Transvenous cardioversion for the management of recurrent ventricular arrhythmias

The efficacy of transvenous cardioversion and defibrillation for treating life threatening spontaneous ventricular arrhythmias was assessed in a study of 17 patients in a cardiac care unit. Eleven had ventricular tachycardia, five had ventricular fibrillation, and one had both. Transvenous cardioversion successfully terminated tachyarrhythmias on 42 separate occasions in ten patients. Stable electrode positions could not be achieved in two patients, recurrent late displacement occurred in one, and four patients had no further arrhythmias requiring cardioversion once the lead was placed. The energy levels required for successful cardioversion ranged from 0.05 J to 25 J for ventricular tachycardia and from 1 J to 25 J for ventricular fibrillation. The nine successful shocks of 1 J or less did not require sedation or general anaesthesia. High energy (25 J) endocardial shocks were unsuccessful in terminating arrhythmias in two patients, one with ventricular tachycardia and the other with both ventricular tachycardia and fibrillation. Minor unwanted effects of endocardial shocks occurred in five patients. These were acceleration of ventricular tachycardia in two patients and complications of pacing via the special lead in three others: failure of sensing occurred in all three and one patient also had a transient rise in pacing threshold. A postmortem examination in one patient who had received three unsuccessful high energy shocks revealed localised endocardial necrosis at the site of the distal electrode. Transvenous cardioversion offers advantages over external cardioversion but at present practical difficulties limit its application to patients with recurrent ventricular arrhythmias that cannot readily be controlled by conventional methods.     

Transvenous cardioversion for the management of recurrent ventricular arrhythmias.

The efficacy of transvenous cardioversion and defibrillation for treating life threatening spontaneous ventricular arrhythmias was assessed in a study of 17 patients in a cardiac care unit. Eleven had ventricular tachycardia, five had ventricular fibrillation, and one had both. Transvenous cardioversion successfully terminated tachyarrhythmias on 42 separate occasions in ten patients. Stable electrode positions could not be achieved in two patients, recurrent late displacement occurred in one, and four patients had no further arrhythmias requiring cardioversion once the lead was placed. The energy levels required for successful cardioversion ranged from 0.05 J to 25 J for ventricular tachycardia and from 1 J to 25 J for ventricular fibrillation. The nine successful shocks of 1 J or less did not require sedation or general anaesthesia. High energy (25 J) endocardial shocks were unsuccessful in terminating arrhythmias in two patients, one with ventricular tachycardia and the other with both ventricular tachycardia and fibrillation. Minor unwanted effects of endocardial shocks occurred in five patients. These were acceleration of ventricular tachycardia in two patients and complications of pacing via the special lead in three others: failure of sensing occurred in all three and one patient also had a transient rise in pacing threshold. A postmortem examination in one patient who had received three unsuccessful high energy shocks revealed localised endocardial necrosis at the site of the distal electrode. Transvenous cardioversion offers advantages over external cardioversion but at present practical difficulties limit its application to patients with recurrent ventricular arrhythmias that cannot readily be controlled by conventional methods.     

Antiarrhythmic,antifibrillatory, and hemodynamic actions of bethanidine sulfate: An orally effective analog of bretylium for suppression of ventricular tachyarrhythmias

Bethanidine sulfate is a chemical and pharmacologie analog of bretylium tosylate that has virtually identical antifibrillatory and inotropic actions on the heart. Bretylium is the only drug approved by the Food and Drug Administration specifically for the “prophylaxis and treatment of ventricular fibrillation.” Unlike bretylium, which is poorly absorbed from the gut and limited to parenteral use, oral bethanidine is absorbed rapidly. Bethanidine was given to 23 patients with recurrent multiple drug refractory ventricular tachycardia and fibrillation. Eighteen patients (78%) had complete suppression of spontaneous or electrophysiologically inducible tachyarrhythmias; 3 were improved and 2 had no benefit. In 6 of a 9 patient subgroup studied by programmed electrophysiologic drug testing, bethanidine completely prevented previously inducible ventricular tachyarrhythmias at the maximal stimulus tested (including 4 extrastimuli and burst-pacing at 10 times threshold). Cardiac output measured in 6 patients 1 to 2 hours after bethanidine was increased in 4, unchanged in 2, and decreased in 1. Ten patients on long-term therapy with bethanidine and protriptylene (to prevent orthostatic hypotension) have been free of arrhythmias from 2 to 26 (average 13) months.     

Therapy of ventricular tachycardia

Therapeutic modalities for ventricular tachycardia include antiarrhythmic drugs, direct current cardioversion, electrical pacing and surgical intervention. Lidocaine, procainamide and bretylium are all capable of controlling recurrent ventricular tachycardia; bretylium has the advantage of also being antifibrillatory and of raising the threshold for ventricular fibrillation. Lidocaine and bretylium are available only in i.v. form. Procainamide is available in i.v. as well as oral form. Other oral antiarrhythmic agents include quinidine, disopyramide, beta-blockers such as propranolol and verapamil. The latter may be useful in ventricular arrhythmias induced by ischemia; of these, only beta-blockers appear to significantly raise the threshold for ventricular fibrillation. Control of ventricular ectopy does not always preclude ventricular tachycardia and ventricular fibrillation. In treating ventricular tachycardia, bretylium tosylate is generally given 5 to 10 mg/kg i.v. over 10 to 20 minutes. Given too rapidly, it may cause nausea and vomiting. Orthostatic hypotension, a common side effect, generally abates with continued use and may be ameliorated with tricyclic antidepressants such as protriptyline. Significant supine hypotension may be encountered in patients with acute myocardial infarction and may be managed with pressor agents or fluids, or both. The antiarrhythmic efficacy of bretylium was analyzed in 40 patients. Five etiologic groups were defined by cardiac catheterization: 19 patients had atherosclerotic heart disease, 6 had primary myocardial disease, 4 had mitral valve prolapse, 4 had rheumatic heart disease and 7 had miscellaneous or no heart disease. All patients had recurrent ventricular tachycardia (VT); 23 had ventricular fibrillation (VF) as well. Other antiarrhythmic agents had failed in 38 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bretylium tosylate: a newly available antiarrhythmic drug for ventricular arrhythmias.

Bretylium tosylate (Bretylol) has recently been approved for parenteral use against resistant ventricular arrhythmias. The pharmacologic action of bretylium is complex, and its antiarrhythmic action differs significantly from other drugs. Bretylium is an adrenergic neuronal blocking agent taken up selectively at peripheral adrenergic nerve terminals, where it initially releases norepinephrine (sympathomimetic effect) and then produces adrenergic neuronal blockade. It has direct cardiac membrane effect to prolong action potential duration and effective refractory period but, unlike other membrane active antiarrhythmic agents, does not depress conduction velocity or automaticity. Bretylium increases ventricular fibrillation threshold and prevents the decrease in ventricular fibrillation threshold associated with myocardial ischemia. It does not depress myocardial contractility. Clinical studies have shown parenteral bretylium to be effective in suppressing ventricular arrhythmias, particularly recurrent, drug resistant ventricular tachycardia or ventricular fibrillation.     

Electrophysiologic testing of bretylium tosylate in sustained ventricular tachycardia

We used programmed ventricular stimulation to test intravenous bretylium tosylate in 10 consecutive patients with inducible sustained ventricular tachycardia (usually refractory to type I antiarrhythmic agents). These 10 patients had previously documented sustained ventricular tachycardia and/or ventricular fibrillation complicating stable heart disease. Following control inductions of sustained ventricular tachycardia, bretylium 10 mg/kg was infused over 30 minutes. Thirty minutes after this infusion, sustained ventricular tachycardia could be induced in 9 of the 10 patients (one of these nine patients also had bretylium-potentiated spontaneous ventricular tachycardia). Tachycardia induced in the nine patients after bretylium was similar to control tachycardia with respect to morphology and cycle length (333 +/- 16 msec after bretylium versus 330 +/- 16 msec during control). However, five of the nine patients tolerated induced tachycardia less well after bretylium (exacerbated hypotension). In one patient, ventricular tachycardia could not be induced after intravenous bretylium.     

Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate

Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QT_c interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.     

Determinants of the outcome of electrophysiologic study in patients with ventricular tachyarrhythmias

To determine those factors predictive of the ability to both initiate and suppress ventricular tachyarrhythmias during electrophysiologic study, the results of programmed cardiac stimulation were evaluated in 261 patients: 66 presenting with nonsustained ventricular tachycardia, 91 with sustained ventricular tachycardia and 104 with ventricular fibrillation. Multivariate logistic regression analysis revealed that the presenting arrhythmia was a potent and independent predictor of the ability to provoke ventricular arrhythmias at electrophysiologic study; a history of myocardial infarction and male sex were also significant independent predictors. Of patients presenting with sustained ventricular tachycardia, 89% (81 of 91) had inducible ventricular arrhythmias compared with 61 (40 of 66) and 66% (69 of 104) of patients with nonsustained ventricular tachycardia and ventricular fibrillation, respectively. Complete suppression of inducible arrhythmias could be achieved in only 52% (34 of 66) of patients with sustained ventricular tachycardia, compared with 73 (24 of 33) and 75% (46 of 61) of patients presenting with nonsustained ventricular tachycardia and ventricular fibrillation, respectively. Multivariate analysis showed that the major independent determinants of the ability to suppress inducible arrhythmias were the number of drug trials performed before electrophysiologic study (inversely correlated) and the nature of the induced arrhythmia. The nature of the presenting clinical arrhythmia is, therefore, a highly significant and independent predictor of the ability to induce ventricular arrhythmias during electrophysiologic testing and an important determinant of the ability to suppress induced arrhythmias in patients with spontaneous ventricular tachyarrhythmias.     

Treatment of recurrent ventricular tachycardia and fibrillation with aprindine

Twenty-three patients with recurrent ventricular tachycardia or ventricular fibrillation, or both, were treated with aprindine, a new antiarrhythmic agent. It was found that: (1) no patient had a recurrence of ventricular fibrillation after aprindine therapy was begun, except as a terminal event subsequent to the development of acute myocardial infarction and cardiogenic shock or refractory congestive heart failure; (2) 6 patients experienced ventricular tachycardia after the loading dose, but with continued aprindine therapy the ventricular tachycardia was suppressed in 3 of these 6 patients, and a fourth patient was asymptomatic during brief paroxysms of ventricular tachycardia; (3) in 2 patients, aprindine was ineffective and was discontinued; (4) electrical cardioversion was not required in any patient receiving aprindine; (5) premature ventricular extrasystoles were decreased in 18 of the 23 patients treated with aprindine; (6) aprindine was discontinued in 1 patient because of intolerable side effects, although ventricular arrhythmias were suppressed in this patient; and (7) 5 patients died from acute myocardial infarction or severe heart failure while receiving aprindine.     

Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias

Low energy endocardial cardioversion was attempted in 23 patients with 30 arrhythmias, of whom only four were receiving additional drug treatment. Four had atrial flutter, five atrial fibrillation, three intra-atrioventricular nodal tachycardia, two atrioventricular re-entrant tachycardia, 13 ventricular tachycardia, and three ventricular fibrillation. A pacing lead with special large surface area electrodes--the active electrode positioned either in the right atrium or in the right ventricular apex and the indifferent electrode in the right atrium, superior vena cava, or inferior vena cava--was used together with a low energy defibrillator. A total of 114 shocks was delivered, 26 of which were atrial. One episode of atrial flutter was terminated, but atrial fibrillation and atrioventricular nodal tachycardia were not terminated in any of the patients. Both patients with atrioventricular tachycardia were successfully treated, as were eight of the patients with ventricular tachycardia. Atrial fibrillation was produced in three patients and non-sustained ventricular tachycardia in one, ventricular tachycardia was accelerated in two, and ventricular fibrillation induced in five. Fourteen patients experienced severe discomfort and seven mild or moderate discomfort, and only one found the procedure painless. One patient was anaesthetised throughout the procedure. Low energy endocardial cardioversion is not universally successful even at the highest energies tolerable, and with the present electrode and pulse waveforms some patients may suffer considerable discomfort.     

Efficacy of a tiered therapy defibrillator system used to treat recurrent ventricular arrhythmias refractory to drugs.

OBJECTIVE--To evaluate an implantable tiered therapy defibrillator system that delivered antitachycardia pacing treatment for slower well tolerated ventricular tachycardias and cardioversion or defibrillation for fast tachycardias or ventricular fibrillation. METHODS--A tiered treatment device (Ventritex Cadence V-100) was implanted in 30 patients with ventricular tachycardia that was refractory to drugs. Efficacy was evaluated by the responses of induced or spontaneous arrhythmias to the treatments delivered. RESULTS--Antitachycardia pacing successfully terminated 80% of episodes of ventricular tachycardia induced by non-invasive programmed stimulation, but acceleration was brought about by pacing in six patients in 10% of episodes. During a follow up of two to 17 (mean seven) months, 18 patients (60%) had recurrence of ventricular arrhythmias. Antitachycardia pacing terminated ventricular tachycardia in 17 of 18 patients in 87% of episodes. Twelve patients received shocks for ventricular tachycardia or fibrillation. Failure of pacing, with subsequent cardioversion, occurred in nine patients (50%) in one or more episodes. Acceleration of tachycardia by pacing occurred in 10 patients in 5% of episodes. Only two of these patients had experienced acceleration of previously induced arrhythmia. Five patients had spontaneous fast ventricular tachycardia or fibrillation treated by cardioversion or defibrillation. Spurious treatment was delivered in nine patients (30%), during atrial fibrillation in five, sinus tachycardia in two, and because of fracture of the sensing lead system in two patients. The retrieval of stored intracardiac electrograms was of clinical value in assessing spurious treatment. CONCLUSIONS--Tiered treatment was effective in terminating recurrent ventricular arrhythmias in these selected patients. Most episodes were treated successfully by pacing, and resistant tachycardias, pacing induced acceleration, or haemodynamically compromising arrhythmias were treated by shocks.     

Internal transvenous low energy cardioversion for the treatment of cardiac arrhythmias.

Low energy endocardial cardioversion was attempted in 23 patients with 30 arrhythmias, of whom only four were receiving additional drug treatment. Four had atrial flutter, five atrial fibrillation, three intra-atrioventricular nodal tachycardia, two atrioventricular re-entrant tachycardia, 13 ventricular tachycardia, and three ventricular fibrillation. A pacing lead with special large surface area electrodes--the active electrode positioned either in the right atrium or in the right ventricular apex and the indifferent electrode in the right atrium, superior vena cava, or inferior vena cava--was used together with a low energy defibrillator. A total of 114 shocks was delivered, 26 of which were atrial. One episode of atrial flutter was terminated, but atrial fibrillation and atrioventricular nodal tachycardia were not terminated in any of the patients. Both patients with atrioventricular tachycardia were successfully treated, as were eight of the patients with ventricular tachycardia. Atrial fibrillation was produced in three patients and non-sustained ventricular tachycardia in one, ventricular tachycardia was accelerated in two, and ventricular fibrillation induced in five. Fourteen patients experienced severe discomfort and seven mild or moderate discomfort, and only one found the procedure painless. One patient was anaesthetised throughout the procedure. Low energy endocardial cardioversion is not universally successful even at the highest energies tolerable, and with the present electrode and pulse waveforms some patients may suffer considerable discomfort.     

Clinical transvenous cardioversion of recurrent life-threatening ventricular tachyarrhythmias: Low energy synchronized cardioversion of ventricular tachycardia and termination of ventricular fibrillation in patients using a catheter electrode

The purpose of this study was to test the efficacy, safety, and patient tolerance of transvenous cardioversion and defibrillation in patients who had recurrent ventricular tachyarrhythmias. In five of seven patients, a truncated exponential shock of 0.025 to 2.0 joules synchronized to the QRS complex terminated 47 episodes of recurrent sustained ventricular tachycardia (VT). Cardioversion threshold was ≤ 0.25 joule in three patients and 0.75 to 2.0 joules in two patients. Shocks of 0.75 joule and 2.0 joule failed to terminate VT in one patient each; higher energies were not tried because of hemodynamic decompensation. In one patient, a shock of 25 joules terminated ventricular fibrillation (VF) on three occasions, and in another patient a shock of 1.0 joule terminated atrial fibrillation on one occasion. Shocks ≤ 0.5 joule were well tolerated by the awake unsedated patient. One hundred forty of 141 synchronized shocks (including subthreshold shocks) produced no repetitive ventricular activity. In one seriously ill patient who had received multiple antiarrhythmic drugs and required balloon counterpulsation for hemodynamic support, on a single occasion each a synchronized transvenous shock and a synchronized conventional transthoracic shock produced ventricular flutter and ventricular fibrillation (VF), respectively. We conclude that synchronized transvenous cardioversion by a catheter electrode offers promise as a new therapeutic approach.     

Electrophysiologic and hemodynamic studies in patients resuscitated from cardiac arrest

Fifty-two patients resuscitated from cardiac arrest underwent electrophysiologic studies. The earliest documented arrhythmia at the time of initial or recurrent (18 patients) cardiac arrest was ventricular fibrillation (30 patients) or ventricular tachycardia (20 patients); in 2 patients no arrhythmia was documented before defibrillation. Programmed ventricular stimulation revealed inducible arrhythmias in 33 patients (63 percent). Of the 30 patients with ventricular fibrillation as the initial arrhythmia, 13 had inducible arrhythmias—ventricular fibrillation (4 patients), sustained ventricular tachycardia (6 patients) and nonsustained ventricular tachycardia (3 patients). In the 20 patients with ventricular tachycardia as the initial arrhythmia, sustained ventricular tachycardia was initiated in 17 patients and torsade de pointes in 1. Patients with inducible arrhythmias had longer mean A-H and H-V intervals than those without inducible arrhythmias (91.1 versus 76.6 ms and 62.5 versus 50.3 ms, respectively). Prolonged H-V intervals (17 of 33) and intraventricular conduction defects (18 of 33) were more common in patients with than in those without inducible arrhythmias (4 of 19 and 7 of 19, respectively). Mean cardiac index was lower (2.4 versus 3.9 liters/min per m²), left ventricular end-diastolic pressure higher (17.0 versus 9.4 mm Hg), and ejection fraction lower (36.1 versus 57.2 percent) in the group with inducible arrhythmias than in those in whom no arrhythmia could be induced. These data suggest that (1) ventricular tachycardia often precipitates cardiac arrest; and (2) electrophysiologic testing may provide data on which to base therapy in patients resuscitated from cardiac arrest.     

Predictors of inducible sustained ventricular tachyarrhythmias in patients with coronary artery disease

To determine predictors of inducible sustained ventricular tachycardia or fibrillation by programmed electrical stimulation in patients with coronary artery disease and ventricular tachyarrhythmias, 14 clinical and angiographic variables were analyzed in 60 consecutive patients. All patients had angiographically documented coronary artery disease and symptomatic ventricular arrhythmias (sustained ventricular tachycardia in 21, ventricular fibrillation in 21 and nonsustained ventricular tachycardia in 18). Baseline programmed electrical stimulation while the patient was not taking antiarrhythmic drugs was performed with use of single, double and triple extrastimuli and burst pacing from two right ventricular sites. The variables analyzed were presenting arrhythmia; presence, frequency and complexity of ventricular ectopic activity on baseline 24 h electrocardiographic (Holter) monitoring; greater than or equal to 70% narrowing in either the left anterior descending, proximal left anterior descending, right coronary or circumflex coronary artery (independently assessed); single, double or triple vessel coronary disease; anterior, apical or inferior wall motion abnormalities; segmental dyskinesia and ejection fraction. Thirty-seven patients (62%) had inducible sustained ventricular tachycardia (rate greater than 100 beats/min, duration greater than 30 s or requiring cardioversion) and two patients (3%) had ventricular fibrillation induced. Eleven patients (18%) had nonsustained ventricular tachycardia (duration greater than or equal to 3 beats, less than 30 s) induced and 10 patients (17%) had no inducible arrhythmia (duration less than 3 beats). Multivariate stepwise logistic regression analysis identified three independent variables predictive of inducible sustained ventricular arrhythmias: sustained ventricular tachycardia as the presenting arrhythmia (p = 0.004), proximal left anterior descending artery lesion (p = 0.002) and anterior wall motion abnormality (p = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Control of refractory cardiac arrhythmias with amiodarone.

Amiodarone hydrochloride was used to treat 19 patients with symptomatic arrhythmias refractory to quinidine sulfate, procainamide hydrochloride, disopyramide phosphate, antazoline hydrochloride, lidocaine hydrochloride, bretylium tosylate, propranolol hydrochloride, phenytoin sodium, and practotol acetanilide given to the limit of tolerance. In 17 patients, attacks were completely controlled. Arrhythmias treated successfully included recurrent supraventricular tachycardias, recurrent supraventricular tachycardias with Wolff-Parkinson-White syndrome, and refractory ventricular arrhythmias including recurrent ventricular tachycardia and ventricular fibrillation complicating acute coronary heart disease. Control was confirmed by continuous ECG monitoring both in the hospital and when ambulatory and was maintained for up to four years. Attacks of supraventricular tachycardia were reduced from 7.9/mo to one attack every 53.5 months on amiodarone. Hospital admissions for arrhythmias were reduced from 34 the year before treatment to none the year after. Therefore, amiodarone is an excellent drug for control of many refractory arrhythmias, but two patients with recurrent atrial fibrillation were refractory to this treatment.     

Clinical and electrophysiologic assessment of oral flecainide acetate for recurrent ventricular tachycardia: Evidence for exacerbation of electrical instability

Four patients with recurrent, symptomatic ventricular tachycardia (VT) refractory to conventional antiarrhythmic agents were given flecainide acetate to control arrhythmias. Ventricular stimulation studies were performed in all patients before and 1 to 2 weeks after initiation of oral flecainide therapy. Before flecainide, all patients had easily inducible VT that was morphologically identical to their spontaneously occurring arrhythmia. Flecainide increased the mean PR interval (from 0.17 to 0.23 second), mean QRS duration (from 0.08 to 0.12 second) and mean ventricular effective refractory period (from 235 to 270 ms). Mean corrected QT interval did not change (0.51 second).In 2 patients, VT could not be induced during follow-up stimulation studies. One patient has been treated successfully for 10 months, with no clinically apparent episodes of VT. One patient had recurrent nonsustained VT and was withdrawn from the study as a treatment failure after 6 months of therapy. Two patients had inducible, polymorphous VT that degenerated into ventricular fibrillation that required 2 countershocks before the successful restoration of sinus rhythm. One of these patients had VT stimulation by atrial pacing at a cycle length of 320 ms in the postflecainide electrophysiologic study. VT was not inducible by atrial pacing during this patient's preflecainide study.Thus, sustained oral flecainide administration may precipitate serious electrical instability in susceptible patients, and ventricular stimulation studies and other clinical variables may be useful in selecting patients with recurrent VT who may benefit or may be endangered by oral flecainide therapy.     

Mexiletine for refractory-ventricular arrhythmias: Results using serial electrophysiologic testing

Mexiletine was administered during serial drug testing to 35 patients with electrically inducible ventricular arrhythmias and to 6 with recurrent ventricular tachycardia that could not be induced or terminated by programmed cardiac stimulation. All patients had arrhythmias resistant to all conventionally available agents. Electrically induced arrhythmias were completely suppressed during mexiletine therapy in 13 patients. In 12 patients no antiarrhythmic regimen was completely suppressive and in 7 of these mexiletine favorably modified the response to programmed stimulation. In four of six patients with frequent episodes of spontaneous ventricular tachycardia that were not inducible by programmed cardiac stimulation, arrhythmia was controlled by mexiletine. The presence of complete arrhythmia suppression with mexiletine during acute testing accurately predicted long-term freedom from recurrent arrhythmia in 16 of 17 patients over a mean follow-up period of 12.6 ± 6 months. Severe adverse neurologic effects were noted early during mexiletine therapy in three patients, but no patient discharged on such therapy experienced major adverse effects. The study demonstrates that mexiletine can provide well tolerated effective prophylaxis against recurrent ventricular arrhythmias in a significant proportion of patients resistant to conventional drugs.     

Amiodarone in patients with recurrent sustained ventricular tachyarrhythmias: results of programmed electrical stimulation and long-term clinical outcome in chronic treatment

Thirty-three patients with clinically recurrent ventricular tachyarrhythmias were treated with amiodarone (200 to 600 mg/day) during a mean follow-up period of 23.7 months. Prior to amiodarone therapy, sustained ventricular tachycardia or ventricular fibrillation was initiated in all patients at control electrophysiologic study; patients failed a mean of 5.7 drugs, as assessed by programmed electrical stimulation. At electrophysiologic study after a loading phase (1000 mg/day for 10 days), 10 patients had no inducible ventricular tachycardia, nine patients had nonsustained ventricular tachycardia, 13 patients had persistent sustained ventricular tachycardia, and one patient had ventricular fibrillation. Patients were continued on amiodarone alone regardless of the findings at the electrophysiologic study, and during follow-up patients with no inducible sustained ventricular tachycardia or fibrillation on amiodarone had no recurrent arrhythmias or sudden death. Six of 14 patients (43%) with sustained ventricular tachyarrhythmias still inducible had recurrent ventricular tachycardia/fibrillation, and four of them died suddenly (29%). Programmed electrical stimulation predicts a good clinical long-term outcome during amiodarone therapy. Patients with persisting fast tachyarrhythmias (cycle length less than or equal to 300 msec) on amiodarone and a low ejection fraction (less than 35%) seem to have a higher incidence of sudden death. In these patients, therapeutic approaches such as antiarrhythmic surgery or implantation of antitachycardia devices should be considered.     

Electrophysiologic testing and follow-up of patients with aborted sudden death

Clinical, electrophysiologic and follow-up data were analyzed for 108 patients with aborted sudden death. The mean follow-up interval was 2 years. All patients underwent baseline drug-free invasive electrophysiologic studies. Seventy-five patients (group I) had inducible ventricular arrhythmias (including nonsustained and sustained ventricular tachycardia and ventricular fibrillation) and 33 patients (group II) had no inducible arrhythmias. Noninducibility was not predictive of a favorable outcome, because the incidence of both sudden death and recurrent ventricular tachycardia was similar in the two groups. Treatment guided by electrophysiologic testing was used in 17 patients; in 13 (17%) in group I arrhythmias became noninducible, and in 4 (5%) sustained ventricular arrhythmias became nonsustained after administration of conventional drugs. There was a significantly higher incidence of sudden death and recurrent ventricular tachycardia in the 4 patients with inducible arrhythmias (n = 3, 75%) compared with the 13 patients whose arrhythmias were noninducible (n = 2, 15%) (p less than 0.05). For the group as a whole, 11% died suddenly and 15% had recurrence of ventricular tachycardia. Sixty-four patients were treated with amiodarone and, of these, four (6%) died suddenly during the follow-up period and nine (14%) had recurrent ventricular tachycardia. Ventricular arrhythmias could be induced in 69% of patients with aborted sudden death but inducibility could be suppressed in only 20% of them. The role of therapy guided by electrophysiologic testing could therefore not be fully assessed. The findings reveal a significant recurrence rate of symptomatic, potentially life-threatening ventricular arrhythmias in medically treated patients with aborted sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)