Electrophysiologic characteristics in initiation of paroxysmal atrial fibrillation from a focal area.
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OBJECTIVES: We investigated the electrophysiologic characteristics in the initiation of paroxysmal atrial fibrillation (PAF) from a focal area. BACKGROUND: The electrophysiologic characteristics in the initiation of PAF are still not clear. METHODS: The study group consisted of 77 patients (M/F = 65/12, age 66 +/- 12 years) with frequent episodes of PAF; we analyzed: 1) 15 cycle lengths of electrical activity before the onset of atrial fibrillation (AF); 2) coupling interval (CI) of the first ectopic beat just before the initiation of AF; and 3) the prematurity of an ectopic beat (prematurity index [PI] = CI/mean of preceding 15 cycle lengths). RESULTS: A total of 111 episodes of sustained AF were identified. Two patterns of AF initiation were observed: group I (59/111, 53%) included the episodes preceded by cycle length oscillation, and group II (52/111, 47%) included the episodes initiated by a single ectopic beat with preceding cycle length relatively constant. The PI of group I episodes was significantly greater than that of group II (0.41 +/- 0.12 vs. 0.34 +/- 0.10, p < 0.01). The CI (267 +/- 54 ms vs. 217 +/- 55 ms, p < 0.05), AF1 (194 +/- 36 ms vs. 153 +/- 37 ms, p < 0.05) and PI (0.49 +/- 0.13 vs. 0.37 +/- 0.11, p < 0.01) of the AF episodes from the superior vena cava (SVC) were significantly longer and greater than those of AF episodes from pulmonary veins (PVs). CONCLUSIONS: In patients with PAF originating from PVs or the SVC, two major initiating patterns were found. Moreover, the electrophysiologic characteristics in the initiation of AF originating from the SVC were also different from those of AF initiating from the PVs. (+info)
Multi atrial maco-re-entry circuits in adults with repaired congenital heart disease: entrainment mapping combined with three-dimensional electroanatomic mapping.
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OBJECTIVES: We sought to characterize re-entry circuits causing intra-atrial re-entrant tachycardias (IARTs) late after the repair of congenital heart disease (CHD) and to define an approach for mapping and ablation, combining anatomy, activation sequence data and entrainment mapping. BACKGROUND: The development of IARTs after repair of CHD is difficult to manage and ablate due to complex anatomy, variable re-entry circuit locations and the frequent co-existence of multiple circuits. METHODS: Forty-seven re-entry circuits were mapped in 20 patients with recurrent IARTs refractory to medical therapy. In the first group (n = 7), ablation was guided by entrainment mapping. In the second group (n = 13), entrainment mapping was combined with a three-dimensional electroanatomic mapping system to precisely localize the scar-related boundaries of re-entry circuits and to reconstruct the activation pattern. RESULTS: Three types of right atrial macro-re-entrant circuits were identified: those related to a lateral right atriotomy scar (19 IARTs), the Eustachian isthmus (18 IARTs) or an atrial septal patch (8 IARTs). Two IARTs originated in the left atrium. Radiofrequency (RF) lesions were applied to transect critical isthmuses in the right atrium. In three patients, the combined mapping approach identified a narrow isthmuses in the lateral atrium, where the first RF lesion interrupted the circuit; the remaining circuits were interrupted by a series of RF lesions across a broader path. Overall, 38 (81%) of 47 IARTs were successfully ablated. During follow-up ranging from 3 to 46 months, 16 (80%) of 20 patients remained free of recurrence. Success was similar in the first 7 (group 1) and last 13 patients (group 2), but fluoroscopy time decreased from 60 +/- 30 to 24 +/- 9 min/procedure, probably related to the increasing experience and ability to monitor catheter position non-fluoroscopically. CONCLUSIONS: Entrainment mapping combined with three-dimensional electroanatomic mapping allows delineation of complex re-entry circuits and critical isthmuses as targets for ablation. Radiofrequency catheter ablation is a reasonable option for treatment of IARTs related to repair of CHD. (+info)
Angerlike behavioral state potentiates myocardial ischemia-induced T-wave alternans in canines.
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OBJECTIVES: The main goal of this study was to determine whether induction of an angerlike state can result in significant levels of T-wave alternans, a marker of electrical instability, in the normal and ischemic heart. BACKGROUND: Outbursts of anger have been implicated in the occurrence of myocardial infarction and sudden cardiac death, but the pathophysiologic mechanisms remain unknown. METHODS: A standardized behavioral challenge of eliciting an angerlike state was conducted before and during a 3-min period of coronary artery occlusion in six canines. RESULTS: Precordial T-wave alternans increased from 0.04 +/- 0.02 at baseline to 1.40 +/- 0.32 mV X ms (p < 0.05) during the angerlike response. When the angerlike state and myocardial ischemia were superimposed, the augmentation in T-wave alternans magnitude (to 3.27 +/- 0.61 mV X ms, p < 0.05) exceeded their additive effects, increasing by 130% over the angerlike state alone (p < 0.05) and by 390% over occlusion alone (p < 0.05). Adrenergic influences were reduced by the beta1-adrenergic receptor blocking agent metoprolol (1.5 mg/kg, intravenous), which diminished T-wave alternans magnitude (p < 0.0004 for all) during the angerlike response (from 1.40 +/- 0.32 to 0.80 +/- 0.17 mV x ms) and during the combined intervention (from 3.27 +/- 0.61 to 1.23 +/- 0.13 mV X ms). In five additional normal anesthetized canines, atrial pacing at 180 beats/min did not increase T-wave alternans magnitude monitored from lead II electrocardiogram. CONCLUSIONS: Provocation of an angerlike state results in T-wave alternans in the normal heart and potentiates the magnitude of ischemia-induced T-wave alternans. Elevation in heart rate during arousal does not appear to be the main factor in the development of alternans in the normal heart but may be an important component during myocardial ischemia. Enhanced adrenergic activity appears to mediate the effects in both the normal and ischemic hearts. T-wave alternans may constitute a useful electrophysiologic measure for clinical use in conjunction with behavioral stress testing or ambulatory monitoring. (+info)
Ablation of atrial fibrillation in the rapid pacing canine model using a multi-electrode loop catheter.
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OBJECTIVES: This investigation details our experience using a loop catheter to ablate atrial fibrillation (AF) in dogs. BACKGROUND: Atrial fibrillation is the most common arrhythmia and has significant morbidity. Maintenance of normal sinus rhythm (NSR) after conversion in many patients is still a challenge. METHODS: A multi-electrode loop catheter was used to create linear atrial lesions to ablate AF in a rapid atrial pacing model in 29 dogs. Rhythm status was assessed over a six-month recovery period, after which tissue analysis was performed. RESULTS: Acute conversion to NSR or atrial tachycardia (AT) was achieved in 90% of cases. Six of 26 conversions occurred after only left atrial (LA) lesions, and two after just right atrial lesions. Sixteen (62%) of 26 lesions that resulted in AF conversion were in the LA, and 11 of these 16 conversions occurred during a lesion connecting the mitral ring to the pulmonary veins. Acute conversion rate was similar with ring and coil electrodes, but AT was more frequent with coil electrodes (63% vs. 31%). At six months 80% of dogs were in NSR, 14% were in AT, and 7% remained in AF. There was an average reduction in P-wave amplitude of 64 +/- 26% after power application. Tissue analysis revealed transmural contiguous lesions when final outcome was NSR, and nontransmural/noncontiguous lesions where AF persisted. CONCLUSIONS: Multi-electrode loop catheters can create contiguous transmural lesions in either atrium to safely and effectively ablate AF and provide a stable long-term rhythm outcome in this dog model. The left atrium appears to be the dominant chamber that sustains AF. Atrial tachycardia is a frequent acute outcome with coil electrodes. (+info)
Early autonomic and repolarization abnormalities contribute to lethal arrhythmias in chronic ischemic heart failure: characteristics of a novel heart failure model in dogs with postmyocardial infarction left ventricular dysfunction.
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OBJECTIVES: Using a model of arrhythmias associated with ischemic left ventricular (LV) dysfunction, this study investigated autonomic and electrophysiologic mechanisms associated with sudden cardiac death (SCD) in chronic heart failure (HF). BACKGROUND: Left ventricular dysfunction from ischemic heart disease is associated with many instances of SCD. Electrophysiologic and autonomic derangements occur in HF, but their contribution to SCD risk is poorly understood. METHODS: Sudden death risk was assessed in 15 dogs with a healed anterior myocardial infarction (MI) during submaximal exercise and brief acute circumflex ischemia. Left ventricular dysfunction was then induced by repetitive circumflex microembolization until LV ejection fraction reached 35%. Before embolization, six dogs were susceptible to SCD, and nine were resistant. RESULTS: Baroreflex sensitivity was lower in susceptible dogs (10 ms/mm Hg +/- 4 ms/mm Hg vs. 20 ms/mm Hg +/- 11 ms/mm Hg, p = 0.04). QT intervals from susceptible dogs were longer after MI (246 ms +/- 26 ms susceptible vs. 231 ms +/- 20 ms resistant, p < 0.001) and prolonged within eight weeks after LV dysfunction was established (from 246 ms +/- 26 ms to 274 ms +/- 56 ms, +11%, p < 0.01). Heart rate in susceptible dogs increased during transient ischemia (+20%) and with progressive LV dysfunction (102 beats/min +/- 28 beats/min baseline to 154 beats/min +/- 7 beats/min LV dysfunction, p = 0.003). All susceptible dogs had spontaneous sustained ventricular tachycardia culminating in SCD. In contrast, QT intervals in resistant dogs prolonged after 24 +/- 6 weeks (from 231 ms +/- 20 ms to 238 ms +/- 15 ms, p < 0.05), and heart rates were unchanged. Only one resistant dog died suddenly with LV dysfunction. CONCLUSIONS: Depressed vagal and elevated sympathetic control of heart rate coupled with abnormal repolarization are associated with high SCD risk when post-MI LV dysfunction develops. (+info)
Variations in diagnostic yield of head-up tilt test and electrophysiology in groups of patients with syncope of unknown origin.
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AIMS: To assess the diagnostic yield of the head-up tilt test and electrophysiology in different groups of patients with syncope of unknown origin established according to simple clinical criteria. METHODS AND RESULTS: Six hundred consecutive patients with syncope of unknown origin submitted to a tilt test. Two hundred and forty seven of them also underwent electrophysiology. Patients were divided into groups according to age at the time of first syncope, ECG findings and the presence of organic heart disease. Positive responses to the tilt test were more common in patients who had suffered their first syncope at an age equal to or below 65 years (group I) than in older patients (group II) (47% vs 33%, P<0.05, OR 1.8, CI 1.2-2.78), and in patients with a normal ECG and without organic heart disease than in the other subgroups of patients (47% vs 37%, P<0.008, OR 1.6). The lowest rate of positive response was observed in older patients with an abnormal ECG and organic heart disease. Electrophysiology disclosed abnormal findings in group II more often than in group I (23% vs 7%, P<0.001, OR 3.7, CI 1.7-9.2). The diagnostic yield from electrophysiology was higher in patients with an abnormal ECG than in those with a normal ECG (22% vs 3.7%, P<0.0005, OR 7.1), and it was especially low in patients with a normal ECG and without organic heart disease (2.6%). CONCLUSION: The diagnostic yield of the tilt test and electrophysiology differs in groups of patients with syncope of unknown origin, established according to simple clinical criteria. These findings have a bearing on selecting the most appropriate test in a particular patient. (+info)
Effects of diacetyl monoxime and cytochalasin D on ventricular fibrillation in swine right ventricles.
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Whether or not the excitation-contraction (E-C) uncoupler diacetyl monoxime (DAM) and cytochalacin D (Cyto D) alter the ventricular fibrillation (VF) activation patterns is unclear. We recorded single cell action potentials and performed optical mapping in isolated perfused swine right ventricles (RV) at different concentrations of DAM and Cyto D. Increasing the concentration of DAM results in progressively shortened action potential duration (APD) measured to 90% repolarization, reduced the slope of the APD restitition curve, decreased Kolmogorov-Sinai entropy, and reduced the number of VF wave fronts. In all RVs, 15-20 mmol/l DAM converted VF to ventricular tachycardia (VT). The VF could be reinduced after the DAM was washed out. In comparison, Cyto D (10-40 micromol/l) has no effects on APD restitution curve or the dynamics of VF. The effects of DAM on VF are associated with a reduced number of wave fronts and dynamic complexities in VF. These results are compatible with the restitution hypothesis of VF and suggest that DAM may be unsuitable as an E-C uncoupler for optical mapping studies of VF in the swine RVs. (+info)
Transmural reentry during acute global ischemia and reperfusion in canine ventricular muscle.
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Coronary occlusion and reperfusion produce tachyarrhythmias. We tested the hypothesis that variations in transmural activation after global ischemia and reperfusion were responsible for arrhythmias. We arterially perfused 36 isolated transmural wedges from canine left ventricular free walls. After > or =100 min of stabilization, the artery was occluded for 25 min, followed by reperfusion at various flow rates. We recorded 256 channels of fluorescent action potentials on transmural surfaces from preocclusion to >15 min after reperfusion. During endocardial pacing at 300 ms, ischemia of > or =570 +/- 165 s (n = 34) produced 1:1 endocardial conduction and then 2:1 and 4:1 block as the wave fronts conducted toward epicardium. Transmural reentry appeared after 535 +/- 146 s of ischemia (n = 31). Further ischemia caused epicardial inactivation and eliminated reentry (n = 24). During reperfusion, tissues progressed through sequences of epicardial inactivation and reappearance of activation with 1:1, 2:1, and 4:1 conduction; both sustained and nonsustained reentry occurred. We conclude that heterogeneous activation responses to endocardial pacing during acute ischemia provide the substrate for initiating reentry, suppressed reentry during further ischemia, and caused reentry during reperfusion. (+info)