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Notes: Ventricular Defibrillation and Cardiac Function. Introduction: The effect of implantable defibrillator shocks on cardiac hemodynamics is poorly understood. The purpose of this study was to test the hypothesis that ventricular defibrillator shocks adversely effect cardiac hemodynamics. Methods and Results: The cardiac index was determined by calculating the mitral valve inflow with transesophogeal Doppler during nonthoracotomy defibrillator implantation in 17 patients. The cardiac index was determined before, and immediately, 1 minute, 2 minutes, and 4 minutes after shocks were delivered during defibrillation energy requirement testing with 27- to 34-, 15-, 10-, 5-, 3-, or 1-J shocks. The cardiac Index was also measured at the same time points after 27- to 34-, and 1-J shocks delivered during the baseline rhythm. The cardiac index decreased from 2.30 ± 0.40 L/min per m2 before a 27- to 34-J shock during defibrillation energy requirement testing to 2.14 ± 0.45 L/min per m2 immediately afterwards (P= 0.001). This effect persisted for 〉4 minutes. An adverse hemodynamic effect of similar magnitude occurred after 15 J (P= 0.003) and 10-J shocks (P= 0.01), but dissipated after 4 minutes and within 2 minutes, respectively. There was a significant correlation between shock strength and the percent change in cardiac index (r = 0.3, P= 0.03). The cardiac index decreased 14% after a 27- to 34-J shock during the baseline rhythm (P 〈 0.0001). This effect persisted for 〈4 minutes. A 1- J shock during the baseline rhythm did not effect the cardiac index. Conclusion: Defibrillator shocks 〉9 J delivered during the baseline rhythm or during defibrillation energy requirement testing result in a 10% to 15% reduction in cardiac index, whereas smaller energy shocks do not affect cardiac hemodynamics. The duration and extent of the adverse effect are proportional to the shock strength. Shock strength, and not ventricular fibrillation, appears to be most responsible for This effect. Therefore, the detrimental hemodynamic effects of high-energy shocks may be avoided when low-energy defibrillation is used.

Notes: Adenosine and Retrograde Fast Pathway Conduction. Introduction: Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. Methods and Results: The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 ± 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P 〈 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 ± 78 vs 333 ± 74 msec, P 〈 0.01), a shorter VA block cycle length (383 ± 121 vs 307 ± 49 msec, P 〈 0.001), and a shorter VA interval during tachycardia (53 ± 23 vs 41 ± 17 msec, P 〈 0.01). Conclusion: Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.

Notes: Cardiac Memory. Introduction: “Cardiac memory” (primary T wave change) is thought to occur after 15 minutes to several hours of right ventricular (RV) pacing. The two components of the temporal change in repolarization are memory and accumulation. The purpose of this study was to examine quantitatively the effect of short periods of ventricular pacing on the human cardiac action potential, using monophasic action potential (MAP) recordings. Methods and Results: Thirty-one patients (ages 43 ± 14 years) with structurally normal hearts undergoing a clinically indicated electrophysiologic procedure were enrolled. Catheters were placed in the right atrium (RA) and RV, and a MAP catheter was positioned at the RV septum. APD90 was calculated from digitized MAP recordings. MAP morphology comparisons were performed using the root mean square (RMS) of the difference between complexes. All pacing was at 500-msec cycle length. There were four pacing protocols: (1) RA pacing was performed for approximately 15 minutes to evaluate temporal stability of the MAP recordings (5 pts); (2) to evaluate the memory phenomenon, four successive 1-minute episodes of RV pacing were interspersed with 2 minutes of RA pacing (5 pts); (3) the accumulation phenomenon was evaluated by assessing the effects of 1, 5, 10, and 15 minutes of RV pacing on the MAP during RA pacing (16 pts); and (4) 20 minutes of RV pacing was followed by 10 minutes of RA pacing to correlate visually apparent T wave changes with changes in MAP recordings (5 pts). In the control patients, no changes in APD90 or RMS analysis were noted during 14.9 ± 1.4 minutes of RA pacing. In the second protocol, RMS of the difference between the baseline MAP complexes and the signal average of the first 50 beats following each of four 1-minute RV pacing trains demonstrated progressively greater differences in morphology after successive episodes of RV pacing. In protocol 3, RMS analysis identified a progressively greater difference between the baseline MAP recording and the average of the first 50 beats after 1,5, 10, and 15 minutes of RV pacing. In protocol 4, visually apparent changes in T waves occurred in parallel with the RMS of the difference between the baseline MAP recordings and the average of the first 50 beats after 20 minutes of RV pacing. Similar changes also were demonstrated by APD90 analysis. Conclusion: This study is the first to demonstrate that episodes of abnormal ventricular activation as short as 1 minute in duration may exert lingering effects on the repolarization process once normal ventricular activation resumes.

Notes: Introduction: A corridor of double potentials along the ablation line has been recognized to be an indicator of complete cavotricuspid isthmus block. Isoproterenol is used to confirm cavotricuspid isthmus block, but the effects of isoproterenol on the double potential interval (DPI), either in the absence or presence of amiodarone, are unknown. Methods and Results: Thirty-two patients with isthmus-dependent atrial flutter underwent successful ablation of the cavotricuspid isthmus. The procedure was performed in the drug-free state in 23 patients, and 2 to 7 days after discontinuation of chronic amiodarone therapy in 9 patients. Electrograms recorded along the ablation line before and during isoproterenol infusion were analyzed after isthmus block was achieved. Double potentials were recorded along the entire ablation line upon achievement of complete isthmus block in all patients. The DPI in 9 patients treated with amiodarone was longer than in the other patients (147 ± 32 msec vs 119 ± 19 msec, P 〈 0.001). The DPI increased as the pacing cycle length shortened in patients treated with amiodarone, but not in the other patients. At all pacing cycle lengths, isoproterenol shortened the DPI to a greater extent in the patients treated with amiodarone than in the other patients. Conclusion: Amiodarone results in rate-dependent prolongation of the DPI during coronary sinus pacing after ablation of the cavotricuspid isthmus. Isoproterenol shortens the DPI despite the presence of complete isthmus block, and this effect is accentuated in the presence of amiodarone. (J Cardiovasc Electrophysiol, Vol. 14, pp. 935-939, September 2003)

Notes: Immediate Recurrence of Atrial Fibrillation. Introduction: An immediate recurrence of atrial fibrillation (IRAF) appears to be more common after early restoration of sinus rhythm with an implantable atrial defibrillator than after elective transthoracic cardioversion, which suggests that the probability of IRAF may be related to the duration of AF. Methods and Results: Transthoracic cardioversion was performed 85 ± 187 days (range 7 minutes to 8 years) after the onset of atrial fibrillation in 315 patients (mean age 61 ± 13 years). IRAF was defined as a recurrence of AF within 60 seconds after restoration of sinus rhythm. IRAF occurred in 56% of patients when cardioversion was performed within 1 hour of the onset of AF compared with 12% of patients when cardioversion was performed after 24 hours of AF (P 〈 0.001). The duration of AF was the only independent predictor of IRAF among the clinical variables of age, gender, structural heart disease, antiarrhythmic drug therapy, and cardioversion energy (P 〈 0.01). Conclusion: IRAF is more likely to occur when the duration of AF is 〈1 hour than when the duration is 〉24 hours. This observation has clinical implications for the most appropriate timing of cardioversion, particularly in patients who receive device therapy for AF. (J Cardiovasc Electrophysiol, Vol. 14, pp. 182-185, February 2003)

Notes: Pulmonary Vein Anatomy. Introduction: The anatomic arrangement of pulmonary veins (PVs) is variable. No prior studies have quantitatively analyzed the effects of segmental ostial ablation on the PVs. The aim of this study was to determine the effect of segmental ostial radiofrequency ablation on PV anatomy in patients with atrial fibrillation (AF). Methods and Results: Three-dimensional models of the PVs were constructed from computed tomographic (CT) scans in 58 patients with AF undergoing segmental ostial ablation to isolate the PVs and in 10 control subjects without a history of AF. CT scans were repeated approximately 4 months later. PV and left atrial dimensions were measured with digital calipers. Four separate PV ostia were present in 47 subjects; 3 ostia were present in 2 subjects; and 5 ostia were present in 9 subjects. The superior PVs had a larger ostium than the inferior PVs. Patients with AF had a larger left atrial area between the PV ostia and larger ostial diameters than the controls. Segmental ostial ablation resulted in a 1.5 ± 3.2 mm narrowing of the ostial diameter. A 28% to 61% focal stenosis was present 7.6 ± 2.2 mm from the ostium in 3% of 128 isolated PVs. There were no instances of symptomatic PV stenosis during a mean follow-up of 245 ± 105 days. Conclusion: CT of the PVs allows identification of anatomic variants prior to catheter ablation procedures. Segmental ostial ablation results in a significant but small reduction in ostial diameter. Focal stenosis occurs infrequently and is attributable to delivery of radiofrequency energy within the PV. (J Cardiovasc Electrophysiol, Vol. 14, pp. 150-155, February 2003)

Notes: Pulmonary Vein Tachycardia. Introduction: The significance of intermittent tachycardia within a pulmonary vein (PV) during an episode of atrial fibrillation (AF) is unclear. The aim of this study was to determine the role that intermittent PV tachycardias play in AF. Methods and Results: In 56 patients with AF, segmental ostial ablation guided by PV potentials was performed to isolate the PVs. The characteristics of intermittent PV tachycardias and the inducibility of AF before and after PV isolation were analyzed prospectively. During AF, a PV tachycardia (mean cycle length 130 ± 30 msec) with exit block to the left atrium was present in 93% of left superior, 80% of left inferior, 73% of right superior, and 7% of right inferior PVs. The site of shortest cycle length during AF alternated between the PVs and left atrium 1 to 13 times per minute. Complete isolation was achieved in 168 (94%) of 178 targeted PVs. In 99% of PVs, tachycardia resolved upon isolation. AF was persistent before and after PV isolation in 100% and 27% of patients, respectively (P 〈 0.001). Conclusion: Intermittent bursts of tachycardia are observed within multiple PVs during persistent AF in a majority of patients. After PV isolation, PV tachycardias almost always resolve, and AF is less likely to be inducible or persistent. These observations suggest a dynamic interplay between the atria and PVs, with intermittent bursts of PV tachycardia being dependent on left atrial input and with the probability of persistent AF diminishing when PV tachycardias are eliminated by PV isolation.

Notes: Introduction: Bursts of tachycardia arising in the pulmonary veins may play an important role in perpetuating atrial fibrillation (AF). However, the role of the coronary sinus (CS) in the perpetuation of AF has been unclear. The aim of this study was to determine whether the CS plays a role in perpetuation of AF. Methods and Results: Pulmonary vein isolation was performed by segmental ostial ablation with radiofrequency energy in 22 consecutive patients with paroxysmal AF. Bipolar and unipolar electrograms recorded in the left atrium and CS were analyzed during atrial pacing from the mitral annulus and during AF. There was a mean of 2.5 ± 0.5 electrical connections between the CS and the left atrium. The electrical connections between the left atrium and CS were ablated with a mean of 6.2 ± 2.7 minutes of radiofrequency energy applied along the atrial side of the inferior mitral annulus. During AF, episodes of intermittent tachycardia alternated between the left atrium and the CS. Among the 22 patients, sustained AF was still inducible in 9 after pulmonary vein isolation. After electrical disconnection of the CS from the left atrium, sustained AF was inducible in only 3 of these 9 patients. Conclusion: The CS may be a source of rapid repetitive electrical activity during AF. The lower probability of inducible sustained AF after electrical disconnection of the CS from the left atrium suggests that the CS may play a role in perpetuating AF. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1329-1336, December 2003)

Notes: Pulmonary Vein Electrograms. Introduction: Accurate discrimination of atrial and pulmonary vein potentials recorded circumferentially within the pulmonary veins is important when performing segmental isolation of the pulmonary veins in patients with atrial fibrillation. Methods and Results: Twenty patients with paroxysmal atrial fibrillation underwent pulmonary vein mapping with a decapolar Lasso catheter during sinus rhythm and during pacing in the distal coronary sinus and left atrial appendage. Bipolar and unipolar electrograms were recorded within the left superior, right superior, and left inferior pulmonary veins. The atrial potentials were larger in the left pulmonary veins than in the right superior pulmonary vein, whereas the pulmonary vein potentials in the superior pulmonary veins were larger than in the left inferior pulmonary vein. The atrial and pulmonary vein potentials usually were readily distinguished during sinus rhythm in the right superior pulmonary vein. Characteristic distribution and morphologies of the atrial potentials as well as the response to distal coronary sinus and left atrial appendage pacing were useful for differentiating the atrial and pulmonary vein potentials in the left pulmonary veins. Conclusion: Atrial and pulmonary vein potentials recorded circumferentially within the pulmonary veins have characteristic features that are useful in distinguishing them from each other.In the left pulmonary veins, discrimination of the atrial and pulmonary vein potentials is aided by coronary sinus or left atrial appendage pacing.