Dissociation of atrial electrograms by right and left atrial pacing in patients with atrioventricular reciprocating tachycardia.

Seventeen patients had atrioventricular (AV) reciprocating tachycardia incorporating an AV bypass tract as the retrograde limb of the tachycardia circuit. High right atrial pacing during tachycardia dissociated the low septal right atrial electrogram in four of seven patients with a left free wall bypass tract, neither of two patients with a right free wall bypass tract, four of six patients with a posteroseptal bypass tract and both patients with an anteroseptal bypass tract. Pacing from the coronary sinus during tachycardia dissociated the atrial electrogram recorded at the os of the coronary sinus in no patient with a left free wall bypass tract, both patients with a right free wall bypass tract, two patients with a posteroseptal bypass tract and one patient with an anteroseptal bypass tract. These findings suggest two distinct inputs to the AV node, with the left-sided input being part of the tachycardia circuit in patients with a left free wall bypass tract and the right-sided input being part of the tachycardia circuit in patients with a right free wall bypass tract. However, in some patients with a septal bypass tract, neither the right- nor the left-sided atrial input appears to be a necessary link in the tachycardia circuit.

Coexistent posteroseptal and right-sided atrioventricular bypass tracts.

Twelve patients with a posteroseptal accessory pathway underwent complete electrophysiologic studies, and four were found to have a second atrioventricular (AV) bypass tract that was right anterior, right anteromedial or right anterolateral in location. In two of these four patients, the presence of the right-sided AV bypass tract was confirmed by intraoperative epicardial mapping or after catheter-induced abolition of retrograde conduction through the posteroseptal bypass tract. In three of the four patients with a dual AV bypass tract, the delta wave pattern was clearly atypical of the pattern seen with an isolated posteroseptal accessory pathway. Instead of a transition from an isoelectric or slightly positive delta wave in lead V1 to markedly positive delta waves in leads V2 to V6, the delta waves were negative or only slightly positive in leads V2 to V5. However, in a fourth patient with dual AV bypass tracts, the only atypical electrocardiographic finding was an intermittently positive delta wave in lead II; at times this patient's electrocardiogram was consistent with an isolated posteroseptal bypass tract, with negative delta waves in the inferior leads. There appears to be an association between posteroseptal and right-sided accessory pathways. In patients with a posteroseptal accessory pathway who are candidates for catheter or surgical bypass tract ablation, a complete mapping study of the tricuspid anulus is mandatory, even when the electrocardiogram is typical of an isolated posteroseptal bypass tract.

Effects of increased heart rate and sympathetic tone on intraventricular electrogram morphology.

Electrogram pattern recognition by way of morphologic analysis has been proposed as a technique that may improve discrimination of ventricular tachycardia from sinus rhythm by antitachycardia devices. The potential impact that increases in heart rate and sympathetic tone could have on such techniques, however, has not been previously determined. A comparative study was undertaken to quantify possible changes in ventricular electrogram morphology using correlation waveform, area of difference, and amplitude analyses in 6 patients during atrial overdrive pacing at cycle lengths of 600 and 400 ms (group A), in 13 patients during infusions of physiologic doses of epinephrine (group B), and in 20 patients undergoing infusions of isoproterenol (group C). Four patients were in both groups A and B. A bipolar intraventricular template of cardiac depolarization during sinus rhythm at rest was compared with depolarization during subsequent passages of sinus rhythm at rest and subsequently increased heart rate. In 36 of 39 patients, waveform configuration as assessed by correlation waveform analysis remained relatively stable during atrial overdrive pacing, epinephrine infusion, and isoproterenol infusion when compared with sinus rhythm at rest. The correlation value did not fall below 0.950 in any patient. Area of difference values for the same 36 patients changed by an average of 6 and 37% during atrial overdrive pacing at cycle lengths of 600 and 400 ms intervals, respectively, by 3% during epinephrine infusion, and by 17% during isoproterenol infusion. In these same patients, there was an average change in electrogram amplitude of -1% during atrial overdrive pacing at 600 ms, 26% during pacing at 400 ms, -1% during epinephrine infusion, and 12% during isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac arrest and sudden death in patients treated with amiodarone for sustained ventricular tachycardia or ventricular fibrillation: risk stratification based on clinical variables.

Multivariate analysis of 11 clinical variables was performed in 104 patients with sustained, symptomatic ventricular tachycardia (VT) or ventricular fibrillation treated with amiodarone to determine variables predictive of subsequent cardiac arrest or sudden death. Twenty-five patients (24%) had fatal or nonfatal cardiac arrest after 7.3 +/- 6.2 months (mean +/- standard deviation) of therapy. Multivariate analysis identified an ejection fraction of less than 0.40, syncope or cardiac arrest before amiodarone therapy, and VT (3 or more consecutive ventricular premature complexes) during predischarge ambulatory electrocardiographic monitoring as variables associated with a high risk of subsequent fatal or nonfatal cardiac arrest (p less than 0.03). Patients who had these 3 clinical variables had a much higher predicted incidence of cardiac arrest at 6 months (62%) and 12 months (76%) than did patients with an ejection fraction greater than 0.40, without syncope or cardiac arrest before amiodarone therapy, and without VT during predischarge ambulatory electrocardiographic monitoring (2% and 5%, respectively) (p less than 0.02). Risk stratification using clinical variables can predict which patients are at high risk of recurrent cardiac arrest or sudden death during amiodarone therapy.

The role of beta-blockade therapy for ventricular tachycardia induced with isoproterenol: a prospective analysis.

Isoproterenol is sometimes required for ventricular tachycardia (VT) induction. However, the role of beta-blockade for treatment of such VT has not been critically assessed. The use of beta-blockade was evaluated prospectively in 14 consecutive patients who required isoproterenol 2.4 +/- 1.3 (+/- S.D.) micrograms/min to induce sustained monomorphic VT (greater than 30 seconds, or requiring termination due to hemodynamic collapse) after a negative baseline study. The VT mechanisms were enhanced automaticity (group A, six patients), triggered automaticity (group B, three patients), and reentry (group C, five patients). Groups A and B had serial intravenous electropharmacologic tests with propranolol alone (0.2 mg/kg), verapamil alone (0.15 mg/kg), and propranolol plus verapamil, and group C had serial tests with propranolol alone, procainamide or quinidine (class Ia drug) alone, and propranolol plus a class Ia drug until VT could no longer be induced. All six patients in group A responded to propranolol alone. In group B, one patient responded to verapamil alone, and two patients responded to propranolol plus verapamil. In group C, three patients responded to propranolol alone, one patient responded to a class Ia drug alone, and one patient responded to propranolol plus a class Ia drug. During a follow-up of 7 to 37 (17.9 +/- 10.7) (+/- S.D.) months, VT has not recurred in any patient. Three patients treated initially with propranolol alone have required substitution of amiodarone due to refractory congestive heart failure. In patients requiring isoproterenol for VT induction, beta-blockade alone appears to be effective in preventing reinduction of VT caused by enhanced automaticity. A heterogeneous response occurs when the VT mechanisms are triggered automaticity or reentry.

Driving restrictions advised by midwestern cardiologists implanting cardioverter defibrillators: present practices, criteria utilized, and compatibility with existing state laws.

Although some patients remain at risk of losing physical control or collapsing after implantation of a cardioverter defibrillator for sustained ventricular arrhythmias, little is known about restrictions advised by arrhythmia specialists to patients with implanted devices concerning physical activities such as driving. In this study, all of the 58 cardiologists implanting cardioverter defibrillators in three contiguous midwestern states were surveyed to determine present practices and the compatibility of these practices with existing state law. Of the 51 respondents (88%), 27 cardiologists (53%) advised only those implanted patients who had had arrhythmia-induced presyncope or physical collapse to cease driving. Twenty two of the remaining cardiologists (43%) advised all implanted patients to cease driving, whereas two cardiologists (4%) never advised any implanted patient to restrict driving. Permanent driving abstinence was advised by seven of the responding cardiologists (14%), while temporary driving abstinence for periods of 2-12 months (mean 6 +/- 3 months) was recommended by the remaining 42 respondents (82%) who advised against driving. The criteria utilized, driving restrictions advised, and durations advised for driving restrictions were not uniform in any of the 13 surveyed university and nonaffiliated cardiology practices with greater than or equal to 2 implanting cardiologists. Overall, 38 cardiologists (74%) advised against driving and recommended durations that equaled or exceed their state's minimum legal requirements, although only 27 of the 51 cardiologists (53%) based their practice upon knowledge of their state's driving laws. The results of this survey suggest that the majority of cardiologists who implant cardioverter defibrillators advise their patients against driving postoperatively.(ABSTRACT TRUNCATED AT 250 WORDS)

Paroxysmal bundle branch block of supraventricular origin: a possible source of misdiagnosis in detecting ventricular tachycardia using time domain analyses of intraventricular electrograms.

Current implantable antitachycardia devices use several methods for differentiating sinus rhythm (SR) from supraventricular tachycardia (SVT) or ventricular tachycardia (VT). These methods include sustained high rate, the rate of onset, changes in cycle length, and sudden onset. Additional methods for detecting VT include techniques based upon ventricular electrogram morphology. The morphological approach is based on the assumption that the direction of cardiac activation, as sensed by a bipolar electrode in the ventricle, is different when the patient is in SR as compared to VT. Whether paroxysmal bundle branch block of supraventricular origin (BBB) can be differentiated from VT has not been determined. In this study, we compared the morphology of the ventricular electrogram during sinus rhythm with a normal QRS (SRNIQRS) or SVT with a normal QRS (SVTNIQRS) with the morphologies of BBB and VT in 30 patients undergoing cardiac electrophysiology studies. Changes in ventricular electrogram morphology were determined using three previously proposed time domain methods for VT detection: Correlation Waveform Analysis (CWA), Area of Difference (AD), and Amplitude Distribution Analysis (ADA). CWA, AD, and ADA distinguished VT from SRNIQRS or SVTNIQRS in 16/17 (94%), 14/17 (82%), and 12/17 (71%) patients, and BBB from SRNIQRS or SVTNIQRS in 15/15 (100%), 13/15 (87%), and 6/15 (40%) patients, respectively. However, the ranges of values during BBB using these methods overlapped with ranges of values during VT in all cases for CWA, AD, and ADA. Hence, BBB may be a source of misdiagnosis in detecting VT when these time domain methods are used for ventricular electrogram analysis.

Ventricular tachycardia detection using bipolar electrogram analysis is site specific.

While algorithms for bipolar intraventricular electrogram analysis have potential use in complementing rate criteria for ventricular tachycardia (VT) detection by implantable antitachycardia devices, the sensitivity of such algorithms to the intracavitary site of electrogram detection has not been determined. In this study, unfiltered (1-500 Hz) electrograms were recorded from a bipolar electrode catheter initially positioned at the right ventricular (RV) apex (site 1) of 12 patients during sinus rhythm (SR1) and during induced monomorphic VT (VT1). Sinus rhythm (SR2) and the identical VT (VT2) were recorded a second time after repositioning the same electrode catheter within the RV apex (site 2) 7-44 mm (mean +/- SD = 15 +/- 10) from its original site. The data were digitized at 1,000 Hz. Templates from SR1 and SR2, respectively, were compared subsequently with individual intraventricular electrograms from 15-25 sec passages of SR1 and VT1 and SR2 and VT2, respectively, using correlation waveform analysis. At site 1, the mean patient correlation coefficient ranged from 0.982-0.998 during SR1 and 0.062-0.975 during VT1. At site 2, the mean patient correlation coefficient ranged from 0.995-0.998 during SR2 and 0.113-0.983 during VT2. Using a correlation threshold of 0.9, VT was differentiated from SR in 11/12 patients (91%) overall: 8/12 patients (67%) at site 1, 9/12 patients (75%) at site 2, and 6/12 patients (50%) at both sites. Thus, while discrimination of VT from SR is feasible with morphological analysis of bipolar right ventricular intracavitary electrograms, the accuracy of bipolar intraventricular electrogram analysis may depend upon intracavitary electrode location in selected patients.

Identification of ventricular tachycardia using intracardiac electrograms: a comparison of unipolar versus bipolar waveform analysis.

Implantable antitachycardia devices suffer a high false-positive rate of delivery of therapy because current detection schemes based upon ventricular rate and rate variations are excessively sensitive at the cost of specificity. Several methods have been proposed for providing complementary information derived from morphologic analysis of intraventricular electrograms in order to increase specificity. The majority of these techniques have utilized bipolar electrogram analysis to detect changes in ventricular activation indicative of ventricular tachycardia. Whether bipolar or unipolar intracardiac electrogram analysis might be preferred for discriminating ventricular tachycardia from sinus rhythm has not been determined. In this study, a previously demonstrated method for identification of ventricular tachycardia using intracardiac electrograms, correlation waveform analysis, was used to analyze both unipolar and bipolar signals during sinus rhythm and ventricular tachycardia recorded during electrophysiology studies of 15 patients with inducible sustained monomorphic ventricular tachycardia. Correlation waveform analysis consistently discriminated between all depolarizations during ventricular tachycardia in 14/15 patients (93%) using either electrogram configuration; 13 of the 14 patients were common to both groups. Of these patients, 8/15 (53%) had greater separation between sinus rhythm and ventricular waveforms with bipolar electrogram analysis while 7/15 (47%) had greater separation with unipolar electrogram analysis. We conclude that morphologic analysis of unipolar and bipolar electrograms may be equally effective in distinguishing ventricular tachycardia from sinus rhythm. For individual patients, either a unipolar or bipolar ventricular configuration may be preferable, and should be chosen on a patient-specific basis during electrophysiology study prior to antitachycardia device implantation.

Discrimination of retrograde from anterograde atrial activation using intracardiac electrogram waveform analysis.

The prevention of pacemaker-mediated tachycardias requires a safe, reliable method for distinguishing retrograde from anterograde atrial activation by dual chamber pacemakers. In this study, a technique was developed to detect the morphological change that occurs in the waveform of the intra-atrial electrogram during retrograde atrial activation. The method employed for waveform analysis is based upon statistical correlation. In 19 patients undergoing electrophysiological studies, atrial electrograms were recorded from bipolar endocardial electrodes during sinus rhythm and 1:1 retrograde atrial depolarization while undergoing right ventricular pacing. Data were digitally sampled at 750, 1,000, and 1,500 Hz. Templates of anterograde atrial depolarization were constructed by signal averaging waveforms from an initial sinus rhythm passage. These were used for analysis of anterograde depolarizations from a subsequent passage of sinus rhythm and a passage of known retrograde atrial depolarization. In all 19 cases, a patient-specific threshold could be derived to separate anterograde from retrograde atrial depolarizations using 1,000 Hz and 1,500 Hz sampling rates. However, at a sampling rate of 750 Hz, separation of anterograde from retrograde atrial activation was possible in only 16/19 patients (84%). We conclude that correlation waveform analysis of a suitably sampled atrial electrogram is a reliable method of discriminating retrograde atrial depolarization from anterograde atrial depolarization in intracardiac electrograms.

Histologic changes and arrhythmogenicity after discharge through transseptal catheter electrode.

Ventricular tachycardia commonly arises within the intraventricular septum and successful catheter ablation of septal tachycardia might be enhanced by transseptal electrode placement. We have evaluated the safety of a transseptal ablation procedure. Arrhythmogenicity and histology were examined after high-energy capacitor discharges were delivered to an intracavitary cathode-anode pair placed on opposite sides of the interventricular septum in pentobarbital-anesthetized dogs. After two discharges of 200 or 100 J proved lethal, paired discharges of 30 or 50 J (10 dogs) or a single discharge of 100 J (four dogs) was used to induce 28 lesions. Acute rhythm changes and risk of induction of ventricular tachycardia by programmed stimulation were measures of arrhythmogenicity. Gross and histologic examination of the hearts after 20 min to 28 days allowed characterization of the evolution of lesions. The conduction system in nearby and remote locations was extensively examined in four dogs. Refractory ventricular fibrillation developed with paired shocks at 200 or 100 J. At lower energy levels, acute ventricular fibrillation occurred with 12 of 20 shocks (60%), but defibrillation was consistently achieved. After ablation, no dog had ventricular tachycardia or fibrillation induced with programmed stimulation. Matching anodal and cathodal lesions spanned the septum without perforation in 10 of 16 dogs, and the lesions were of similar histology. Each contained central areas of hemorrhage surrounded by a region of coagulation necrosis merging with normal myocytes peripherally. There was necrosis and edema without inflammation at 20 min, acute inflammatory cell infiltration at 1 to 2 days, and myocyte replacement by granulation tissue after 6 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy and safety of transcatheter ablation of posteroseptal accessory pathways.

Eight patients with a posteroseptal accessory pathway and symptomatic atrial fibrillation and/or orthodromic reciprocating tachycardia underwent attempted transcatheter ablation of the accessory pathway. A quadripolar electrode catheter was positioned within the coronary sinus such that the proximal pair of electrodes straddled the os. This proximal pair of electrodes was made electrically common and connected to the cathodal output of a defibrillator. A patch electrode placed over the midthoracic spine was connected to the anodal sink of the defibrillator. Two to three transcatheter shocks were delivered, with a cumulative energy of 600 to 900 J. Immediately after the shocks were delivered, retrograde accessory pathway conduction was absent in each patient. Anterograde conduction through the posteroseptal accessory pathway was absent in six patients. In one patient, retrograde accessory pathway conduction was absent and anterograde conduction was present but was slower than at baseline. In this patient, orthodromic tachycardia was no longer inducible and the ventricular rate during induced atrial fibrillation was 150 beats/min, compared with 220 beats/min before the attempted ablation. He has remained asymptomatic without antiarrhythmic drug therapy for 18 months. In one patient, the transcatheter shocks had no long-term effect on accessory pathway conduction. The shocks delivered at the os of the coronary sinus were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Catheter ablation of ventricular tachycardia with intracardiac shocks: results in 33 patients.

Catheter electrical ablation of ventricular tachycardia (VT) was attempted in 33 patients who had recurrent unimorphic VT refractory to 3.7 +/- 1.2 (mean +/- SD) antiarrhythmic drugs. Their mean age was 56 +/- 14 years. Twenty-two patients had coronary artery disease, six had other types of heart disease, and five had no structural heart disease. The mean left ventricular ejection fraction was 0.34 +/- 0.17. Thirty patients had only one documented morphologic type of spontaneous VT, whereas three patients had more than one. One to four shocks of 100 to 300 J each were delivered to the endocardial exit site of VT, as identified by endocardial activation mapping and pace-mapping. In each patient endocardial activation at the exit site of VT preceded the onset of the QRS complex (mean activation time -50 +/- 30 msec). Pace-mapping was possible in 26 patients, and in all but two patients the QRS complexes during VT and during pacing at the exit site of VT were very similar in at least 10 of 12 electrocardiographic leads. In 29 patients, shocks were delivered between an endocardial electrode (cathode) and a patch electrode on the chest wall (anode). Seven patients (including three who first received shocks using an external anode) whose VT originated in the septum received transseptal shocks between two electrodes positioned on either side of the septum. The procedure was successful in 15 patients (45%), who had no recurrence of VT either on no antiarrhythmic therapy or on the same regimen that was ineffective before ablation, over a follow-up period of 15.5 +/- 10 months (range 5 to 35). The ablation attempt was unsuccessful in 18 patients (55%). There were no significant differences in clinical and electrophysiologic variables between patients with and without a successful outcome. Seven nonfatal complications occurred in six patients: sustained nonclinical VT immediately after the shock, ventricular fibrillation on days 5 and 6 after ablation, neurologic deficits (n = 2), atrioventricular block (n = 2), and brachial artery thrombosis. In conclusion, catheter electrical ablation of VT has modest efficacy and is relatively safe in a selected group of patients who have predominantly one configuration of unimorphic VT.