33 research outputs found

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    A new animal model of atrial flutter

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    A new, simple and reliable model of atrial flutter utilizing postpericardiotomy pericarditis was developed in the dog. Using a sterile technique, the pericardium was opened by way of a right thoracotomy, Teflon-coated, stainless steel wire electrodes were fixed to three selected sites on the atria and exteriorized, the atrial surfaces were generously dusted with talcum powder and a single layer of gauze was placed on the free left and right atrial walls. The dogs were allowed to recover. Subsequently, the inducibility of atrial flutter and selected electrophysiologic properties of the atria were determined by daily programmed atrial stimulation studies with the dogs in the conscious, nonsedated state.Atrial flutter could be induced in 23 of 25 dogs initially studied. It was sustained (that is, lasting ≥5 min) in 17 of the 23. Neither atrial excitability, Intraatrial conduction time nor atrial refractoriness determined by pacing and recording from the three fixed sites predicted the inducibility of atrial flutter. One hundred thirty-nine episodes of atrial flutter induced in these 23 dogs were analyzed. The mean sustained atrial flutter cycle length was 131 ± 20 ms (mean ± SD) (range 100 to 170); the atrial flutter cycle length was 150 ms or more in 23 episodes, between 120 and 150 ms in 64 episodes and 120 ms or less in 52 episodes.In five dogs, the stability of the atrial flutter cycle length during sustained atrial flutter was studied and shown to be remarkably stable in all five until interrupted by rapid atria) pacing 35 to 95 minutes after its induction. Seventeen dogs were submitted to reoperation for epicardial mapping purposes and atrial flutter could be induced in the open chest state in 12. In conclusion, this sterile pericarditis model of atrial flutter in the canine heart proved to be highly reliable, reproducible and easy to create

    Intermediate septal accessory pathways: Electrocardiographic characteristics, electrophysiologic observations and their surgical implications

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    AbstractIntermediate septal accessory pathways are located in close proximity to the atrioventricular (AV) node and His bundle, have unique features that distinguish them from typical anterior and posterior accessory pathways and have been associated with a high risk for unsuccessful pathway division and the production of complete AV block after surgery. Between July 1986 and May 1990, 4 of 70 patients (3 men and 1 woman; mean age 33 ± 13 years) undergoing surgery for accessory pathway division were found to have an intermediate septal accessory pathway. The presenting arrhythmia was atrial fibrillation with rapid anterograde conduction over the accessory pathway in two patients and recurrent orthodromic reciprocating tachycardia in two patients.In all patients, the delta wave on the electrocardiogram (ECG) was inversed in lead V1, but two patterns of delta wave configuration were observed. In three patients (type 1 intermediate septal accessory pathway), the delta wave was upright in lead II, inverted in lead III and isoelectric in lead aVF; the transition from a negative to an upright delta wave occurred in lead V2. The fourth patient exhibited a different delta wave pattern (type 2 intermediate septal accessory pathway). The delta wave was upright in each of leads II, III and aVF; the transition from a negative to an upright delta wave occurred at lead V3.Intraoperative electrophysiologic study localized the atrial insertion of type 1 pathways to the midpoint of Koch's triangle close to the AV node. In the one patient with a type 1 pathway in which both anterograde and retrograde accessory pathway conduction was present, preoperative catheter mapping demonstrated that earliest retrograde atrial activation occurred near the foramen ovale. Intraoperative mapping during anterograde conduction over the type 1 pathway demonstrated earliest epicardial ventricular activation to occur simultaneously at the crux and the base of the aorta. The atrial insertion of the type 2 intermediate septal accessory pathway was localized to the apex of Koch's triangle in close proximity to the bundle of His. Preoperative catheter mapping revealed that earliest retrograde atrial activation occurred on the His bundle electrogram. Intraoperative mapping during anterograde conduction over the type 2 pathway demonstrated that earliest epicardial ventricular activation occurred anteriorly at the base of the aorta.Intraoperative ablation of the intermediate septal accessory pathway was accomplished by cooling the endocardium at the site of pathway insertion on the atrial side of the tricuspid anulus with a 5 mm cryoprobe. Patients with a type 1 intermediate septal accessory pathway had preservation of AV conduction, but the patient with the type 2 pathway did not and required permanent pacing. At late follow-up study, no patient has had return of intermediate septal accessory pathway conduction. Distinguishing an intermediate septal accessory pathway close to the AV node (type 1) from one close to the His bundle (type 2) is useful to predict both surgical success and success without the production of permanent complete AV block

    Value of early postoperative epicardial programmed ventricular stimulation studies after surgery for ventricular tachyarrhythmias

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    The value of early postoperative epicardial programmed ventricular stimulation studies after electrophysiologically-directed surgery for ventricular tachyarrhythmia was assessed in 34 patients who underwent epicardial stimulation within 7 to 30 days (mean 9.8) of surgery and were followed up for at least 6 months. The antiarrhythmic operation performed was an endocardial ventriculotomy (full encircling or limited), an endocardial resection, a wall resection or a combination of these procedures. All these interventions were directed by intraoperative mapping during sinus rhythm. Temporary epicardial wire electrodes left at the time of surgery rather than endocardial catheter electrodes were used to perform the pacing. The stimulation protocol included the introduction of up to three ventricular extrastimuli and incremental burst ventricular pacing performed at twice diastolic threshold (9.2 ± 5.8 mA for the right ventricle and 6.0 ± 3.5 mA for the left ventricle). A study was considered positive when ventricular tachycardia, defined as 10 or more consecutive ventricular beats, was induced by any pacing modality.Nineteen patients (Group I) had a negative study: after stimulation of both ventricles in 15 patients and of the left ventricle only in 4. Fifteen patients (Group II) had a positive study: after stimulation of the right ventricle in nine patients and of the left ventricle in six. The two groups were comparable with respect to preoperative clinical status, surgical procedures performed and postoperative ejection fraction. No arrhythmic events were observed in Group I during a mean follow-up period of 19.5 months (range 4 to 37), whereas seven arrhythmic events (47% incidence) occurred (p = 0.0008) in Group II during a mean follow-up period of 17.7 months (range 5 to 39). These arrhythmic events were sudden death (five patients) and sustained ventricular tachycardia (two patients).It is concluded that temporary epicardially-placed electrodes can be used satisfactorily to perform programmed ventricular stimulation studies in the postoperative period, thereby avoiding the cardiac catheterizations otherwise necessary to perform these studies. In addition, the protocol used in this report of epicardial programmed ventricular stimulation early after surgery for ventricular tachyarrhythmia predicts a good outcome if the study is negative and identifies patients at a high risk for future arrhythmic events when positive

    Preferential effect of procainamide on the reentrant circuit of ventricular tachycardia

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    AbstractTransient entrainment was used to test the hypotheses that 1) procainamide prolongs the cycle length of ventricular tachycardia in patients with coronary artery disease because it has a preferential effect on the reentrant tachycardia circuit, and 2) regions of slow conduction in the reentrant circuit are more susceptible to the effect of procainamide than are other areas of the ventricles. In five patients with prior myocardial infarction, sustained ventricular tachycardia with identical QRS configuration was inducible before and after intravenous infusion of procainamide. Transient entrainment of ventricular tachycardia was demonstrated at two or more cycle lengths by rapid pacing in the baseline state and after procainamide. Rapid pacing was performed from the same site during sinus rhythm at the cycle lengths that demonstrated transient entrainment of ventricular tachycardia. The conduction interval to the transiently entrained site during ventricular tachycardia (orthodromic interval) was compared with the conduction interval to the same site during pacing in sinus rhythm (antidromic interval).The mean tachycardia cycle length increased by 27% after procainamide administration (p = 0.002). The antidromic conduction intervals were prolonged by 9 % (p = 0.06) compared with a 28% increase in the mean orthodromic conduction interval (p = 0.002). The difference between the orthodromic and antidromic conduction intervals increased by 40% (p = 0.003). Prolongation of the tachycardia cycle length after procainamide administration correlated positively with increases in the orthodromic conduction intervals (r = 0.94, p = 0.02) but not with changes in the antidromic intervals (r = −0.08, p = NS). The effect of procainamide on the difference between orthodromic and antidromic conduction intervals correlated strongly with changes in the cycle length of venetricular tachycardia (r = 0.97 p = 0.006).Thus, procainamide has a preferential effect on the reentrant circuit of ventricular tachycardia compared with other areas of ventricular myocardium. In addition, these results are compatible with the hypothesis that the effect of procainamide is more marked in regions of conduction delay in the reentrant circuit

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    A prospective evaluation of intracoronary ethanol ablation of the atrioventricular conduction system

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    AbstractThe clinical efficacy and complications associated with ablation of the atrioventricular (AV) conduction system by the selective infusion of ethanol into the AV node artery were prospectively assessed in 12 consecutive patients with medically refractory atrial arrhythmias. Six of the patients had previously failed to have permanent complete AV block created with direct current or radiofrequency catheter ablation. The AV node artery was cannulated with a 0.016 in. (0.041 cm) guide wire in all 12 patients. It was also possible to advance a 2.7F infusion catheter into the AV node artery in all patients.Transient AV block was induced by selective injections into the AV node artery of iced saline solution (8 patients) and of radiographic contrast agent (ioxaglate) (10 patients). The infusion of 2 ml of ethanol (96%) induced immediate complete AV block in all 10 patients who demonstrated AV block with ioxaglate. The escape rhythm exhibited a narrow QRS complex preceded by p His bundle deflection in nine patients and left bundle branch block in one patient. The immediate mean rate of the escape rhythm was 45.3 ± 13.4 beats/min. In two patients who demonstrated reflux of contrast agent into the distal right coronary artery with selective injections into the AV node artery, transient ST segment elevation developed in the inferior electrocardiographic leads with the infusion of ethanol. There was no change in the left ventricular ejection fraction from the baseline value (0.53 ± 0.12) to that measured after ablation (0.55 ± 0.11) and no patient developed wall motion abnormalities. All 10 patients developing complete AV block after ethanol infusion were discharged without AV conduction. After a mean follow-up period of 134.8 days (range 48 to 216), AV conduction returned in three patients (noted at 6 days and 4 and 6 weeks, respectively, after the procedure) who were discharged with complete heart block. Intracoronary ablation of the AV conduction system by the selective infusion of ethanol into the AV node artery can be performed with a low risk of serious complications. However, reflux of ethanol into the distal right coronary artery may occur. In addition, AV conduction may return in approximately 30% of patients who initially develop complete AV block

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