Ablation of atrial tachycardia originating from the vicinity of the atrioventricular node: significance of mapping both sides of the interatrial septum.

OBJECTIVES: The purpose of the study was to examine the value of right- and left-sided mapping to identify the site of tachycardia origin. BACKGROUND: Focal atrial tachycardia may originate from the vicinity of the atrioventricular node from either side of the interatrial septum. METHODS: In 16 patients undergoing radiofrequency catheter ablation of perinodal atrial tachycardia, activation mapping of the right and left side of the interatrial septum was performed. RESULTS: Atrial tachycardia originated from the right side of the interatrial septum in 10 patients (group A) and from the left side in 6 patients (group B). On the right side, earliest atrial activity preceded the onset of the P-wave by 49 +/- 15 ms in group A and by 38 +/- 8 ms in group B (NS), and it preceded the signal recorded from the right atrial appendage by 59 +/- 19 ms in group A and by 60 +/- 13 ms in group B (NS). On the left side, earliest activity preceded the onset of the P-wave by 27 +/- 16 ms in group A and by 51 +/- 6 ms in group B (<0.01), and it preceded the signal obtained from the right atrial appendage by 38 +/- 19 ms in group A and by 73 +/- 9 ms in group B (<0.01). Atrial tachycardias were successfully eliminated in all patients without impairment of atrioventricular conduction. During follow-up, two patients had a recurrence of tachycardia. CONCLUSIONS: Mapping of only the right side cannot exclude a left-sided origin. Therefore, mapping of both sides of the interatrial septum is required prior to ablation of focal atrial tachycardia originating from the vicinity of the atrioventricular node.

Successful treatment of idiopathic left ventricular outflow tract tachycardia by catheter ablation or minimally invasive surgical cryoablation.

Idiopathic right ventricular outflow tract tachycardia is readily amenable to radiofrequency catheter ablation. However, treatment modalities for left ventricular outflow tract tachycardia are not well defined. Out of 37 patients with idiopathic outflow tract tachycardia referred for catheter ablation, in 3 patients tachycardia originated from the left ventricular outflow tract. On the surface ECG, all left ventricular tachycardias exhibited an inferior axis with a predominant negative QRS complex in lead I. Heart rate during tachycardia ranged from 115 to 170 beats/min. During electrophysiological testing, 1 patient had inducible tachycardia on orciprenaline challenge, 1 patient had inducible tachycardia at baseline, and 1 patient had incessant tachycardia. In two patients, earliest ventricular activation was recorded from the endocardial left ventricular outflow tract at an anterolateral and an anterior site, respectively. A distinct high frequency spike preceded the QRS onset by 66/78 ms. Application of radiofrequency energy successfully eliminated tachycardia at these sites. In one patient, tachycardia originated from the epicardial left ventricular outflow tract. Mapping of the anterior interventricular vein revealed a fractionated low amplitude signal occurring 46 ms before QRS onset. After failure of catheter ablation from the corresponding endocardial site, successful minimally invasive surgical focal cryoablation of the epicardial target region was performed. During a follow-up period ranging from 7 to 12 months, all patients remained free of tachycardia. In conclusion, ventricular tachycardia arising from the left ventricular outflow tract may require endo- and epicardial mapping. Successful treatment is achieved by radiofrequency catheter ablation or minimally invasive surgical cryoablation.

Irregularity of the ventricular rhythm during atrial fibrillation: effect of slow atrioventricular nodal pathway ablation.

BACKGROUND: The contribution of dual atrioventricular (AV) nodal pathway physiology to the irregularity of the ventricular rhythm during atrial fibrillation has not been clarified. HYPOTHESIS: This study was performed to assess the effects of slow AV nodal pathway ablation on the irregularity of the ventricular rhythm during atrial fibrillation. METHODS: Irregularity of the ventricular rhythm was quantified using analysis of heart rate variability. In 20 patients with AV nodal reentrant tachycardia, absolute heart rate variability during atrial fibrillation was quantified before and after slow AV nodal pathway ablation by the standard deviation of all NN intervals (SDNN). Relative heart rate variability was determined by computing the coefficient of variation, SDNN normalized for the standard deviation of the mean ventricular cycle length (MVCL-AF). RESULTS: The slope of the regression between MVCL-AF and SDNN was significantly more gradual after slow pathway ablation (slope 0.39 vs. 0.23, p < 0.001). Coefficient of variation increased in 12 patients with heart rates > 120 beats/min at baseline (18.6 +/- 3.9 vs. 22.1 +/- 2.7% MVCL-AF, p < 0.05), but decreased in 8 patients with heart rates < 120 beats/min at baseline (25.6 +/- 3.1 vs. 22.2 +/- 2.2% MVCL-AF, p = 0.05). Furthermore, coefficient of variation correlated with MVCL-AF only at baseline (slope 0.034, r = 0.66), but no relation was found after slow pathway ablation (slope 0, r = 0). CONCLUSIONS: Slow AV nodal pathway ablation alters the relation between absolute heart rate variability and mean ventricular rate during atrial fibrillation and eliminates cycle length dependency of relative heart rate variability. These data indicate that dual AV nodal pathway physiology contributes to the irregularity of the ventricular rhythm during atrial fibrillation.

Unusual locations for adenosine-sensitive accessory atrioventricular pathways with decremental conduction.

INTRODUCTION: Accessory AV pathways with decremental conduction are uncommon and, in particular, are thought not to occur at the anterior portion of the mitral annulus. METHODS AND RESULTS: This report describes successful catheter ablation in three patients with accessory AV pathways that were adenosine sensitive and showed decremental conduction properties. The pathways were located at the anteroseptal, anteroparaseptal, and anterolateral aspects of the mitral annulus. CONCLUSION: Accessory pathways with decremental conduction do occur anywhere around the mitral annulus, even in the area of fibrous continuity between the aortic leaflet of the mitral valve and the aortic valve itself.

Atrioventricular nodal reentry tachycardia in patients with sinus node dysfunction: electrophysiologic characteristics, clinical presentation, and results of slow pathway ablation.

INTRODUCTION: Sinus node dysfunction (SND) is frequently associated with impaired AV conduction. This study investigated the electrophysiologic properties of dual AV nodal pathways in patients suffering from both SND and AV nodal reentrant tachycardia (AVNRT). METHODS AND RESULTS: Two groups of patients with slow-fast AVNRT underwent invasive electrophysiologic testing and catheter ablation of the slow pathway. Group A comprised 10 patients with SND (age 70 +/- 8 years). Group B included 10 age-matched patients without SND (age 69 +/- 7 years; P = NS) who served as controls. Patients of group A exhibited prolongation of the anterograde Wenckebach cycle lengths (WBCLs) of both the fast pathway (559 +/- 96 vs 361 +/- 38 msec; P < 0.01) and the slow pathway (409 +/- 57 vs 339 +/- 32 ms; P < 0.01). However, the delta between the WBCLs of the fast and the slow pathways was larger in patients of group A (150 +/- 80 vs 22 +/- 20 msec; P < 0.01). Retrograde fast pathway conduction was well preserved with no difference in WBCLs (356 +/- 42 vs 330 +/- 47 msec; P = NS). Cycle lengths of AVNRT were longer in group A (468 +/- 46 vs 363 +/- 37 msec; P < 0.01). Clinically, all patients of group A suffered from multiple episodes of AVNRT per week, which was not the case in any patient of group B (P < 0.01). Catheter ablation of the slow pathway eliminated AVNRT in all patients without complications. CONCLUSIONS: Patients with AVNRT and SND exhibit characteristic electrophysiologic alterations of both AV nodal pathways. Clinically, this results in significantly more frequent episodes of tachycardia. Slow pathway ablation appears to be safe and effective in these patients.

Demonstration of retrograde conduction over an atriofascicular accessory pathway.

INTRODUCTION: Absence of retrograde conduction over a right atriofascicular accessory pathway causing reciprocating tachycardia has been considered a hallmark of this clinical entity. METHODS AND RESULTS: This report describes successful catheter ablation in a patient presenting with the distinctive pattern of preexcited left bundle branch block tachycardia utilizing a right atriofascicular accessory pathway. This pathway, however, exhibited the unique capability of ventriculoatrial conduction. Both anterograde and retrograde conduction were characterized by "node-like" properties. CONCLUSION: Demonstration of retrograde accessory pathway conduction in this particular setting does not exclude the diagnosis of a single, atriofascicular accessory pathway.

Relation between left atrial size and secondary atrial arrhythmias after successful catheter ablation of common atrial flutter.

Catheter ablation provides an effective cure for patients with typical atrial flutter. However, these patients may have the potential to develop atrial tachyarrhythmias other than common atrial flutter. This study examines clinical and echocardiographic predictors for the occurrence of uncommon atrial flutter or atrial fibrillation after abolition of common atrial flutter. The study population comprised 17 patients (12 men, 5 women, age 32-74 years) who underwent successful radiofrequency catheter ablation of common atrial flutter. Common atrial flutter did not recur in any patient during a median follow-up time of 8 (range 1-25) months. Within a median of 7 (range 1-223) days, however, symptomatic atrial tachyarrhythmias occurred in 8 of 17 patients (47%): uncommon atrial flutter (n = 4); atrial fibrillation (n = 3); and both uncommon atrial flutter and atrial fibrillation in one patient. Preablation left atrial volume was significantly larger in patients who developed secondary arrhythmias compared with patients who remained in sinus rhythm (57.9 +/- 15.6 vs 43.7 +/- 16.4 cm3, P < 0.05). Enlarged left atrial volume dichotomized at 51 cm3 independently predicted postablation atrial arrhythmias (X2 = 5.11, rel. risk = 5.3, P < 0.05). On Kaplan-Meier analysis, time to occurrence of postablation atrial arrhythmias was significantly shorter in patients with enlarged left atrium (P < 0.02). In conclusion, symptomatic uncommon atrial flutter and atrial fibrillation develops in a substantial proportion of patients after successful ablation of common atrial flutter. Out of a series of clinical and echocardiographic parameters, preablation left atrial size is the best predictor for the occurrence of these postablation atrial arrhythmias.

Effect of slow pathway ablation on ventricular rate during atrial fibrillation. Dependence on electrophysiological properties of the fast pathway.

BACKGROUND: Catheter ablation of the posteroseptal right atrium has been proposed for control of ventricular rate in patients with tachycardic atrial fibrillation (AF). However, the exact mechanism of rate control is unclear. Because the ablation site corresponds to the location of the slow pathway in patients with AV nodal reentry tachycardia (AVNRT), we investigated whether selective ablation of this posterior AV nodal input can provide a sufficient reduction in heart rate during AF. METHODS AND RESULTS: In 30 patients with AVNRT, conduction properties of the AV nodal pathways were determined before and after slow pathway ablation. AF was induced by burst pacing at baseline and after ablation, and the mean ventricular cycle length was determined. After slow pathway ablation, the mean ventricular cycle length during AF increased (449 +/- 98 versus 515 +/- 129 milliseconds, P < .01). At baseline, the mean ventricular cycle length correlated with the Wenckebach cycle length of both the slow (r = .90) and fast (r = .86) pathways. After ablation, the mean ventricular cycle length was extremely well determined by the Wenckebach cycle length of the fast pathway (r = .94). However, the slope of the regression line was significantly steeper compared with baseline (1.50 versus 0.77, P < .0001), illustrating that the reduction in ventricular rate was not as evident if the fast pathway had a short Wenckebach cycle length. CONCLUSIONS: Selective elimination of the slow pathway reduces ventricular rate during AF. However, in patients with a short Wenckebach cycle length of the anterior AV nodal input that causes tachycardic AF, this effect may be insufficient to provide adequate control of ventricular rate.

Alterations of orthodromic circus movement tachycardia by dual atrioventricular nodal pathways in a patient with Wolff-Parkinson-White syndrome.

In a patient with a left sided accessory pathway (AP) three different types of orthodromic circus movement tachycardia were observed: (1) narrow QRS complex tachycardia with a stable cycle length (CL); (2) wide QRS complex tachycardia with a functional bundle branch block ipsilateral to the AP, which, paradoxically, had a shorter CL. The decrease in CL was due to a decrease of the AH interval; and (3) narrow QRS complex tachycardia with alternating CL, due to alternations of the AH interval. These phenomena were attributed to a concomitant dual atrioventricular (AV) node, which was eventually proven after successful catheter ablation of the AP.

Impaired subsidiary pacemaker function in patients with a right bundle branch block created prior to complete catheter ablation of the AV junction.

The impact of a right bundle branch block (RBBB), inadvertently created prior to complete ablation of the atrioventricular (AV) junction, on the intrinsic subsidiary pacemaker function was investigated. In 31 patients suffering from intractable supraventricular tachyarrhythmia, catheter ablation of the AV junction was performed using direct current (n = 13) or radiofrequency (n = 18) energy. In 16/31 patients a RBBB was created prior to complete AV ablation. Subsidiary pacemaker function was evaluated after a mean period of 5 months. Following 5 min of ventricular pacing (70 beats.min-1) escape interval and spontaneous heart rate were measured. In patients with a RBBB there was a trend towards a longer escape interval (2979 +/- 2559 vs 1867 +/- 1254 ms, P = ns) and a significantly lower intrinsic heart rate (38 +/- 14 vs 47 +/- 8 beats.min-1, P < 0.05). Pacemaker dependency was only observed among patients with a RBBB (4/16 vs 0/15, P < 0.05). HV intervals were shorter in those energy discharges resulting in a RBBB as compared to those inducing a complete heart block (52 +/- 8 vs 66 +/- 6 ms, P < 0.05). Creation of a RBBB prior to complete ablation of the AV junction results in impaired intrinsic subsidiary pacemaker function; the most proximal catheter position should be carefully sought to minimize the risk of pacemaker dependency.

Pacing-induced myocardial ischemia does not affect the endothelial release of coagulant and fibrinolytic factors into the coronary circulation.

The present study addresses the potential effects of pacing-induced myocardial ischemia on the secretion of coagulant and fibrinolytic factors within the coronary circulation. In 6 patients undergoing programmed ventricular stimulation with repeated induction of clinical ventricular tachycardia, the coronary release of tissue-type plasminogen activator (t-PA) antigen, plasminogen activator inhibitor (PAI) capacity, von Willebrand factor antigen (WF:Ag), and prostacyclin (6-keto-PGF 1a) was measured. Blood samples were collected simultaneously from the ascending aorta and the coronary sinus at baseline and immediately after the induction of ventricular tachycardia. The occurrence of pacing-induced myocardial ischemia was established by myocardial net lactate production. Myocardial ischemia was induced in every patient by repeated pacing trials. Pacing-induced ischemia did not affect the coronary release of any of the above factors. Consequently, there was no alteration of transcardiac gradients of thrombin-antithrombin complexes and D-dimer. The present results indicate that pacing-induced myocardial ischemia does not affect the release of coagulant and fibrinolytic endothelial factors or prostacyclin into the coronary circulation.

Evoked potentials in severe herpes simplex encephalitis.

Diagnostic and prognostic value of evoked potentials (EP) were studied in 5 patients with severe herpes simplex encephalitis (HSE). Latency of the third negative cortical N70 peak, elicited by median nerve stimulation, was prolonged in 3 survivors with Glasgow coma score of less than or equal to 6 (115 vs 71 ms in controls, p less than 0.05), but normal after improvement of the acute disease. N70 right to left interhemisphere difference was increased initially in the 4 survivors (26 vs 3 ms in controls, p less than 0.05) indicating focal brain involvement, a crucial finding in HSE. The first cortical N20 peak was preserved in all survivors even during deep coma where evaluation of brain function is difficult. Auditory brainstem EP were normal in all patients and useful to exclude brainstem death. In severe HSE, somatosensory long-latency EP are an effective monitor of the level of impaired consciousness and can detect brain focal signs. Short-latency N20 components may be predictive of the outcome.

Prognostic role of inducible ventricular tachycardia in patients with dilated cardiomyopathy and asymptomatic nonsustained ventricular tachycardia.

We studied the prognostic relevance of inducible ventricular tachycardia in 32 patients with dilated cardiomyopathy and spontaneous nonsustained asymptomatic ventricular tachycardia. Programmed ventricular stimulation included basic drive cycle lengths of 600, 500, 430, 370, 330 and 300 msec at single, double, and triple extrastimuli. Ventricular tachycardia (greater than or equal to 6 beats) was initiated in 7 patients (22%), with sustained monomorphic ventricular tachycardia being seen in 4 of them. During median follow-up of 21 months (13-44), 14 patients died. Sudden cardiac death occurred in two of the seven patients with inducible tachycardia and in only one of the 25 patients in whom it was not possible to induce tachycardia. Although patients with inducible tachycardia did not differ clinically from those in whom tachycardia could not be induced, the projected mean survival time was significantly shorter in those with inducible tachycardia (10 months vs. 32 months, P = 0.04). For late sudden cardiac death, the positive predictive value of inducible tachycardia was 28%. The negative predictive value was 96%. We conclude that induction of ventricular tachycardia by programmed stimulation might indicate poorer prognosis in patients with dilated cardiomyopathy.

Effect of heart rate on Doppler measurements of resistive index in renal arteries.

The effect of heart rate on Doppler measurements of the resistive index (RI) in renal arteries was studied in eight patients by varying paced heart rate to eliminate intrinsic and extrinsic factors influencing renal vascular resistance. A Doppler spectrum was obtained in renal segmental arteries. The RI was calculated at increasing heart rates from 70 to 120 beats per minute. There was a statistically significant decrease in RI with increasing heart rate (heart rate of 70: RI = 0.7 +/- 0.06; heart rate of 120: RI = 0.57 +/- 0.06; P less than .001), while blood pressure and cardiac output remained constant. To overcome this source of variance, the observed RI can be corrected for heart rate by using the following regression equation. For a heart rate of 80 beats per minute, corrected RI = observed RI - 0.0026(80 - observed heart rate). In interpreting the RI in renal allograft examinations, the actual heart rate of a patient must be taken into account. However, the clinical significance of standardizing the RI for heart rate requires further investigation.

Combined sotalol and flecainide given at low dosage in patients with the Wolff-Parkinson-White syndrome.

We determined the effects of combined sotalol (160 mg/day) and flecainide (200 mg/day) in 15 patients with the Wolff-Parkinson-White syndrome. After medication given for 3 days, the plasma levels were 0.8 +/- 0.3 micrograms/ml for sotalol and 232 +/- 104 ng/ml for flecainide. Electrophysiologic testing showed complete blockade of the accessory pathway in 4 patients and a decrease in the anterograde conduction capacity by 27% in the remainder. The effect on the accessory pathway was unrelated to the resting conduction properties. Initiation of circus movement tachycardia was prevented in 5 of 11 patients. During a median period of 28 months of follow-up, 87% of patients were either free of tachycardia or satisfactorily improved. No proarrhythmic or adverse drug effects were observed.

Electrophysiologic determinants of recurrent atrial flutter after successful termination by overdrive pacing.

The potential ability of electrophysiologic abnormalities to predict recurrence of atrial flutter was evaluated. Twenty-five patients with chronic atrial flutter resistant to combined digitalis and quinidine therapy were studied electrophysiologically after restoration of sinus rhythm by overdrive pacing or by eventual direct current cardioversion. Recurrence of atrial flutter was observed in 12 patients during a mean follow-up period of 17 months (range 3 to 50). Electrophysiologic testing included programmed high right atrial stimulation at a paced drive cycle length of 600 ms and incremental pacing up to 200-ms paced intervals. When coupling intervals of 90% of the drive cycle length were compared to coupling intervals of 48% of the drive cycle length, the increase in S1A1 interval, defined as the interval between the stimulus artifact and the atrial activation near the atrioventricular junction, was greater in patients with subsequent recurrence of atrial flutter (47 +/- 11 vs 21 +/- 18 ms). Stepwise logistic regression analysis identified the S1A1 increase to be the sole independent predictor of recurrence (p = 0.0082) while previous episodes of atrial flutter or the presence of organic heart disease were identified as dependent variables. Reclassification showed a 91% sensitivity and a 92% specificity. Correct classification was achieved in 92% of patients. The initiation of atrial dysrhythmia had no predictive value. The assessment of the S1A1 interval by programmed atrial stimulation appears helpful in delineating the patient risk of recurrent atrial flutter after termination by overdrive pacing.

Inadvertent catheter-induced right bundle branch block in a patient with preexistent left bundle branch block and recurrent macroreentrant ventricular tachycardia.

This article describes the inadvertent, catheter-induced induction of right bundle branch block resulting not only in transient complete infra-His heart block but also in temporary interruption of the macroreentry circuit of ventricular tachycardia. A patient with preexistent left bundle branch block and spontaneous ventricular tachycardia based upon the bundle branch reentry mechanism underwent electrophysiological testing for the evaluation of sotalol drug efficacy. In search of an optimal His-bundle recording, the manipulation of a 6 Fr quadripolar catheter caused a right bundle branch block, thus advancing the preexistent left bundle branch block to complete heart block. Retrograde ventriculoatrial conduction remained unaffected. The macroreentrant tachycardia with left bundle branch block configuration was no longer inducible. While the patient continued on unchanged sotalol medication (320 mg/d) he required temporary pacing for 16 hours until the block subsided. A subsequent induction attempt demonstrated initiation of the tachycardia. Finally, guided by invasive testing, the patient successfully received amiodarone therapy (300 mg/d). The patient completed an uneventful follow up of 27 months. No progression of conduction delay was observed. This case suggests that the inadvertent induction of right bundle branch block prevents the initiation of ventricular tachycardias relying on bundle branch reentry. Therefore, missed diagnosis or misinterpretation of antiarrhythmic drug efficacy might occur if there is no electrophysiological reevaluation after right bundle branch recovery.