Outcomes of Catheter Ablation of Ventricular Tachycardia in the Setting of Structural Heart Disease.

Sustained ventricular tachycardias are common in the setting of structural heart disease, either due to prior myocardial infarction or a variety of non-ischemic etiologies, including idiopathic dilated cardiomyopathy, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy. Over the past two decades, percutaneous catheter ablation has evolved dramatically and has become an effective tool for the control of ventricular arrhythmias. Single and multicenter observational studies as well as several prospective randomized trials have begun to investigate long-term outcomes after catheter ablation procedures. These studies encompass a wide range of mapping and ablation techniques, including conventional activation mapping/entrainment criteria, substrate modification guided by pacemapping, late potential and abnormal electrogram ablation, scar de-channeling, and core isolation. While large-scale, multicenter prospective randomized clinical trials are somewhat limited, the published data demonstrate favorable outcomes with respect to a reduction in overall ventricular tachycardia (VT) burden, reduction of implantable cardioverter defibrillator (ICD) shocks, and discontinuation of anti-arrhythmic medications across varying disease subtypes and convincingly support the use of catheter ablation as the standard of care for many patients with VT in the setting of structural heart disease.

Ablation of ventricular tachycardia.

Ablation is an important management tool for the treatment of ventricular arrhythmias. Even at experienced centers ventricular tachycardia ablation carries a minor but significant risk for potential complications, including vascular and thromboembolic complications, air embolism, volume overload and the precipitation of congestive heart failure, cardiac tamponade from catheter perforation or from steam pop with RF energy delivery, valve or subvalvular support structure disruption, conduction system disruption with development of heart block, coronary artery injury when ablating in the coronary cusps region or trying to gain access to the LV chamber, precipitation of cardiogenic shock from ablation of viable myocardium in patients with marginal reserve and failure to resuscitate or precipitation of cardiogenic shock from repeated VT induction, and with epicardial ablation the potential complications of epicardial access, coronary arteries and phrenic nerve damage. Recognition of these risks is paramount for their avoidance with careful pre-procedure planning and intraprocedural technique being essential to minimize the potential for complications.

Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy.

BACKGROUND: Conventional activation mapping is difficult without inducible, stable ventricular tachycardia (VT). METHODS AND RESULTS: We evaluated 16 patients with drug refractory, unimorphic, unmappable VT. Nine patients had ischemic and 7 had nonischemic cardiomyopathy. All patients had implantable defibrillators and had experienced 6 to 55 VT episodes during the month before treatment. Patients underwent bipolar catheter mapping during baseline rhythm. The amount of endocardium with an abnormal electrogram amplitude was estimated using fluoroscopy in 3 patients and a magnetic mapping system (CARTO) in 13 patients. For the magnetic mapping, normal endocardium was defined by an amplitude >1.5 mV; this measurement was based on sinus rhythm maps in 6 patients who did not have structural heart disease. Radiofrequency point lesions extended linearly from the "dense scar," which had a voltage amplitude <0.5 mV, to anatomic boundaries or normal endocardium. To limit radiofrequency applications, 12-lead ECG during VT and pacemapping guided placement of linear lesions. No new antiarrhythmic drug therapy was added. The amount of endocardium demonstrating an abnormal electrogram amplitude ranged from 25 to 127 cm(2). A total of 8 to 87 radiofrequency lesions (mean, 55) produced a median of 4 linear lesions that had an average length of 3.9 cm (range, 1.4 to 9. 4 cm). Twelve patients (75%) have been free of VT during 3 to 36 months of follow-up (median, 8 months); 4 patients had VT episodes at 1, 3, 9, and 13 months, respectively. Only one of these patient had frequent VT. CONCLUSIONS: Radiofrequency linear endocardial lesions extending from the dense scar to the normal myocardium or anatomic boundary seem effective in controlling unmappable VT.

Electroanatomic left ventricular mapping in the porcine model of healed anterior myocardial infarction. Correlation with intracardiac echocardiography and pathological analysis.

BACKGROUND: Catheter ablation for ventricular tachycardia in healed infarction is limited to patients with inducible, tolerated arrhythmias. Strategies that would allow mapping during sinus rhythm might obviate this limitation. METHODS AND RESULTS: Two sets of experiments were performed in adult pigs to refine a new technique for left ventricular mapping. First, detailed endocardial maps were done in 5 normal pigs and 7 pigs 6 to 10 weeks after left anterior descending coronary artery infarction to characterize electrograms in normal and infarcted tissue by electroanatomic mapping (CARTO, Biosense). Electrogram recording sites were verified by intracardiac echo (ICE, 9 MHz) and grouped by location: infarct (area of akinesis by ICE), border (0.5-cm perimeter of akinetic area), and remote. Compared with remote sites, electrograms from infarct sites had smaller amplitudes (1.2+/-0.5 versus 5.1+/-2.1 mV, P<0.001), longer durations (74.2+/-26.3 versus 36.3+/-6.4 ms, P<0.001), and more frequent notched or late components. Border zone electrograms were intermediate in amplitude and duration. Second, infarct characterization by electroanatomic mapping was compared with pathological (exclusion of triphenyltetrazolium chloride staining) and ICE measurements. Infarct size by pathology correlated with the area defined by contiguous electrograms with amplitude

Living anatomy of the atrioventricular junctions. A guide to electrophysiologic mapping. A Consensus Statement from the Cardiac Nomenclature Study Group, Working Group of Arrhythmias, European Society of Cardiology, and the Task Force on Cardiac Nomenclature from NASPE.

Current nomenclature for the atrioventricular (AV) junctions derives from a surgically distorted view, placing the valvar rings and the triangle of Koch in a single plane with antero-posterior and right-left lateral coordinates. Within this convention, the aorta is considered to occupy an anterior position, although the mouth of the coronary sinus is shown as being posterior. Although this nomenclature has served its purpose for the description and treatment of arrhythmias dependent on accessory pathways and atrioventricular nodal reentry, it is less than satisfactory for the description of atrial and ventricular mapping. To correct these deficiencies, a consensus document has been prepared by experts from the Working Group of Arrhythmias of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology. It proposes a new anatomically sound nomenclature that will be applicable to all chambers of the heart. In this report, we discuss its value for description of the AV junctions, establishing the principles of this new nomenclature.

Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: evidence for distinct mechanisms.

To determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infused at a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia. The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 +/- 4 vs. 7.4 +/- 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 +/- 78 vs. 450 +/- 81 ms, p = NS) and QRS duration (184 +/- 38 vs. 185 +/- 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of pacing current strength on indexes of myocardial activation in humans: influence of chronic infarction and polarity of pacing.

The effects of current strength (threshold to 20 mA) and pacing polarity (bipolar versus unipolar) on indexes of ventricular activation during endocardial pacing (cycle length 400 to 500 ms) from 10 normal and 17 abnormal left ventricular sites were assessed in 19 patients. Abnormal sites were infarcted and demonstrated an electrogram duration greater than 70 ms and amplitude less than 3 mV during sinus rhythm. Bipolar pacing was performed from poles 1 (cathode) and 3 (1 cm interelectrode distance) of a quadripolar catheter. Unipolar cathodal pacing was performed from the tip electrode (pole 1). Local activation was indexed by the interval from the pacing stimulus to 1) the onset of the QRS complex, 2) the largest rapid deflection of the local electrogram, and 3) the end (total duration) of the local electrogram recorded from poles 2 and 4 of the quadripolar catheter used for left ventricular pacing. Distant activation was indexed by the interval from pacing stimulus to electrograms recorded at the right ventricular apex and outflow tract. Bipolar and unipolar pacing of normal sites produced a modest homogeneous reduction of all activation times by 3 to 11 ms (median) with increments in current strength from threshold (0.8 mA) to 20 mA. Bipolar pacing of abnormal sites showed marked (up to 110 ms) and heterogeneous changes in local (median 22 to 30 ms) as well as distant (median 14 to 23 ms) activation times with increases in current strength from threshold (2.7 mA) to 20 mA.(ABSTRACT TRUNCATED AT 250 WORDS)

Arrhythmias induced by device antitachycardia therapy due to diagnostic nonspecificity.

New technology has produced automatic cardioverter-defibrillators capable of delivering antitachycardia pacing, as well as low and high energy shocks and backup bradycardia pacing. These expanded treatment options have led to a wider range of clinical applications for such devices, including the treatment of ventricular tachycardias with longer cycle lengths, which may overlap the cycle lengths of some supraventricular arrhythmias. The diagnostic capability of these devices, although improved, has not advanced sufficiently to ensure reliable discrimination between all supraventricular and ventricular arrhythmias. Two cases are presented in which device-mediated pacing therapy, triggered by supraventricular arrhythmias, induced ventricular tachycardia requiring additional therapeutic intervention. This report illustrates the therapeutic versatility and some of the potential pitfalls, of the recently developed devices and reviews the status of automatic arrhythmia identification technology.

Value of ventricular electrogram recordings in the diagnosis of arrhythmias precipitating electrical device shock therapy.

An antitachycardia pacemaker-cardioverter-defibrillator that is capable of storing ventricular electrograms before and after delivery of device shock therapy was implanted in 16 patients. Three of the patients experienced out-of-hospital device shock therapy preceded by minimal symptoms. Although limitations of electrogram analysis exist and are discussed, careful analysis and registration of electrograms during all supraventricular and ventricular rhythms observed during in-hospital testing served as an important reference for subsequent arrhythmia diagnosis. By analyzing the electrogram rate and RR interval stability and configuration, a definitive diagnosis was established in all three patients (atrial fibrillation, polymorphic ventricular tachycardia and rate-sensing lead disruption, respectively). Thus, the ability to store ventricular electrograms before shock therapy represents a major advance in the management of patients who receive an electrical device to treat ventricular tachyarrhythmia.

Sustained ventricular tachyarrhythmias during the early postinfarction period: electrophysiologic findings and prognosis for survival.

Forty patients with sustained tachycardia occurring 3 to 65 days after myocardial infarction underwent programmed ventricular stimulation within 3 months of the infarction. Patients were characterized clinically by a complicated initial 48 hours of hospitalization for their acute infarction (85% of study group). The development of bundle branch block in association with infarction occurred with an unusually high frequency (32%). Ventricular tachycardia similar in configuration to spontaneous arrhythmia was induced with programmed ventricular stimulation in 33 (83%) of the 40 patients. In 15 (45%) of these 33 patients, additional morphologically distinct ventricular tachycardia not seen clinically was initiated. The induction of ventricular tachycardia was not significantly related to the time after myocardial infarction at which spontaneous ventricular tachycardia was initially observed. Only 20 of the 40 patients are alive after a mean follow-up period of 20 +/- 15 months. Twelve of the 20 deaths were sudden cardiac deaths. Sixteen of the 33 patients with inducible ventricular tachycardia died; 8 of the 16 deaths were sudden. By comparison, four of the seven patients with no inducible ventricular tachycardia died (probability [p] = not significant), all suddenly. The mode of therapy did not influence subsequent survival. It appears that in patients with sustained ventricular tachycardia occurring more than 48 hours after a recent myocardial infarction, ventricular tachycardia similar to that clinically observed can usually be induced by programmed stimulation. In addition, multiple morphologically distinct ventricular tachycardias, some of which have not been previously observed, are frequently induced. Finally, the prognosis for survival is poor, regardless of inducibility or mode of therapy, and may in part be related to a changing arrhythmia substrate.

Effect of rate and coupling interval on endocardial R wave amplitude variability in permanent ventricular sensing lead systems.

OBJECTIVES: We have observed sensing errors in third generation implantable cardioverter-defibrillators that appear to be caused by variation in the R wave amplitude during sinus rhythm, particularly after premature beats. The purpose of this study was to quantify spontaneous R wave variability during sinus rhythm and to determine whether abrupt changes in cycle length further augment R wave amplitude variability. BACKGROUND: Pacemaker sensing algorithms presume a relatively constant R wave signal to establish a sensing threshold. The concept of a fixed sensing threshold is not as applicable in third-generation cardioverter-defibrillators, which depend on automatic gain amplifiers to rapidly detect ventricular fibrillation. These devices may be susceptible to undersensing during sinus rhythm if significant variability in R wave signal characteristics occurs. METHODS: Twelve patients with combination bradycardia pacing cardioverter-defibrillators were studied. The device used (Cadence, Ventritex) allowed recording of real time, telemetered electrograms from the sensing lead system. Measurements were made of the maximal range of the R wave amplitude during sinus rhythm and in response to abrupt changes in heart rate produced by premature atrial and ventricular stimuli. RESULTS: The maximal range in R wave amplitude during sinus rhythm was 1.7 +/- 1.3 mV, or 23.7 +/- 19.2% of the mean R wave amplitude. The R wave amplitude variability increased with abrupt changes in cycle length, with a range of 2.8 +/- 1.5 mV, or 38.8 +/- 18.3% of the mean R wave amplitude (p < 0.05 compared with sinus rhythm). In most patients, R wave amplitude and coupling interval demonstrated an inverse proportional relation. CONCLUSIONS: There is substantial variability in the R wave amplitude during sinus rhythm measured by permanent ventricular sensing lead systems, and this variability is further augmented by abrupt changes in cycle length. This phenomenon may explain the occurrence of undersensing of sinus rhythm in implantable cardioverter-defibrillators with automatic gain sense amplifiers.

Importance of abortive shock capability with electrogram storage in cardioverter-defibrillator devices.

OBJECTIVES: This study evaluates the ability of a third-generation cardioverter-defibrillator to abort energy delivery and the importance of electrogram storage in analyzing the aborted events. BACKGROUND: In the Cadence Tiered Therapy Defibrillator, when a tachycardia satisfies detection criteria for cardioversion or defibrillation therapy, high voltage capacitors begin charging. The Cadence defibrillator continues monitoring the rhythm during charging and if the rate decreases to below the rate triggering therapy, charging is terminated. This event is registered as an aborted shock. The defibrillator also has the ability to store intracardiac electrogram recordings of the electrical events that precipitate device therapy or aborted shocks. METHODS: During a mean follow-up interval of 10 +/- 7 months, 55 aborted events were registered by the Cadence defibrillator in 18 of the 49 patients who received it. Thirty-two stored ventricular electrograms of events leading to aborted shocks were available for analysis in 15 patients. RESULTS: Intracardiac electrogram recordings demonstrated the probable electrical events leading to these aborted shocks included nonsustained ventricular tachycardia (n = 10), nonsustained rapid polymorphic ventricular tachycardia/ventricular fibrillation (n = 2), atrial fibrillation (n = 5), supraventricular tachycardia (n = 2) and electrical noise (n = 13). Eleven patients had a therapeutic intervention initiated as a consequence of the diagnostic information provided by analysis of intracardiac electrogram recordings. Four of the 15 patients had no changes made. During a follow-up period of 9 +/- 5 months after therapy was altered, no patient had subsequent aborted shocks. Five patients have had seven appropriate shocks for sustained ventricular tachycardias. CONCLUSIONS: The ability of Cadence defibrillator to continue tachycardia sensing during capacitor charging and to abort shock therapy for self-terminating events prevented unnecessary shocks in 18 (37%) of the 49 patients. Intracardiac electrogram recordings were critical for instituting appropriate therapy that may have prevented unnecessary device charging and inappropriate discharges.

Polymorphic ventricular tachycardia induced by programmed stimulation: response to procainamide.

OBJECTIVES: This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). BACKGROUND: Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. METHODS: Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. RESULTS: We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p < 0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. CONCLUSIONS: The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the application of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

Usefulness of electrophysiologic study to determine the clinical tolerance of arrhythmia recurrences during amiodarone therapy.

The relation of clinical and electrophysiologic variables to outcome was evaluated in 121 patients treated with amiodarone for sustained ventricular tachyarrhythmias. Electrophysiologic study was performed in all patients a mean of 14 days after beginning amiodarone therapy. Forty-six patients who were given oral amiodarone therapy experienced arrhythmia recurrence. Multivariate analysis was performed using 16 clinical and electrophysiologic variables to determine which factors were associated with 1) arrhythmia recurrence and 2) a poorly tolerated arrhythmia recurrence (that is, cardiac arrest or sudden cardiac death) during oral amiodarone therapy. No variable predicted arrhythmia recurrence. Five variables correlated significantly with a poorly tolerated arrhythmia recurrence. Hemodynamic stability of the arrhythmia induced on electrophysiologic testing during amiodarone therapy had the best predictive value (p less than 0.001). Younger age, lower ejection fraction, a poorly tolerated rhythm at clinical presentation and absence of left ventricular aneurysm were also associated with a poorly tolerated arrhythmia recurrence. Only 3 of 57 patients who had a well tolerated arrhythmia induced on electrophysiologic testing during amiodarone therapy had recurrence of a poorly tolerated arrhythmia versus 19 of 47 who had hemodynamically unstable arrhythmias induced during amiodarone therapy (p less than 0.001). Thus, electrophysiologic testing during amiodarone therapy appears useful in identifying patients who are prone to have catastrophic arrhythmia recurrences and could allow for the institution of additional or alternative modes of therapy.

Characterization of the excitable gap in human type I atrial flutter.

OBJECTIVES: We sought to characterize the excitable gap of the reentrant circuit in atrial flutter. BACKGROUND: The electrophysiologic substrate of typical atrial flutter has not been well characterized. Specifically, it is not known whether the properties of the tricuspid valve isthmus differ from those of the remainder of the circuit. METHODS: Resetting was performed from two sites within the circuit: proximal (site A) and distal (site B) to the isthmus in 14 patients with type I atrial flutter. Resetting response patterns and the location where interval-dependent conduction slowing occurred were assessed. RESULTS: Some duration of a flat resetting response (mean +/- SD 40.1 +/- 20.9 ms, 16 +/- 8% of the cycle length) was observed in 13 of 14 patients; 1 patient had a purely increasing response. During the increasing portion of the resetting curve, interval-dependent conduction delay most commonly occurred in the isthmus. In most cases, the resetting response was similar at both sites. In three patients, the resetting response differed significantly between the two sites; this finding suggests that paced beats may transiently change conduction within the circuit or the circuit path, or both. CONCLUSIONS: Some duration of a flat resetting response was observed in most cases of type I atrial flutter, signifying a fully excitable gap in all portions of the circuit. The isthmus represents the portion of the circuit most vulnerable to interval-dependent conduction delay at short coupling intervals.

Repetitive monomorphic tachycardia from the left ventricular outflow tract: electrocardiographic patterns consistent with a left ventricular site of origin.

OBJECTIVES: This study sought to characterize the electrocardiographic patterns predictive of left ventricular sites of origin of repetitive monomorphic ventricular tachycardia (RMVT). BACKGROUND: RMVT typically arises from the right ventricular outflow tract (RVOT) in patients without structural heart disease. The incidence of left ventricular sites of origin in this syndrome is unknown. METHODS: Detailed endocardial mapping of the RVOT was performed in 33 consecutive patients with RMVT during attempted radiofrequency ablation. Left ventricular mapping was also performed if pace maps obtained from the RVOT did not reproduce the configuration of the induced tachycardia. RESULTS: Pace maps identical in configuration to the induced tachycardia were obtained from the RVOT in 29 of 33 patients. Application of radiofrequency energy at sites guided by pace mapping resulted in elimination of RMVT in 24 (83%) of 29 patients. In four patients (12%), pace maps obtained from the RVOT did not match the induced tachycardia. All four patients had a QRS configuration during RMVT with precordial R wave transitions at or before lead V2. In two patients, RMVT was mapped to the mediosuperior aspect of the mitral valve annulus, near the left fibrous trigone; catheter ablation at that site was successful in both. In two patients, RMVT was mapped to the basal aspect of the superior left ventricular septum. Catheter ablation was not attempted because His bundle deflections were recorded from this site during sinus rhythm. CONCLUSIONS: RMVT can arise from the outflow tract of both the right and left ventricles. RMVTs with a precordial R wave transition at or before lead V2 are consistent with a left ventricular origin.

Narrowing of the superior vena cava-right atrium junction during radiofrequency catheter ablation for inappropriate sinus tachycardia: analysis with intracardiac echocardiography.

OBJECTIVES: The study explored the potential for tissue swelling and venous occlusion during radiofrequency (RF) catheter ablation procedures using intracardiac echocardiography (ICE). BACKGROUND: Transient superior vena cava occlusion has been reported following catheter ablation procedures for inappropriate sinus tachycardia (IST). Presumably, venous occlusion could occur owing to thrombus formation or tissue swelling with resultant narrowing of the superior vena cava-right atrial (SVC-RA) junction. METHODS: Intracardiac echocardiography (9 MHz) was used to guide ablation catheter position and for continuous monitoring during RF application in 13 ablation procedures in 10 patients with IST. The SVC-RA junction was measured prior to and following ablation. Successful ablation was marked by abrupt reduction in the sinus rate and a change to a superiorly directed p-wave axis. RESULTS: Eleven of 13 procedures were successful, requiring 29 +/- 20 RF lesions. Prior to the delivery of RF lesions, the SVC-RA junction measured 16.4 +/- 2.9 mm. With RF delivery, local and circumferential swelling was observed, causing progressive reduction in the diameter of the SVC-RA junction to 12.6 +/- 3.3 mm (24% reduction, p = 0.0001). A reduction in SVC-RA orifice diameter of > or = 30% compared to baseline was observed in five patients. CONCLUSIONS: The delivery of multiple RF ablation lesions, often necessary for cure of IST, can cause considerable atrial swelling and resultant narrowing of the SVC-RA junction. Smaller venous structures, such as the coronary sinus and the pulmonary veins, would also be expected to be vulnerable to this complication. Thus, ICE imaging may be helpful in preventing excessive tissue swelling leading to venous occlusion during catheter ablation procedures.

Postoperative lead-related complications in patients with nonthoracotomy defibrillation lead systems.

OBJECTIVES: This study sought to document postoperative complications attributable to nonthoracotomy defibrillation lead systems in a large cohort. BACKGROUND: The incidence of postoperative complications specifically associated with nonthoracotomy defibrillation lead systems is unknown. METHODS: Postoperative lead-related complications were evaluated in 170 patients with a nonthoracotomy defibrillation lead system who were followed up for a mean (+/- SD) of 17 +/- 12 months. Each system incorporated one or more intravascular leads. In 117 patients (69%), the system incorporated a subcutaneous defibrillation patch. All implantations were performed in an operating room by cardiothoracic surgeons. Defibrillation thresholds were measured at implantation, before hospital discharge (mean 3 +/- 2 days) and at 4 to 18 weeks after implantation. Patients were evaluated every 2 to 3 months after implantation or as indicated by clinical exigency. RESULTS: Twenty-seven patients (15.9%) were diagnosed with a lead-related complication that either extended the initial hospital period or led to a second hospital admission. Complications included endocardial lead or subcutaneous defibrillation patch dislodgment in eight patients (4.7%), which was diagnosed between 2 and 345 days after implantation; endocardial or subcutaneous patch lead fracture in six (3.5%), which was diagnosed between 53 and 600 days after implantation; subcutaneous patch mesh fracture in one, which was diagnosed at 150 days after implantation; subclavian vein thrombosis in three (1.8%), which was diagnosed at 2 to 50 days after implantation; and unacceptably elevated defibrillation threshold (within 5 J of maximal device output) in nine (5.3%), which was documented at one of the two postimplantation evaluations in eight patients or at the time of failure to terminate a spontaneous ventricular tachycardia in one. Seventeen of the 27 patients required reoperation for correction of their complication. In addition, system infection requiring complete explantation occurred in seven other patients (4.1%) at an interval from implantation ranging from 14 to 120 days. CONCLUSIONS: Postoperative complications related to a nonthoracotomy defibrillation lead system were common and frequently required reoperation for correction. The rate of system explantation due to infection was also significant. Postoperative defibrillation testing and vigilant outpatient follow-up evaluation are necessary to ensure normal lead function.

Conduction block in the inferior vena caval-tricuspid valve isthmus: association with outcome of radiofrequency ablation of type I atrial flutter.

OBJECTIVES: We sought to 1) correlate conduction block in the isthmus of the right atrium between the inferior vena cava and the tricuspid annulus with the efficacy of catheter ablation of type I atrial flutter, and 2) characterize the effects of ablative lesions on the properties of isthmus conduction. BACKGROUND: There are few data on the mechanism of persistent suppression of recurrence of atrial flutter by catheter ablation. METHODS: Thirty-five patients with type I atrial flutter underwent catheter mapping and ablation. Radiofrequency lesions were applied in the isthmus. Transisthmus conduction before and after the lesions was assessed during atrial pacing in sinus rhythm from the medial and lateral margins of the isthmus at cycle lengths of 600, 400 and 300 ms and the native flutter cycle length. Isthmus conduction block was defined using multipolar recording techniques. There were three treatment groups: group 1 = radiofrequency energy applied during flutter, until termination (n = 14); group 2 = radiofrequency energy applied during atrial pacing in sinus rhythm from the proximal coronary sinus at a cycle length of 600 ms, until isthmus conduction block was observed (n = 14); and group 3 = radiofrequency energy applied until an initial flutter termination, after which further energy was applied during atrial pacing in sinus rhythm until isthmus conduction block was observed (n = 7). RESULTS: In group 1, after the initial flutter termination, isthmus conduction block was observed in 9 of the 14 patients. In each of these nine patients, flutter could not be reinitiated. In each of the remaining five patients, after the initial flutter termination, isthmus conduction was intact and atrial flutter could be reinitiated. Ultimately, successful ablation in each of these patients was also associated with isthmus conduction block. In groups 2 and 3, isthmus conduction block was achieved during radiofrequency energy application, and flutter could not subsequently be reinitiated. Before achieving conduction block, marked conduction slowing or intermittent block, or both, was observed in some patients. In some patients, isthmus conduction block was pacing rate dependent. In addition, recovery from conduction block was common in the laboratory and had a variable time course. At a mean follow-up interval of 10 months (range 1 to 21), the actuarial incidence of freedom from type I flutter was 80% (recurrence in three patients at 7 to 15 months). CONCLUSIONS: Isthmus conduction block is associated with flutter ablation success. Conduction slowing or intermittent block, or both, in the isthmus can occur before achieving persistent block. Recovery of conduction after achieving block is common. Follow-up has revealed a low rate of flutter recurrence after achieving isthmus conduction block, whether the block was achieved in conjunction with termination of flutter.

Cycle length-dependent effects on normal and abnormal intraventricular electrograms: effect of procainamide.

The effect of procainamide (mean concentration 9.1 +/- 2.0 micrograms/ml) on cycle length-dependent changes in electrographic characteristics was determined in 10 patients with prior myocardial infarction. Intracardiac bipolar electrograms were recorded from an abnormal left ventricular site in the distribution of prior (greater than 6 month) myocardial infarction and from a normal right ventricular site. Pacing was performed for 15 beats from the right ventricular apex at cycle lengths of 600 (or 500), 400 and 300 ms. In the control state, the QRS width, the normal electrogram and in 9 of the 10 patients the abnormal electrogram did not change with decreasing cycle lengths. After procainamide the mean QRS width increased from 203 +/- 32 to 240 +/- 50 ms (+18%, p less than 0.01) at a paced cycle length of 600 (or 500) ms, from 198 +/- 34 to 245 +/- 59 ms (+24%, p less than 0.01) at a paced cycle length of 400 ms and from 197 +/- 36 to 258 +/- 67 ms (+31%, p less than 0.01) at a paced cycle length of 300 ms.(ABSTRACT TRUNCATED AT 250 WORDS)