Ventricular tachycardias mimicking those arising from the right ventricular outflow tract.

INTRODUCTION: Ablation of ventricular tachycardia (VT) arising from the right ventricular outflow tract (RVOT) has proven highly successful, yet VTs with similar ECG features may originate outside the RVOT. METHODS AND RESULTS: We reviewed the clinical, echocardiographic, and ECG findings of 29 consecutive patients referred for ablation of monomorphic VT having a left bundle branch block pattern in lead V1 and tall monophasic R waves inferiorly. Nineteen patients (group A) had VTs ablated from the RVOT, and 10 patients (group B) had VTs that could not be ablated from the RVOT. The QRS morphology during VT or frequent ventricular premature complexes was the only variable that distinguished the two groups. During the target arrhythmia, ECGs of group B patients displayed earlier precordial transition zones (median V3 vs V5; P < 0.001), more rightward axes (90 +/- 4 vs 83 +/- 5; P = 0.002), taller R waves inferiorly (aVF: 1.9 +/- 1.0 vs 2.4 +/- 0.5; P = 0.020) and small R waves in lead V1 (10/10 vs 9/19; P = 0.011). Radiofrequency catheter ablation from the RVOT failed to eliminate VT in any group B patient, but ablation from the left ventricular outflow tract (LVOT) eliminated VT in 2 of 6 patients in whom left ventricular ablation was attempted. CONCLUSION: The absence of an R wave in lead V1 and a late precordial transition zone suggest an RVOT origin of VT, whereas an early precordial transition zone characterizes VTs that mimic an RVOT origin. The latter VTs occasionally can be ablated from the LVOT. Recognition of these ECG features may help the physician advise patients and direct one's approach to ablation.

Interactions between electronic article surveillance systems and implantable cardioverter-defibrillators.

BACKGROUND: In patients with implantable cardioverter-defibrillators (ICDs). inappropriate shocks have been reported with exposure to electronic article surveillance systems. The risk to patients with ICDs of walking through or lingering near surveillance systems requires further investigation. METHODS AND RESULTS: We evaluated the response in ICD function in 170 subjects during a 10- to 15-second midgate walk-through of and during extreme (2 minutes within 6 in of the gate) exposure to 3 common article surveillance systems. Complete testing was done in 169 subjects. During a 10- to 15-second (very slow) walk-through of the 3 surveillance systems, no interactions were observed that would negatively affect ICD function. During extreme exposure (169 subjects) and during extreme exposure and pacing via the ICD (126 subjects), interactions between the ICD and the article surveillance systems were observed in 19 subjects. In 7 subjects, this interaction was clinically relevant and would have likely (3 subjects) and possibly (4 subjects) resulted in ICD shocks. In 12 subjects, the interaction was minor. CONCLUSIONS: It is safe for a patient with an ICD to walk through electronic article surveillance systems. Lingering in a surveillance system may result in an inappropriate ICD shock.

Short-term rapid ventricular pacing prolongs ventricular refractoriness in patients.

BACKGROUND: Traditional concepts suggest that ventricular refractoriness should gradually shorten during rapid pacing and gradually return to baseline after termination of pacing. Animal data, however, have shown that under certain circumstances sustained rapid ventricular rates can prolong refractoriness and action potential duration and, thereby, promote ventricular arrhythmias. METHODS AND RESULTS: In humans we evaluated the effect of rapid pacing (cycle length 400 msec for 30 min from either the right ventricular apex [RVA, 13 patients] or high right atrium [HRA, 11 patients]) on the ventricular effective refractory period (VERP) as measured from the RVA, using the extrastimulus method (drive train 500 msec). A control group of seven patients had serial measurements of VERPs in the absence of pacing. For a given patient, all VERPs were measured at constant stimulus output (twice diastolic threshold) from the same ventricular site and at the same drive train cycle length. VERPs obtained immediately following rapid pacing did not differ from those at baseline (P = 0.46); however, VERPs obtained 15 minutes post pacing were prolonged compared with baseline VERPs (231 +/- 20 msec vs 246 +/- 23 msec, P < 0.0026). Pacing site has no impact on VERP prolongation. There was no effect of time on VERP in the absence of pacing. CONCLUSION: In contrast to traditional concepts of refractoriness, after the termination of sustained rapid ventricular rates, VERP prolonged. This phenomenon could help explain the observation of torsades de pointes in some patients after atrioventricular junction ablation or the administration of a Class IA antiarrhythmic agent to convert atrial fibrillation with rapid ventricular response to sinus rhythm.

Phenylephrine increases T wave shock energy required to induce ventricular fibrillation.

INTRODUCTION: Previous reports in experimental models have suggested that ventricular fibrillation threshold (VFT) can be changed by manipulating cardiac neural tone using agents such as phenylephrine. The purpose of this study was to determine whether phenylephrine increased the energy required to induce VF in humans undergoing such induction using DC energy applied to the T wave. METHODS AND RESULTS: In this prospective investigation, 18 consecutive patients with previously implanted cardioverter defibrillators had induction of VF by placing DC monophasic shocks into the T wave coupled 310 msec after the eighth paced ventricular complex at 400 msec. The T wave shock energy was titrated from 0.2 to 12 J until sustained VF or ventricular tachycardia was induced. Phenylephrine was infused either before the first or second VF induction in a randomized fashion to increase systolic blood pressure by more than 20 mmHg. The mean energy required to induce VF was 1.1 J at baseline and increased to 1.7 J during phenylephrine infusion (P = 0.036). The mean arterial pressure increased from 88 to 114 mmHg (P < 0.001), and the mean sinus cycle length increased from 850 to 1070 msec (P < 0.001). Ten of 13 (77%) patients with sinus cycle length prolongation had increased energy requirements to induce VF compared with only 1 of 5 patients (20%) without sinus cycle length prolongation (P < 0.05). CONCLUSION: Phenylephrine increases VFT in humans presumably by reflex activation of the baroreceptors decreasing sympathetic and/or increasing parasympathetic cardiac efferent effects.

Driving issues related to arrhythmic syncope.

The safety of driving in patients with cardiac arrhythmias is a common concern. Although the risk of driving in these patients cannot be reduced to zero, available data and expert consensus suggest that most patients with arrhythmias can return to driving with a relatively low risk of harm to themselves and others, that is, a risk within the limits deemed acceptable by society. Specific recommendations for allowing patients with various cardiac rhythm abnormalities to drive are reviewed in detail.

Defibrillation shocks over epicardial patches produce sympathetic neural dysfunction in man.

INTRODUCTION: The purpose of this study was to determine the effect of direct current (DC) shocks on cardiac sympathetic innervation in humans using I-123-metaiodobenzylguanidine (MIBG) scintigraphy. Decreased efferent sympathetic neural function has been demonstrated following > 10-J DC shocks delivered through epicardial patch electrodes in dogs. To evaluate the effect of DC shocks on cardiac sympathetic innervation in humans, we performed MIBG scintigraphy in 11 patients (ages 46 to 75 years) prior to and after receiving shocks from an implantable cardioverter defibrillator (ICD). METHODS AND RESULTS: This study was performed during an ICD generator change in 7 patients with epicardial patch electrodes and at the time of initial ICD implantation in 4 patients: 2 with epicardial patch electrodes, and 2 with a transvenous ICD system. All patients had spontaneous and inducible ventricular tachycardia. Prior to ICD implantation and remote from any cardioversions or shocks, baseline MIBG and thallium-201 scintigraphy were performed. Repeat MIBG scintigraphy was performed after delivery of ICD shocks and compared with the baseline scans to determine the effect of the shock on sympathetic neural function. The baseline scans revealed focal areas of reduced MIBG uptake in areas of thallium perfusion defects in all patients except the patient without structural heart disease whose scans were normal. Postshock, patients with epicardial patch electrodes who received at least one 24-J shock and had the postshock MIBG scan performed within 4 hours demonstrated no cardiac uptake of MIBG. Two patients with epicardial patch electrodes had no change in the postshock MIBG scans: 1 had a maximal shock of 20 J, and the other had the postshock scan delayed for 11 hours. The 2 patients with a transvenous lead system demonstrated no change in the postshock MIBG scan when compared with baseline. CONCLUSIONS: This study demonstrates that following DC shocks delivered over epicardial patch electrodes, there is diffuse reduction in MIBG uptake that probably represents cardiac sympathetic neural dysfunction that appears to be transient. Sympathetic function does not appear to be affected by shocks delivered over a transvenous lead system.

Spontaneous echo contrast following delivery of a shock from a transvenous implantable cardioverter defibrillator.

Spontaneous echo contrast has never been described in association with cardiac defibrillation. In this report, we present a patient who developed dense echo contrast as a result of a shock delivered from a transvenous defibrillator system.

Ablative therapy for ventricular arrhythmias.

Radiofrequency catheter ablation techniques have enjoyed successful applications in patients with a wide variety of supraventricular tachycardias, especially the Wolff-Parkinson-White syndrome and atrioventricular nodal reentry. More recent reports have shown successful applications in patients with atrial tachycardias and atrial flutter. In addition to these, there are now reports of success during attempts to use radiofrequency techniques to eliminate ventricular tachycardia (VT), both in patients without structural heart disease (idiopathic VT) and patients with structural heart disease (primarily coronary artery disease). Techniques to map sites for ablation in patients with idiopathic VT usually include identifying early endocardial activation and using pace mapping. Success rates for ablation of idiopathic VT have been very high (over 90%) in patients with VT arising from the right ventricular outflow tract. Success rates have not been quite as high when VTs arising from sites other than the right ventricular outflow tract are targeted in the patient with idiopathic VT. In patients with VT caused by coronary artery disease, early endocardial activation and pace mapping can be unreliable. In these patients, searching for mid-diastolic potentials or showing concealed entrainment have proved more reliable. When these latter techniques are applied, success rates in eliminating a single focus of VT in a patient with coronary artery disease has been reported to be as high as 60% to 80%. Future therapies will include new energy sources, new (larger and/or cooled) electrodes, and multipoint catheter mapping, possibly using body surface mapping techniques.

Elimination of AV nodal reentrant tachycardia with 2:1 VA block by posteroseptal ablation.

AV nodal reentry capable of VA block during tachycardia was successfully eliminated using a posteroseptal ablation pulse delivered well away from the site of earliest atrial activation during tachycardia. A possible explanation is that the arrhythmia represented typical AV nodal reentrant tachycardia with transient intra-atrial conduction block during tachycardia.

Multiple accessory pathways in the permanent form of junctional reciprocating tachycardia.

The permanent form of junctional reciprocating tachycardia (PJRT) has been successfully eliminated by ablation of the accessory pathway responsible for the tachycardia. The coexistence of multiple accessory pathways responsible for different, long RP-interval tachycardias was not documented previously. Five patients with PJRT underwent radiofrequency catheter ablation of accessory pathways. Three of 5 patients had 2 accessory pathways each: 1 had 2 left free wall accessory pathways, another had a right posterior free wall and right posteroseptal pathway, whereas the third had 2 right posteroseptal pathways approximately 1 cm apart. The remaining 2 patients each had 1 right posteroseptal accessory pathway. Seven of 8 pathways were successfully ablated with a median of 3 radiofrequency pulses. No patient developed complications. Peak serum creatine kinase ranged from 131 to 311 IU/liter, with peak MB fraction 7 to 17 IU/liter, or 5 to 11%. Follow-up electrophysiologic study, 29 to 70 days after ablation, revealed no inducible tachycardia and no evidence of accessory pathway conduction, except for the 1 pathway not ablated. All patients remained asymptomatic 17 to 29 months after ablation. Thus, patients with PJRT can have several accessory pathways that can be safely and effectively eliminated with radiofrequency catheter ablation.

Regional cardiac sympathetic denervation in patients with ventricular tachycardia in the absence of coronary artery disease.

OBJECTIVES: The aim of this study was to determine whether patients with ventricular arrhythmias in the absence of coronary artery disease also have abnormalities in sympathetic innervation. BACKGROUND: We have previously shown by cardiac sympathetic scintigraphy using iodine-123-metaiodobenzylguanidine (I-123-MIBG) that patients with ventricular tachycardia after myocardial infarction have regional cardiac sympathetic denervation. It is not known whether patients with ventricular tachycardia in the absence of coronary artery disease also have regional cardiac sympathetic denervation. METHODS: We performed cardiac I-123-MIBG and thallium-201 single-photon emission computed tomographic (SPECT) scans at rest in 18 patients (mean age 47 +/- 18 years) with cardiomyopathy (n = 6), left ventricular hypertrophy (n = 1), valvular disease (n = 2) or a structurally normal heart (n = 9) who presented with monomorphic (n = 15) or polymorphic (n = 3) ventricular tachycardia. These scans were compared with scans in 12 control patients without ventricular tachycardia (mean age 30 +/- 17 years) who had cardiomyopathy (n = 3) or a structurally normal heart (n = 9). Cardiac sympathetic denervation was defined as myocardial areas having thallium uptake with reduced or absent I-123-MIBG uptake. RESULTS: Twelve (67%) of 18 patients with ventricular tachycardia had regional cardiac sympathetic denervation compared with 1 (8%) of 12 patients who did not have ventricular tachycardia (p = 0.002). In the nine patients with a structurally normal heart and ventricular tachycardia, five (55%) patients had regional cardiac sympathetic denervation compared with zero of nine control patients with a structurally normal heart (p = 0.029). Five patients underwent right ventricular radiofrequency ablation for ventricular tachycardia, and sympathetic denervation was adjacent to the ablation site in one of these patients. CONCLUSIONS: Patients with ventricular tachycardia in the absence of coronary artery disease have abnormal cardiac sympathetic innervation detectable by cardiac sympathetic scintigraphy. The role of regional cardiac sympathetic denervation in arrhythmogenesis remains to be determined.

Characteristics of Ca(2+)-activated K+ channels isolated from the left ventricle of a patient with idiopathic long QT syndrome.

Early afterdepolarizations (EADs), possibly caused by reduced K+ conductance, have been hypothesized to cause the long QTU interval and ventricular tachyarrhythmias (VT) in patients with the long QT syndrome (LQTS). In a 26-year-old woman with aborted sudden death as a consequence of the idiopathic LQTS, we recorded with a contact electrode left ventricular endocardial EADs that were enhanced by epinephrine and phenylephrine. Because of uncertain efficacy and side effects achieved with beta-adrenoceptor blockade, the patient underwent left-sided cardiac sympathectomy, at which time we obtained left ventricular biopsy tissue. Crude membrane vesicles were prepared from this tissue and single-channel activity was studied after incorporation of the vesicles in an artificial lipid bilayer (phosphatidylserine, phosphatidylethanolamine, 4:5 weight ratio in decane) in the tip of a patch clamp pipette. Bath and pipette contained 100 mmol/L KCI and 25 mmol/L N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) at pH 7.4. We recorded K+ conducting channels with a mean slope conductance of 49.9 +/- 4.7 picosiemens (pS) (n = 5). Channel open probability was increased by the addition of 1 to 10 mumol/L Ca2+ to the experimental chamber. Addition of charybdotoxin (1-3 nmol/L), a known specific inhibitor of Ca(2+)-activated K+ channels, blocked channel activity. These results are the first to demonstrate Ca(2+)-activated K+ channels from a patient with idiopathic LQTS. These channels appear to show normal characteristics when studied in an artificial planar lipid bilayer.

Radiofrequency catheter ablation of Mahaim fibers at the tricuspid annulus.

BACKGROUND: The purpose of this study was to test the feasibility of radiofrequency catheter ablation of Mahaim fibers at the tricuspid annulus. METHODS AND RESULTS: Four patients who fulfilled criteria for having Mahaim fibers and preexcited reciprocating tachycardia underwent radiofrequency catheter ablation. Three patients had atriofascicular connections, and one patient had an atrioventricular connection. The mean age was 27 years (age range, 11-48 years). All patients had highly symptomatic tachycardias, producing syncope in one patient and presyncope in the remaining three patients. Symptoms were present for a mean of 13 years (range, 4-23 years). All pathways conducted only anterogradely, and preexcitation resulted in a left bundle branch block QRS morphology. Adenosine caused block in the accessory pathway in the three patients in whom it was tested. The stimulus to delta interval increased by 75 msec (range, 35-90 msec) during rapid atrial pacing. The atrial insertion of the Mahaim fiber was in the right lateral atrium in one patient, right posterolateral atrium in two patients, and right posterior atrium in one patient. The ventricular insertion was in the distal right bundle branch in three patients and in the posterolateral right ventricle near the tricuspid annulus in the patient with an atrioventricular connection. Stimulus to delta wave mapping was used to help localize the atrial insertion of the atriofascicular connections. A mean of 15 radiofrequency pulses (range, 10-19 pulses) delivered to the tricuspid annulus in the posterior to lateral regions eliminated accessory pathway conduction in all patients. No complications occurred. Tachycardia did not recur during a mean follow-up of 8 months (range, 2-15 months). CONCLUSIONS: Radiofrequency current applied to the tricuspid annulus can safely eliminate tachycardia in patients with Mahaim fibers.

Differential effects of isoproterenol on sustained ventricular tachycardia before and during procainamide and quinidine antiarrhythmic drug therapy.

BACKGROUND: Autonomic modulation, especially increased sympathetic activity may play a role in the genesis of ventricular arrhythmias. The purpose of this study was to determine whether beta-sympathetic stimulation with isoproterenol would alter sustained ventricular tachycardia (VT) circuits similarly during the drug-free and antiarrhythmic drug-treated states. METHODS AND RESULTS: Twenty-five patients with repeatedly inducible, hemodynamically stable, sustained VT were evaluated by programmed ventricular stimulation. In the antiarrhythmic drug-free state, isoproterenol (0.03 microgram/kg per minute) shortened the following intervals (in milliseconds; mean +/- SEM; 25 patients; paired t test): sinus cycle length (792 +/- 37 to 568 +/- 18; (p < 0.001), ventricular paced QT interval (386 +/- 8 to 348 +/- 6; p < 0.001), ventricular paced QRS duration (185 +/- 4 to 182 +/- 4; p = 0.014), ventricular effective (238 +/- 5 to 208 +/- 4; p < 0.001) and functional (261 +/- 6 to 227 +/- 5; p < 0.001) refractory periods, and the VT cycle length (VTCL) (311 +/- 9 to 291 +/- 9; p < 0.001). Isoproterenol (0.03 microgram/kg per minute) was administered during 31 antiarrhythmic drug trials (procainamide, n = 18; quinidine, n = 13) in 22 patients. Isoproterenol shortened the sinus cycle length, QT interval during ventricular pacing, and ventricular effective and functional refractory periods before and during procainamide and quinidine therapy (ANOVA; isoproterenol effect, p < or = 0.0002 for all). The amount of decrease in these intervals with isoproterenol was the same before and during procainamide and quinidine therapy (ANOVA interaction, p = NS for all). The QRS duration during ventricular pacing and VTCL were also shortened by isoproterenol before and during procainamide (baseline, n = 17; QRS, 182 +/- 4 to 178 +/- 4 msec; VTCL, n = 18, 314 +/- 11 to 291 +/- 11 msec; during procainamide, QRS, 218 +/- 7 to 197 +/- 6 msec; VTCL, 422 +/- 15 to 359 +/- 11 msec) and quinidine (baseline, n = 13; QRS, 190 +/- 6 to 185 +/- 5 msec; VTCL, n = 12, 298 +/- 10 to 280 +/- 9 msec; during quinidine, QRS, 223 +/- 9 to 208 +/- 8 msec; VTCL, 415 +/- 14 to 355 +/- 10 msec) (isoproterenol effect p < or = 0.0003 for all). However, the amount of decrease in QRS duration and VTCL with isoproterenol was greater during procainamide and quinidine than in the drug-free state (ANOVA interaction, p < or = 0.02 for all). These changes continued to be significant when normalized for the initial QRS duration and VTCL (p < or = 0.03 for all). CONCLUSIONS: Isoproterenol affects presumed reentrant sustained VT circuits less in the absence of antiarrhythmic drugs but markedly attenuates the antiarrhythmic drug-induced slowing of sustained VT. To the extent that the change in QRS duration reflects a change in conduction within the VT circuit, these data imply that the attenuation of drug-induced slowing of VT by isoproterenol is due to a greater change in conduction rather than refractoriness.

Radiofrequency ablation for atrioventricular node reentrant tachycardia: comparison between fast (anterior) and slow (posterior) pathway ablation.

OBJECTIVES: We compared the electrophysiologic effects on atrioventricular (AV) node physiology of selective "fast" versus selective "slow" pathway radiofrequency ablation in 42 patients with drug-resistant AV node reentrant tachycardia who underwent 51 ablation attempts to prevent tachycardia recurrence while preserving AV conduction. BACKGROUND: The recent introduction of radiofrequency ablation to treat AV node reentrant tachycardia allows the opportunity to study the effects of selective elimination of the different limbs involved in AV node reentrant tachycardia. METHODS: Selective fast pathway ablation was attempted in 13 patients by delivering radiofrequency energy anteriorly across the tricuspid valve anulus. Selective slow pathway ablation was attempted in 29 patients by delivering radiofrequency energy posteriorly across the tricuspid valve anulus at sites where putative slow pathway potentials were recorded. RESULTS: Selective fast pathway ablation eliminated AV node reentrant tachycardia without AV block in 6 (46%) of 13 patients after one ablation session and in an additional 3 patients (69% of total) after repeat ablation sessions. Slow pathway ablation eliminated AV node reentrant tachycardia without AV block in 26 (90%) of 29 patients after one radiofrequency ablation session and in an additional 2 patients (97% of total) after repeat ablation sessions. Selective fast pathway ablation increased the PR interval (140 to 220 ms, p = 0.0001) and AH interval (66 to 153 ms, p = 0.0001), whereas slow pathway ablation did not change these intervals. Fast pathway radiofrequency ablation caused retrograde block in 7 (64%) of 11 patients, whereas no patients undergoing slow pathway ablation developed selective retrograde block. Single AV node echo beats were commonly induced after slow but not fast pathway ablation (17 of 29 patients vs. 1 of 11 patients, respectively, p = 0.01) and did not predict recurrence of AV node reentrant tachycardia. CONCLUSIONS: Successful selective radiofrequency ablation of fast or slow pathways in patients with AV node reentrant tachycardia resulted in different electrophysiologic properties after ablation. Slow pathway ablation produced more successful outcomes, with a decreased prevalence of recurrent AV node reentrant tachycardia or AV block.

Catheter ablation for cardiac arrhythmias.

With the introduction of radiofrequency energy, catheter ablation has become an established technique for managing many cardiac rhythm disturbances. High efficacy and safety have been reported for accessory pathway ablation, selective fast and slow atrioventricular nodal pathway ablation to eliminate atrioventricular nodal reentrant tachycardia (while preserving atrioventricular conduction), atrioventricular junctional ablation to control the ventricular response to atrial tachyarrhythmias, ablation of the right bundle branch to eliminate bundle branch reentrant ventricular tachycardia, and ablation of the site of tachycardia origin in patients with ventricular tachycardia unassociated with structural heart disease. In addition, there has been active investigation into ablation techniques for more complex arrhythmias such as atrial tachycardia, atrial flutter, and ventricular tachycardia associated with structural heart disease.

Five-year follow-up of 589 patients treated with amiodarone.

Between 1977 and 1986, 589 patients (age, 57 +/- 13 years; 464 men and 125 women) received amiodarone for ventricular fibrillation (VF; 147 patients), sustained (VT-S; 242 patients) or nonsustained (VT-NS; 80 patients) ventricular tachycardia, or supraventricular tachycardia (SVT; 120 patients). Mean left ventricular ejection fraction was 36 +/- 17%, with 23% in New York Heart Association functional class I, 49% in class II, 25% in class III, and 3% in class IV. Sixty-two percent had ischemic heart disease. Follow-up was 32 +/- 27 months (mean +/- SD). Life table analysis revealed that patients with VF, VT-S, and VT-NS had a cumulative incidence of sudden death of 9% at 1 year, increasing by about 3% per year. By years 2 and 5, the cumulative incidence of sudden death, VF, or VT-S recurrence was 26% and 38% and the percent of patients still taking amiodarone was 54% and 32%. For patients with SVT at years 2 and 5, the cumulative incidence of sudden death was 1% and 3%, and of sudden death or SVT recurrence the cumulative incidence was 20% and 29%. The percent of patients still taking amiodarone was 67% and 43%. Of 14 clinical variables assessed, New York Heart Association functional class was the best predictor of sudden death and arrhythmic failure and no other variable added independent predictive power. Older age and lower left ventricular ejection fraction were independent predictors of drug failure (sudden death or arrhythmic failure or need to discontinue amiodarone because of side effects). We conclude that despite its side effect profile, amiodarone is an effective and reasonably well-tolerated antiarrhythmic drug.