function in Animals. The main goal of this article was to review animal experimental work on the effect of asynchronous activation on ventricular pump function. During normal sinus rhythm and atrial pacing, the Purkinje system contributes significantly to the rapid electrical activation of the ventricles. In contrast, during ventricular pacing the impulse is almost exclusively conducted through the normal myocardium. As a consequence, electrical activation of the ventricles becomes asynchronous and has an abnormal sequence. The abnormal impulse conduction causes considerable disturbances to occur in regional systolic fiber shortening, mechanical work, blood flow, and oxygen consumption; low values occurring in early activated regions and values above normal being present in late activated regions. Many animal studies have now shown that the abnormal electrical activation, induced by ventricular pacing, leads to a depression of systolic and diastolic LV function. Pacing at the right ventricular apex (the conventional pacing site) reduces LV function more than pacing at the high ventricular septum or at LV sites. In canine hearts with experimental LBBB, LV pacing significantly improves LV pump function. Differences in LV pump function between (combinations of) pacing sites are poorly correlated with QRS duration. Therefore, the cause of the depression of LV function during abnormal electrical activation appears to be a combination of the asynchrony and the sequence of activation. These experimental findings justify continuing attention for optimizing the site(s) of ventricular pacing in patients with normal and abnormal ventricular impulse conduction. [source] | ||||||||||