Reliable pace termination of postoperative atrial fibrillation in the canine sterile pericarditis model: Implications for atypical atrial flutter.

BACKGROUND: We have identified a reentrant circuit in the pulmonary vein region, which drives the atria, producing fibrillatory conduction, as one mechanism of postoperative atrial fibrillation (POAF) in the canine sterile pericarditis model. OBJECTIVE: In this model, we tested the hypothesis that overdrive pacing from a site at or near such a reentrant circuit would interrupt it and thereby terminate POAF. METHODS: We studied 11 sterile pericarditis dogs on postoperative days 1-4. Atrial electrograms (AEGs) were recorded during POAF, overdrive pacing, and pace termination from 3 sites simultaneously: Bachmann's bundle, posterior left atrium, and right atrial appendage. When recorded AEGs demonstrated regular activation, pace termination was attempted at that site by delivering a drive train starting with 4 consecutive beats at a cycle length (CL) of 2-5 ms shorter than that of the intrinsic CL. RESULTS: Sixteen episodes of sustained POAF (>5 minutes) diagnosed by electrocardiogram were induced. During all episodes of POAF, AEGs recorded from the left atrium exhibited regular activation, ie, constant AEG morphology and CL. When capture of the reentrant circuit by overdrive pacing occurred (mean 13 ± 5, range 5-23 beats), all 16 POAF episodes were successfully terminated. In all termination episodes, at the end of pacing but prior to the return of sinus rhythm, there was disorganized atrial activation in the previously organized sites (mean 2 seconds, range 0.1-8 seconds). However, these beats did not sustain POAF in the absence of a reentrant circuit ("driver"). CONCLUSION: Overdrive pacing from a site demonstrating regular activation during sustained POAF terminated the POAF by interrupting the reentrant circuit.

Termination of a tachyarrhythmia by flunarizine is not a specific marker for a triggered mechanism.

BACKGROUND: Prior studies have indicated that tachyarrhythmia termination by flunarizine demonstrates a triggered mechanism. This concept was not confirmed in atrial tachyarrhythmias. OBJECTIVE: The purpose of this study was to test the hypothesis that flunarizine will not terminate reentrant atrial flutter (AFL). METHODS: We administered flunarizine (2 mg/kg intravenously over 2 minutes) in 11 episodes of reproducibly inducible, sustained AFL in eight canines with sterile pericarditis. If flunarizine terminated AFL, we studied AFL reinducibility. We also studied pacing thresholds, refractoriness, and intra-atrial conduction time during closed-chest studies and pacing at selected cycle lengths (CLs) from selected sites before and after flunarizine administration. Atrial mapping (510 electrodes) assessed the epicardial activation sequence during AFL and its termination in six episodes. Four AFL episodes were studied in the closed-chest state. RESULTS: Flunarizine increased AFL CL in all episodes (mean 21 ms; range 7-49 ms), which is explained by slowing conduction in the AFL reentrant circuit, principally in the area of slow conduction. AFL was terminated in 10/11 episodes after drug initiation (mean 3.7 minutes; range 0.5-6.5 minutes) by block in the area of slow conduction. AFL was then not immediately reinducible until >20 minutes after drug administration. Flunarizine had no meaningful effect on atrial pacing thresholds for capture or refractoriness and only affected conduction time in the area of slow conduction in the reentrant circuit. CONCLUSIONS: Flunarizine (1) causes progressive slowing and block in the area of slow conduction of the AFL reentrant circuit in the canine sterile pericarditis model and (2) is effective in terminating reentrant AFL and so is not a specific marker for a triggered mechanism.

Routine transesophageal echocardiography for the evaluation of cerebral emboli in elderly patients.

BACKGROUND: Approximately 20% of cerebral infarctions are cardioembolic in nature. Transesophageal echocardiography (TEE) is widely regarded as the initial study of choice for evaluating cardiac source of embolism. Although the majority of cerebrovascular accidents occur in elderly patients, the value of TEE in this population is poorly defined. METHODS: We compared 491 patients older than 65 years with suspected embolic stroke or transient ischemic attack (TIA) who had undergone TEE evaluation between April 2000 and February 2004 to an age-, sex-, and time-matched control group that consisted of 252 patients. Studies were reviewed for abnormalities associated with thromboembolic disease. RESULTS: The overall incidence of stroke risk factors was significantly higher in the study than in the control group. However, the four patients with left atrial thrombi had a history of atrial fibrillation. Although ascending and aortic arch sessile atheromata were observed more frequently in the study than control group, there were no significant differences in the incidence of either complex or mobile aortic atheromata. The incidence of atrial septal aneurysm was higher in the stroke/TIA group, but not in association with patent foramen ovale. Finally, there were also no differences in the incidence of spontaneous echocontrast, and/or patent foramen ovale between study and control groups. CONCLUSIONS: We conclude: (1) There is a higher incidence of abnormalities implicated as sources of thromboembolic disease on TEE in elderly patients with cerebral infarctions, but (2) this incidence is driven by the presence of sessile aortic atheroma and atrial septal aneurysm. Until the benefits of specific therapies for these conditions are known, routine TEE in elderly patients with suspected embolic neurological events appears to be unwarranted.