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.

Antitachycardia devices: realities and promises.

Nonpharmacologic therapy for ventricular arrhythmias has gained growing attention with the development of the implantable cardioverter-defibrillator. In addition, the reports of adverse effects of drug therapy from several studies, including the Cardiac Arrhythmia Suppression Trial (CAST), have supported the need for these devices. The development of new implantable cardioverter-defibrillators that have the capability of antitachycardia pacing, bradycardia pacing, cardioversion and defibrillation has enhanced their clinical utility. The currently available implantable cardioverter-defibrillators have been shown to significantly improve survival after sudden cardiac arrest in patients with life-threatening ventricular arrhythmias. Newer devices with expanded capabilities may reduce mortality even further. In this report the features of currently available antitachycardia devices and implantable cardioverter-defibrillators are reviewed and the features and current implant data on newer antitachycardia devices are discussed.

Parasympathetic and sympathetic alterations of Mobitz type II heart block.

This study examined the effects of changes in parasympathetic and sympathetic tone on the cycle length at which Mobitz type II second degree atrioventricular (AV) block occurred. Four patients who had electrocardiographic evidence of type II AV block and confirmation of block in the His-Purkinje system during electrophysiologic study were evaluated. These patients received intravenous atropine (1.0 to 2.4 mg), propranolol (0.15 mg/kg body weight) or isoproterenol (1 and 2 micrograms/min) alone or in combination. In two of three patients receiving propranolol, the atrial pacing cycle length at which 1:1 His-Purkinje conduction occurred was prolonged relative to control (from 360 to 470 ms and 440 to 590 ms, respectively). In contrast, atropine in the presence of beta-adrenergic blockade shortened the cycle length at which 1:1 His-Purkinje conduction occurred in three of four patients receiving the drug (470 to 390, 630 to 570 and 590 to 560 ms, respectively). Isoproterenol also improved His-Purkinje conduction in the one patient receiving this drug. No agent affected the duration of the HV interval during spontaneous sinus rhythm or right atrial pacing. Thus, drugs that alter autonomic tone influence abnormal His-Purkinje conduction minimally during sinus rhythm but, importantly, may modulate the atrial pacing cycle length at which type II AV block occurs.

Determination of the earliest site of ventricular activation in Wolff-Parkinson-White syndrome: application of digital continuous loop two-dimensional echocardiography.

Surgical and transcatheter ablation of accessory atrioventricular (AV) connections (Wolff-Parkinson-White syndrome) requires accurate localization of the accessory pathway. In a canine model of endocardial pacing, a continuous loop two-dimensional echocardiographic technique was developed for determining the earliest site of ventricular activation. This technique was then used to localize accessory AV connections in patients. Echocardiographic images were acquired on videotape and converted to a digital continuous loop format, from which the earliest site of systolic motion was determined. In six dogs, using six distinct endocardial sites, two blinded observers accurately identified the earliest site of ventricular activation in 31 (86%) of 36 and 32 (89%) of 36 locations. Determination of the earliest site of ventricular activation with the continuous loop digital technique was superior to standard analog analysis in overall accuracy (p less than 0.02) and in intraobserver variability (p less than 0.004). After validation of this technique, 21 patients with 22 accessory AV connections with anterograde conduction were studied. The earliest site of mechanical activity was determined during sinus (10 patients) or atrial paced (11 patients) rhythms by two blinded observers and compared with electrophysiologic mapping and surface electrocardiograms. Digitally processed echocardiograms correctly localized the earliest site of ventricular activation in 18 of 22 connections and predicted an adjacent location in the remaining 4.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

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.

Arrhythmogenic effects of antiarrhythmic drugs: a study of 506 patients treated for ventricular tachycardia or fibrillation.

Antiarrhythmic therapy in 506 consecutive patients undergoing 1,268 antiarrhythmic drug trials for ventricular tachycardia or ventricular fibrillation was reviewed for evidence of arrhythmogenic drug effect defined as the occurrence of a new form of ventricular tachyarrhythmia temporally associated with initiation of drug therapy or dosage increase. Arrhythmogenic effects occurred in 6.9% of patients and 3.4% of drug trials. This ranged from a high of 11.8% caused by encainide to none occurring with procainamide, tocainide or beta-adrenergic blocking drugs. The incidence of arrhythmogenesis was significantly greater in patients whose presenting arrhythmia was sustained ventricular tachycardia than it was in those who presented with nonsustained ventricular tachycardia or ventricular fibrillation (p = 0.02). Decreased systolic function measured echocardiographically at the base of the left ventricle was associated with an increased incidence of arrhythmogenic effects (p = 0.006) whereas global left ventricular ejection fraction was not. Age, gender, cardiac diagnosis, location of prior myocardial infarction and New York Heart Association functional class for heart failure were not related to the occurrence of drug-induced arrhythmias. These findings emphasize the need for in-hospital cardiac monitoring during initiation of antiarrhythmic drug therapy for ventricular tachyarrhythmias.

Regional sympathetic denervation after myocardial infarction in humans detected noninvasively using I-123-metaiodobenzylguanidine.

Transmural myocardial infarction in dogs produces denervation of sympathetic nerves in viable myocardium apical to the infarct that may be arrhythmogenic. It is unknown whether sympathetic denervation occurs in humans. The purpose of this study was to use iodine-123-metaiodobenzylguanidine (MIBG), a radiolabeled guanethidine analog that is actively taken up by sympathetic nerve terminals, to image noninvasively the cardiac sympathetic nerves in patients with and without ventricular arrhythmias after myocardial infarction. Results showed that 10 of 12 patients with spontaneous ventricular tachyarrhythmias after myocardial infarction exhibited regions of thallium-201 uptake indicating viable perfused myocardium, with no MIBG uptake. Such a finding is consistent with sympathetic denervation. One patient had frequent episodes of nonsustained ventricular tachycardia induced at exercise testing that was eliminated by beta-adrenoceptor blockade. Eleven of the 12 patients had ventricular tachycardia induced at electrophysiologic study and metoprolol never prevented induction. Sympathetic denervation was also detected in two of seven postinfarction patients without ventricular arrhythmias. Normal control subjects had no regions lacking MIBG uptake. This study provides evidence that regional sympathetic denervation occurs in humans after myocardial infarction and can be detected noninvasively by comparing MIBG and thallium-201 images. Although the presence of sympathetic denervation may be related to the onset of spontaneous ventricular tachyarrhythmias in some patients, it does not appear to be related to sustained ventricular tachycardia induced at electrophysiologic study.

Pharmacokinetic and electrophysiologic interactions of amiodarone and procainamide.

The effects of amiodarone on the pharmacokinetic and electrophysiologic properties of procainamide were examined in eight patients treated for recurrent ventricular arrhythmias who received intravenous procainamide, 6 to 15 mg/kg, at control and after 1 to 2 weeks of oral amiodarone treatment. Compared with control, procainamide plasma clearance decreased from 0.43 +/- 0.12 L/kg-hr to 0.33 +/- 0.12 L/kg-hr (P less than 0.01), plasma elimination half-life increased from 3.77 +/- 0.64 hours to 5.21 +/- 0.42 hours (P less than 0.01), and volume of distribution was unchanged from 2.31 +/- 0.74 L/kg to 2.47 +/- 0.90 L/kg during amiodarone treatment. As single agents, intravenous procainamide and oral amiodarone produced equivalent increases in QRS duration, rate-corrected QT interval, right ventricular effective refractory period, and cycle length of induced ventricular tachycardia. After the addition of intravenous procainamide to amiodarone the QRS duration, rate-corrected QT interval, and, in six of eight patients, ventricular tachycardia cycle length were significantly increased compared with control or either drug alone, suggesting additive electrophysiologic effect. However, acceleration of induced ventricular tachycardia occurred in one patient with combined treatment, suggesting a potential for adverse electrophysiologic interactions. These findings indicate that amiodarone has pharmacokinetic and electrophysiologic interactions with procainamide and suggest that the intravenous dose of procainamide be reduced by 20% to 30% during concurrent drug administration.

Supernormal conduction in accessory atrioventricular connections.

Prospective electrophysiologic evaluation of 74 patients with ventricular preexcitation revealed 4 patients who had supernormal anterograde conduction over an accessory atrioventricular pathway. In each patient, anterograde conduction over the accessory pathway was present at relatively slow sinus rates, but the accessory pathway anterograde effective refractory period was substantially prolonged. During premature atrial stimulation, a "window" of supernormal conduction was identified at which closely coupled atrial extrastimuli conducted over the accessory pathway, whereas longer premature intervals resulted in accessory pathway block. Causes other than supernormal conduction to explain this phenomenon, for example, phase 4 block, were unlikely in each case. Although the mechanism of supernormal conduction in humans is unknown, the electrophysiologic findings in our patients are similar to those reported in patients with supernormal conduction in the His-Purkinje system.

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.

Survivors of cardiac arrest: prevention of recurrence by drug therapy as predicted by electrophysiologic testing or electrocardiographic monitoring.

Sixty-two patients (44 men and 18 women, aged 15 to 75 years) resuscitated from at least 1 cardiac arrest unrelated to acute myocardial infarction were studied. No patient was taking antiarrhythmic drugs at the time of the initial cardiac arrest. Thirty-five patients had coronary artery disease (CAD) and 27 did not. Before drug therapy, control electrophysiologic studies induced ventricular tachycardia (VT) in 43 of 58 patients (74%) (30 of 35 with CAD and 17 of 27 without CAD). At control continuous electrocardiographic monitoring for 48 hours or longer, only 19 of 62 patients (31%) had spontaneous VT, 5 of whom had no VT induced at control electrophysiologic study. Mean follow-up was 22 months. Fourteen of 41 patients, 8 of 25 with and 6 of 16 without CAD, had VT suppressed with drugs during serial electrophysiologic testing, and none had a recurrent arrhythmic event. VT was suppressed in 12 of 14 patients receiving conventional drugs. Of 27 patients with VT induced during all drug studies, 6 died from cardiac arrest and 4 had recurrent VT. Drug efficacy in 20 patients was guided by continuous electrocardiographic monitoring, and 4 of 9 patients in whom VT and ventricular pairs were suppressed by drug therapy, as documented by continuous electrocardiographic monitoring for 48 hours or longer, died of cardiac arrest. Overall, 26 patients were discharged receiving amiodarone therapy, and 5 died of cardiac arrest and 3 had recurrent sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Subthreshold conditioning stimuli prolong human ventricular refractoriness.

This study tested whether a subthreshold stimulus (Sc) inserted before a premature stimulus prolonged the right ventricular effective refractory period in humans, and whether the degree of effective refractory period lengthening was influenced by heart rate, Sc current intensity or Sc pulse duration. Sc at current intensity 10 mA and pulse width 2 ms prolonged mean effective refractory period from 255 ms to 277 ms (p less than 0.001, n = 20). The increase in effective refractory period was similar in 6 patients studied at pacing cycle lengths 600 (259 to 289 ms) and 400 ms (236 to 258 ms). When Sc current intensities were varied at 2, 5 or 10 mA at a constant pulse duration of 100 ms the effective refractory period progressively prolonged by 6, 40 and 81 ms respectively (p less than 0.02, n = 6). The pulse duration of Sc at a constant current of 10 mA significantly influenced effective refractory period prolongation. With Sc pulse durations of 2, 10, and 100 ms the effective refractory period prolonged by 16, 33 and 66 ms respectively (p less than 0.01, n = 7). Thus, subthreshold impulses prolong the effective refractory period in human right ventricular myocardium. The prolongation of effective refractory period depended on Sc current intensity and pulse duration but was independent of heart rate at the cycle lengths tested. The use of subthreshold stimuli as antiarrhythmic therapy may be feasible in some patients.

Development of the implantable transvenous cardioverter.

The development of the transvenous cardioverter, from the initial animal studies, to the clinical studies using temporary leads, to the initial permanent implants is described. Shocks less than or equal to 2.0 joules synchronized to the QRS complex and delivered through a specially designed catheter electrode placed in the apex of the right ventricle successfully terminate most episodes of ventricular tachycardia in patients. The implanted unit which also serves as a demand ventricular pacemaker, can be used to perform programmed electrophysiologic studies. Future devices must be capable of defibrillation and more accurate arrhythmia detection.

Propafenone treatment of recurrent ventricular tachycardia: comparison of continuous electrocardiographic recording and electrophysiologic study in predicting drug efficacy.

Propafenone was administered to 29 patients who had multiple episodes of recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) despite previous antiarrhythmic therapy. All patients had 24-hour continuous electrocardiographic recording and electrophysiologic study in a drug-free control state and while receiving maximum doses of propafenone. During propafenone treatment, the mean frequency of ventricular premature complexes (VPCs) decreased 74% (p less than 0.05). There was more than an 83% decrease in VPC frequency in 17 of 29 patients, and 11 patients had 99 to 100% decreases. Propafenone prevented VT induction at electrophysiologic study in 6 patients, whereas another 12 patients were judged to have satisfactory electrophysiologic responses on the basis of slower VT rates and absence of hemodynamic compromise during VT. After long-term treatment from 2 to 26 months, 9 patients continued propafenone without evidence of recurrent arrhythmia. Six of these 9 patients had not VT induction at electrophysiologic study while receiving propafenone. The decrease in VPC frequency produced by propafenone was a poor predictor of a successful electrophysiologic study and of long-term therapy. In conclusion, propafenone has potential as an effective antiarrhythmic agent, but better methods to stratify risk for recurrence of VT and VF are needed.

Prospective evaluation of a discriminant function for prediction of recurrent symptomatic ventricular tachycardia or ventricular fibrillation in coronary artery disease patients receiving amiodarone and having inducible ventricular tachycardia at electrophysiologic study.

Induction of ventricular tachycardia (VT) at electrophysiologic study in patients taking amiodarone poorly predicts recurrence of VT. Consequently, a discriminant function was developed (using parameters based on retrospective data) that appeared to identify high-risk patients. These parameters included ventricular effective refractory period, corrected QT interval, initiation of a repetitive ventricular response and the mode of VT induction. In the present study these parameters were prospectively evaluated in 60 patients with coronary artery disease and sustained VT or ventricular fibrillation (VF), in whom VT was still induced at electrophysiologic study during amiodarone therapy. Thirteen patients had recurrent events (sudden death in 8 and sustained VT in 5) and 47 patients had no symptomatic arrhythmia recurrence (follow-up for 16 +/- 2 months, mean +/- standard error of the mean). The ventricular effective refractory period, corrected QT interval and presence of a repetitive ventricular response did not discriminate between patients with and without symptomatic arrhythmia recurrence. However, an easier mode of VT induction during amiodarone therapy versus control was highly predictive of arrhythmia recurrence: 9 of 13 (69%) recurrences were in this group. In contrast, only 4 of 44 (9%) patients who had either the same or harder mode of VT induction had a recurrent event. Overall, 9 of 16 (56%) patients with an easier mode of VT induction had a recurrence, including 6 of the 8 patients with subsequent sudden cardiac death. It is concluded that electrophysiologic testing during amiodarone therapy is useful to identify high-risk patients.

Encainide for atrial fibrillation associated with Wolff-Parkinson-White syndrome.

Thirty-six patients with a history of atrial fibrillation and Wolff-Parkinson-White syndrome were treated with oral encainide, 175 +/- 44 mg/day, after undergoing baseline drug-free electrophysiologic studies. The mean age was 38 +/- 15 years, with structural heart disease present in only 3 patients. Nine patients had only paroxysmal atrial fibrillation and 27 patients had both atrial fibrillation and atrioventricular reciprocating tachycardia (AVRT). Symptoms were present for a mean of 195 +/- 168 months and were treated with an average of 2.7 +/- 1.6 drugs before encainide. Anterograde block in the accessory pathway occurred in 12 of 30 patients (40%) and retrograde block accessory pathway occurred in 10 of 24 patients in whom comparison could be made. AVRT was initiated in 29 of 36 patients during the control study and could be initiated in 19 of 29 patients while receiving encainide. Drug efficacy was determined by the clinical response judged completely effective, partially effective or ineffective. During a mean follow-up of 30.1 +/- 25 months, 24 patients (67%) continued to take encainide. Encainide was completely effective in 14 of 24 patients and partially effective in another 7 patients. Noncardiac side effects were mild and generally resolved, and required discontinuance in only 1 patient. More frequent AVRT occurred in 2 patients, but was managed with dose reduction and the addition of a beta blocker. Three patients had ventricular tachycardia requiring discontinuance; however 2 of 3 patients had a history of ventricular tachycardia before receiving encainide. Encainide is an effective and safe agent for treating atrial fibrillation in patients with Wolff-Parkinson-White syndrome.

Encainide for treatment of atrioventricular reciprocating tachycardia in the Wolff-Parkinson-White syndrome.

Oral encainide, varying from 75 to 300 mg/day (mean 174 mg/day), was administered to 52 patients with drug-resistant atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed before and during drug treatment. Encainide resulted in anterograde accessory pathway block in 15 of 37 (41%) and retrograde accessory pathway block in 11 of 46 (24%) patients. In patients with residual accessory pathway conduction, encainide significantly prolonged the shortest pacing cycle length maintaining anterograde (261 +/- 26 to 404 +/- 85 ms) and retrograde (279 +/- 46 to 436 +/- 87 ms) accessory pathway conduction, as well as the anterograde accessory pathway effective refractory period (271 +/- 32 to 329 +/- 73 ms). AVRT could not be induced during encainide therapy in 20 of 49 patients (41%). In the remaining patients, AVRT cycle length increased (319 +/- 44 to 426 +/- 90 ms, p less than 0.001) due to prolongation of HV and ventriculoatrial intervals. During follow-up (mean 38.5 months), 30 patients continued to take the drug and 7 patients with favorable drug response subsequently elected to undergo surgical accessory pathway ablation (71% overall favorable response). Encainide was ineffective in 11 patients, was discontinued because of drug intolerance in 2 patients and exacerbated ventricular tachycardia in 2 patients. Lack of AVRT inducibility at encainide electrophysiologic study did not always predict recurrence-free follow-up. Encainide is an effective and well-tolerated drug to prevent recurrence of AVRT in patients with Wolff-Parkinson-White syndrome.

Encainide for treatment of supraventricular tachycardias associated with the Wolff-Parkinson-White syndrome.

Thirty-three patients with supraventricular tachycardia associated with the Wolff-Parkinson-White syndrome were treated with encainide for 26 months (mean). Encainide at a mean dosage of 187 mg/day abolished or markedly decreased episodes of palpitations in 24 of 33 (73%), and no patient had syncope or required cardioversion while receiving the drug. Encainide was well tolerated and was discontinued in only 2 patients because of side effects (6%). Only 1 patient (3%) had a proarrhythmic effect while taking encainide (ventricular tachycardia). Fourteen of 16 patients (88%) with atrial fibrillation continue receiving encainide. Episodes of palpitations have been abolished or markedly decreased and no patient has had syncope or required cardioversion. All 14 of these patients had either anterograde block in the accessory pathway during atrial fibrillation or greater than or equal to 75 ms increase in the shortest R to R interval formed by 2 preexcited QRS complexes. Encainide prolonged refractory periods of the atrial (p = 0.064) and ventricular (p = 0.061) muscle. It prolonged the cycle length at which 1:1 conduction of the accessory pathway in both the anterograde and retrograde directions occurred (both, p less than 0.001). Induction of atrioventricular-reciprocating tachycardia (AVRT) was prevented in 36% of patients at repeat electrophysiologic study. The AVRT cycle length increased 112 ms (mean, p less than 0.001) in those patients in whom AVRT was still inducible. The loss of delta waves recorded with the 12-lead scalar electrocardiogram during encainide therapy was a significant predictor of anterograde accessory pathway block (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Antiarrhythmic and electrophysiologic effects of oral propafenone.

Twenty-six patients had ventricular tachycardia initiated at control electrophysiologic study and had a repeat study during oral propafenone therapy. Ten patients had had sustained ventricular tachycardia, 6 cardiac arrest and 10 symptomatic, nonsustained ventricular tachycardia. Twenty-two patients had heart disease, 18 of whom had coronary artery disease. During propafenone therapy, ventricular tachycardia could not be initiated during programmed ventricular stimulation in 5 patients, and in 21 patients the cycle length of induced ventricular tachycardia increased from 246 +/- 42 ms at control to 355 +/- 96 ms (p less than 0.001). Seventeen patients were discharged with propafenone therapy and have been followed for a mean of 11 months. No symptomatic ventricular tachycardia recurred in the 5 patients without inducible ventricular tachycardia during drug treatment. Six of 12 patients with inducible ventricular tachycardia during the drug study have remained asymptomatic. In conclusion, propafenone substantially prolongs the cycle length of ventricular tachycardia, and initiation of ventricular tachycardia by programmed ventricular stimulation at drug study does not preclude a favorable clinical outcome.