Long-term clinical outcome of ventricular tachycardia or fibrillation treated with amiodarone

The determinants of long-term clinical outcome were studied in 42 patients with recurrent ventricular tachycardia (VT) or ventricular fibrillation (VF) who were treated with amiodarone as the sole antiarrhythmic agent. Of the 42 patients, 11 (26%) either died suddenly or had recurrent, symptomatic, sustained VT during a mean follow-up period of 10 months (range 0.3 to 45). Of the 19 patients without inducible VT/VF during electrophysiologic study while receiving amiodarone, 1 patient died suddenly but no patient had recurrent VT/VF. Ten of the 23 patients (43%) with persistently inducible arrhythmia have died suddenly or have had recurrent VT/VF. Using survival and stepwise logistic regression analyses, 2 significant independent predictors of recurrent arrhythmia were identified; persistently inducible VT during electrophysiologic testing in patients receiving amiodarone therapy (p < 0.002) and the left ventricular ejection fraction at rest (p < 0.05). The predictive accuracy of the response to serial electrophysiologic testing during amiodarone therapy was 67%, the sensitivity was 58% and the specificity was 91%. Thus, serial electrophysiologic testing is useful for determining the prognosis in patients with inducible VT/VF treated with amiodarone.     

Electrophysiologic effects of bepridil in patients with refractory ventricular tachycardia assessed by programmed electrical stimulation

The effect of intravenous bepridil, a new calcium antagonist with class I and III properties, was tested in 21 patients with sustained ventricular tachyarrhythmias refractory to a mean of five antiarrhythmic agents as assessed by programmed right ventricular stimulation. At control electrophysiologic study without antiarrhythmic agents, sustained monomorphic ventricular tachycardia (VT) was initiated in 20 patients and ventricular fibrillation (VF) was initiated in one patient. After 3 mg/kg of bepridil was administered, VT was still inducible in 19 patients (3 patients had self-terminating VT); the other 2 patients had no inducible VT after bepridil. Bepridil prolonged significantly the QTc interval, the effective refractory period, and the cycle length of induced ventricular tachycardia. Two patients with no inducible VT after intravenous bepridil were placed on oral bepridil (300 mg/day). One patient died suddenly and one patient died of progressive heart failure. The results seem to indicate that the efficacy of bepridil in patients with refractory ventricular tachycardia is limited.     

Intravenous amiodarone in the treatment of refractory life-threatening cardiac arrhythmias in the critically ill patient

Eleven critically ill patients with life-threatening cardiac arrhythmias refractory to currently approved antiarrhythmic drugs were treated with intravenous amiodarone. Two patients had acute myocarditis, five had acute myocardial infarction, two had left ventricular failure secondary to ischemic heart disease, one had Wolff-Parkinson-White syndrome, and one manifested postoperative atrial fibrillation. Eight of the patients had severe cardiac failure and five had hypotension requiring intravenous dopamine. Five patients were treated for recurrent ventricular fibrillation, two for recurrent ventricular tachycardia, and four for recurrent atrial arrhythmlas. Six patients had repeated cardioversions. The arrhythmias had lasted a mean of 88.3 hours resistant to a mean of 2.7 different intravenous antiarrhythmic drugs. The ventricular arrhythmias did not recur after commencing intravenous amiodarone, but some minor atrial arrhymias occurred for 24 hours. One patient died of intractable left ventricular failure, chronic obstructive lung disease, and respiratory arrest during treatment. The dose of amiodarone was 150 mg over 5 minutes, followed by 600 mg/24 hr for 3 to 4 days; one patient on total parenteral nutrition required intravenous amiodarone for 20 days. Hypotension, cardiac failure, and bradyarrhythmias were not induced by this treatment. Intravenous amiodarone can be used safely in critically ill patients with impaired left ventricular function to control life-threatening refractory cardiac arrhythmias.     

Meobentine sulfate: antiarrhythmic and electrophysiologic effects assessed by programmed electrical stimulation and ambulatory monitoring in patients with complex ventricular tachyarrhythmia. Report of a multicenter evaluation

Five cardiology centers conducted open-label prospective trials of meobentine sulfate, an intravenously and orally available analog of bethanidine, to assess its potential for treatment of recurrent, drug refractory ventricular tachycardia (VT) or fibrillation (VF), and complex ventricular arrhythmias. The study population comprised 26 patients (mean age, 61 years); 18 were men. Coronary artery disease was present in 15, cardiomyopathy in six, and valvular heart disease in three. Patients presented with both VT and VF (seven), sustained VT alone (12), or frequent ventricular ectopy (PVCs) and nonsustained VT (seven). Of the 26 patients, 5 were enrolled in antiarrhythmic studies (chronic PVC suppression) and 21 were enrolled in programmed electrical stimulation (PES) studies. Two of five in the chronic PVC study showed greater than 75% arrhythmia suppression. Among 21 patients in PES studies, there were eight intravenous (16 mg/kg) and 19 oral trials (400 to 1000 mg every 6 hours, 3 days/dose interval). Five of 22 patients showed efficacy at repeat PES study (neither VT nor VF), one showed partial efficacy, and four were not restudied because of clinical arrhythmia (three) and/or adverse effects (two). Overall, three patients (12%) were continued on the drug for an extended period of time. Adverse experience included hypotension in 50% and gastrointestinal effects (nausea, vomiting, or diarrhea) in 56% (oral trials only). Adverse reactions led to drug discontinuation in six and dosage reduction in eight patients. Thus, meobentine may prevent induction of VT or VF or reduce frequency of complex PVCs in selected patients refractory to other antiarrhythmic agents, but the response rate is relatively low. Symptomatic hypotension or gastrointestinal adverse effects are common and may limit utility of meobentine as a chronic oral antiarrhythmic agent.     

Long-term efficacy and toxicity of high-dose amiodarone therapy for ventricular tachycardia or ventricular fibrillation

Amiodarone was administered to 154 patients who had sustained, symptomatic ventricular tachycardia (VT) (n = 118) or a cardiac arrest (n = 36) and who were refractory to conventional antiarrhythmic drugs. The loading dose was 800 mg/day for 6 weeks and the maintenance dose was 600 mg/day. Sixty-nine percent of patients continued treatment with amiodarone and had no recurrence of symptomatic VT or ventricular fibrillation (VF) over a follow-up of 6 to 52 months (mean ± standard deviation 14.2 ± 8.2). Six percent of the patients had a nonfatal recurrence of VT and were successfully managed by continuing amiodarone at a higher dose or by the addition of a conventional antiarrhythmic drug. One or more adverse drug reactions occurred in 51% of patients. Adverse effects forced a reduction in the dose of amiodarone in 41 % and discontinuation of amiodarone in 10% of patients. The most common symptomatic adverse reactions were tremor or ataxia (35 %), nausea and anorexia (8%), visual halos or blurring (6%), thyroid function abnormalities (6%) and pulmonary interstitial infiltrates (5%).Although large-dose amiodarone is highly effective in the long-term treatment of VT or VF refractory to conventional antiarrhythmic drugs, it causes significant toxicity in approximately 50% of patients. However, when the dose is adjusted based on clinical response or the development of adverse effects, 75 % of patients with VT or VF can be successfully managed with amiodarone.     

Intravenous amiodarone in the acute treatment of recurrent symptomatic ventricular tachycardia

Fifteen patients aged 59.3 +/- 11.5 years (mean +/- standard deviation [SD]) had recurrent symptomatic ventricular tachycardia (VT) refractory to at least 2 conventional antiarrhythmic drugs. All patients had organic heart disease; 4 had an acute myocardial infarction. The mean ejection fraction was 0.30 +/- 0.09. TWelve patients had overt congestive heart failure. Five had bundle branch block. Before treatment with intravenous amiodarone, the patients had had 6 to 40 episodes of symptomatic VT over 1 to 8 days of hospitalization. All patients received an initial bolus of 5 mg of amiodarone/kg over 15 minutes. Seven patients also received a continuous infusion of 600 to 1,000 mg of amiodarone over 12 to 24 hours. Additional doses depended on the patients' clinical responses. In 11 of 15 patients, antiarrhythmic drugs that had failed to suppress VT were continued during administration of amiodarone. In 12 of 15 patients acute control of VT was obtained with intravenous administration of amiodarone either alone or in combination with previously ineffective drugs. Three patients continued to have frequent episodes of VT while being treated with intravenous amiodarone. Mobitz type I atrioventricular block developed in 1 patient. No patient had high degree atrioventricular block, symptomatic hypotension, or a clinically apparent worsening of congestive heart failure. The use of intravenous amiodarone represents a significant advance in the acute treatment of frequent life-threatening VT refractory to other drugs. With appropriate monitoring, it can be used safely in patients with congestive heart failure, bundle branch block, or acute myocardial infarction.     

Electrophysiologic testing: predictive of amiodarone efficacy in recurrent sustained ventricular tachycardia?

The role of programmed ventricular stimulation (PVS) was evaluated in 12 patients with recurrent sustained ventricular tachycardia (VT) who were treated with amiodarone as the sole antiarrhythmic agent. At control PVS, sustained VT was induced in 11 patients and nonsustained VT was induced in one patient, as compared with late PVS (mean, 8.6 weeks) when sustained VT was induced in six patients and nonsustained VT was induced in five. Amiodarone significantly prolonged the patients' RR, PR, QRS, and QTc intervals, VT cycle length, and right ventricular effective refractory period. During a mean follow-up of 16 +/- 13.6 months, two patients had recurrent clinical VT. In the patients in whom amiodarone therapy failed (1) sustained VT was induced during late PVS, (2) VT cycle length and symptoms during late PVS and during recurrent clinical VT were similar, and (3) the QTc failed to be prolonged significantly (32.5 +/- 1.6 ms in amiodarone failure vs. 84.1 +/- 27.1 ms in amiodarone success, P<0.05). It is concluded that (1) amiodarone in high-risk patients is clinically effective (88.3%), (2) patients with noninducible VT or nonsustained VT during late PVS did not have recurrent clinical VT, (3) late PVS is probably predictive of electrophysiologic and hemodynamic consequences in patients with recurrent spontaneous VT, and (4) failure of the QTc interval to be prolonged substantially is probably predictive of clinical recurrence of VT.     

Encainide in lethal ventricular arrhythmias evaluated by electrophysiologic testing and decrease in symptoms

Encainide hydrochloride has distinct electrophysiologic properties that suggest active antiarrhythmic properties. Encainide has been administered both intravenously (0.5 to 1.7 mg/kg) and orally (100 to 300 mg/day) to patients with lethal ventricular arrhythmias--ventricular tachycardia (VT) and ventricular fibrillation--and evaluated by electrophysiologic testing. In 62 patients with inducible sustained VT, intravenous encainide prevented initiation in 13 (21%). In 57 patients with refractory sustained VT, oral encainide prevented initiation of VT by programmed stimulation in 17 (30%). The results obtained with intravenous and oral encainide in the same patient were usually concordant (93%). Encainide may worsen ventricular arrhythmia, most typically by converting nonsustained VT into sustained VT during electrophysiologic testing. In patients with lethal ventricular arrhythmia, analysis of symptoms before and during chronic encainide therapy showed that the number and severity of arrhythmia-related symptoms were reduced. Encainide appears to be a useful antiarrhythmic agent.     

Control of refractory life-threatening ventricular tachyarrhythmias by amiodarone

The antiarrhythmic effects and dose-response relationship of amiodarone hydrochloride, 600 to 1200 mg daily, were studied in 22 patients with recurrent life-threatening symptomatic ventricular tachyarrhythmias refractory to two or more conventional antiarrhythmic agents. In all patients the presence of the arrhythmia was confirmed on ECG and/or 24-hour Holter readings. In 10 one or more episodes of cardiac arrest had been documented by ECG. Two patients died prior to initiation or stabilization of therapy; the goal of therapy was attained in all but one patient. Amiodarone abolished all complex premature ventricular contractions (PVCs) and paroxysmal or sustained episodes of ventricular tachycardia (VT) in all 19 remaining patients; In the 15 in whom predrug and serial 24-hour Holter recordings could be obtained and analyzed, the total PVC counts were reduced 90% to 98% by amiodarone. After a mean follow-up of 12 months on chronic amiodarone therapy, there have been no recurrences of VT or ventricular fibrillation and sustained antiarrhythmic response has been confirmed by Holter recordings. One patient died suddenly at home despite complete suppression of PVCs. Amiodarone prolonged the PR (+16.7%; P < 0.05) and QT_c (+22.7%; P < 0.01) intervals without effect on QRS duration. Side effects attributable to the drug were gastrointestinal discomfort, halo vision, proximal muscle weakness, transient elevations of hepatic enzymes, and skin photosensitivity, all being reversible on reduction in dosage which did not compromise antiarrhythmic efficacy. Amiodarone did not aggravate cardiac failure even in patients with low ventricular ejection fractions. This study indicates that amiodarone is an extremely potent and safe agent for the prophylactic control of life-threatening ventricular tachyarrhythmias.     

Efficacy of the combination of low doses of beta-blockers and amiodarone in the treatment of refractory ventricular tachycardia

Thirty one patients aged 56 +/- 16 years with chronic ventricular tachycardias (VT) refractory to 4.4 +/- 1.8 antiarrhythmic drugs, used alone or in combination, were managed by low doses of beta-blocker agents combined with oral amiodarone, either after loading (1.2 g for 7 days, n : 7) or reloading (1.2 g for 4 days, n : 24) of amiodarone. All patients proved refractory to amiodarone alone. Nine VT were also refractory to endocardial catheter fulguration in 8 patients. Twenty one patients had coronary artery disease, 4 had arrhythmogenic right ventricular dysplasia, 4 had dilated cardiomyopathy, 1 had valvular disease, and 1 had no structural heart disease. Twelve patients had an ejection fraction less than 30 p. 100. Ten patients were in NYHA functional class 3. VT was permanent in 3 patients, daily in 5, weekly in 7, paroxysmal in 16. In 14 patients, VT occurred both at day and night. Oral administration of a daily low dose of a beta-blocker agent (acebutolol 100 mg, betaxolol 5-10 mg, metoprolol 50-100 mg, nadolol 20-40 mg, pindolol 2.5 mg, propranolol 30 mg, sotalol 80-160 mg, tertatolol 2.5 mg) combined with 400 mg per day of amiodarone suppressed VT episodes in all patients. None presented heart failure or collapse. The mean reduction of the heart rate was about 17 p. 100. One patient need a definite pacemaker to correct sinus bradycardia. At discharge, exercise ECG (n: 20) induced non sustained VT in 2 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

胺碘酮治疗维吾尔族器质性心脏病人室性心律失常的疗效和安全性

目的：评价胺碘酮治疗维吾尔族器质性心脏病人室性心律失常的疗效和安全性。方法：观察47例维吾尔族器质性心脏病人采用胺碘酮治疗室性心律失常的疗效和安全性，随访1～3年。结果：6例反复发作的持续性室速、室颤病人，首剂3～5mg／kg胺碘酮10min内静脉注射，再以1～1．5mg／min缓慢滴注，室速均被有效终止。以200mg／d胺碘酮作为长期维持量能有效的控制室性早搏(92．7％)。6例静脉注射胺碘酮病人中窦性心动过缓5例、PR间期延长1例；在41例长期口服维持量的病人中甲状腺功能低下者1例、窦性心动过缓18例、QT间期延长22例，但无肺损害发生。结论：采用胺碘酮治疗维吾尔族器质性心脏病人室性心律失常效果满意，安全可靠。     

Efficacy of Nifekalant hydrochloride for life-threatening ventricular tachyarrhythmias in patients with resistance to lidocaine: a study of patients with out-of-hospital cardiac arrest

OBJECTIVES: Class I antiarrhythmic agents are not always effective in the treatment of life-threatening ventricular tachycardia/ventricular fibrillation (VT/VF) especially in patients with cardiopulmonary arrest. Nifekalant hydrochloride(NIF) is a novel class III antiarrhythmic agent for malignant VT/VF. This study prospectively evaluated NIF efficacy for life-threatening VT/VF observed after cardiopulmonary arrest. METHODS: Thirty-two of 145 patients who were transferred to the emergency room in Tokai University Hospital showed VT/VF after resuscitation from cardiopulmonary arrest from June 2000 to March 2001. These 32 patients were treated with 12 mg (mean) epinephrine and 1.0-2.0 mg/kg lidocaine following direct current application(200 to 360J), and then classified into two groups. Eleven patients received intravenous 0.15 to 0.3 mg/kg NIF followed by intravenous infusion of 0.3 to 0.4 mg/kg/hr NIF(NIF group). The other 21 patients received 1.0 to 2.0 mg/kg of lidocaine(non-NIF group). RESULTS: Sinus rhythm was restored in the nine patients(82%) in the NIF group but only four patients (19%) in the non-NIF group. QTc was not prolonged(0.45 +/- 0.04 sec, n = 9) and no torsades de pointes was observed in the NIF group. Two patients survived but the remaining nine patients died in the NIF group. Five patients died of cardiac standstill following sinus bradycardia and repeated sinus arrest within 2 to 27 hr after admission, two patients died of sudden cardiac arrest from sinus rhythm, and two patients died of persistent VT/VF. In contrast, all 21 patients in the non-NIF group died. Seventeen patients died of persistent VT/VF before hospitalization, one patient died of recurrent VT/VF, and three patients died of cardiac standstill following sinus bradycardia. CONCLUSIONS: NIF effectively suppresses VT/VF which is refractory to direct current shock in patients with cardiopulmonary arrest. However, NIF may rather worsen electrophysiological function in the sinus node after administration of high doses of epinephrine, and may induce sinus bradycardia and/or sinus arrest. Careful observation, such as monitoring of electrocardiography and blood pressure and temporary cardiac pacemaker use, is needed to prevent death in patients surviving after cardiopulmonary arrest if NIF is administered following high dose epinephrine infusion.     

Evaluation of bepridil efficacy by electrophysiologic testing in patients with recurrent ventricular tachycardia: Comparison of two regimens

Summary The purpose of the study was to evaluate this effect of different doses of intravenous and oral bepridil on the induction of ventricular tachycardia. Thirty-eight patients underwent electrophysiologic evaluation for recurrent ventricular tachycardia (VT). Sustained monomorphic VT was induced by programmed ventricular stimulation, using up to three extrastimuli in all patients. The effects of intravenous bepridil (2 mg/kg) were evaluated during the initial study. Intravenous bepridil prevented the induction of sustained VT in eight patients (21%). Electrophysiologic study was repeated after oral bepridil. In six patients the study was stopped because of adverse effects or VT recurrence. Thirty-two patients underwent repeat study 7 days later, taking oral bepridil, 500 mg/day (n=16) or 900/day (n=16). A dose of 500 mg/day of bepridil prevented the induction of sustained VT in only one patient. A dose of 900 mg/day of bepridil prevented the induction of sustained VT in eight patients. There were no significant clinical adverse effects, except in one patient receiving intravenous bepridil. The response to intravenous bepridil did not predict the response to oral bepridil. The response to intravenous or oral bepridil was not related to the plasma level of bepridil but was related to a higher left ventricular ejection fraction. Eight patients (21%) in whom VTs were noninducible on oral bepridil were discharged on 300 mg/day of bepridil if their initial loading dose was 500 mg/day or on 600 mg/day if their initial loading dose was 900 mg/day. They remained free of VT during a follow-up of at least 6 months. In conclusion, this study suggests that oral bepridil at the dose of 600 mg/day may be of value in patients with recurrent VT.     

Out-of-hospital cardiac arrest in patients with no overt heart disease: electrophysiologic observations and clinical outcome

Electrophysiologic studies were performed in nine survivors of out-of-hospital cardiac arrest who had no overt heart disease on clinical, hemodynamic and angiographic evaluation. Cardiac arrest occurred during sedentary activity in seven patients and during exercise in two; no patient was on antiarrhythmic drugs at the time of cardiac arrest. Twenty-four hour ambulatory electrocardiographic monitoring demonstrated premature ventricular beats in four patients (44%). Electrophysiologic stimulation induced sustained ventricular tachycardia (VT) or fibrillation (VF) in five patients, nonsustained VT in one patient and less than five ventricular beats in the remaining three patients. Of five patients with inducible sustained VT or VF, four had complete suppression of inducible VT with antiarrhythmic therapy, and none of these four patients died suddenly or had clinical VT after an average follow-up of 27 months (range 12 to 41 months). The remaining patient with inducible sustained VT refused serial electropharmacologic testing, was treated empirically with amiodarone (400 mg/day) and died suddenly eight months later. Of the four patients with noninducible sustained VT or VF, three received no antiarrhythmic therapy and one was given a beta-blocker. None had recurrent cardiac arrest or symptomatic VT after an average follow-up of 17 months (range 13 to 20 months). Thus, inducibility of sustained VT or VF provided a reliable end point for long term antiarrhythmic therapy and noninducibility identified a subset of patients that had an excellent prognosis without specific antiarrhythmic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Suppression of sustained ventricular tachyarrhythmias: a comparison of d,l-sotalol with no antiarrhythmic drug treatment

Objectives. This study evaluates the clinical efficacy of d,l-sotalol in patients with sustained ventricular tachyarrhythmias.Background. D,l-sotalol is an important antiarrhythmic agent to prevent recurrences of sustained ventricular tachyarrhythmias (VT/VF). However, evidence is lacking that an antiarrhythmic agent like d,l-sotalol can reduce the incidence of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.Methods. A prospective study was performed in 146 consecutive patients with inducible sustained ventricular tachycardia or ventricular fibrillation. In 53 patients, oral d,l-sotalol prevented induction of VT/VF during electrophysiological testing and patients were discharged on oral d,l-sotalol (sotalol group). In 93 patients, VT/VF remained inducible and a defibrillator (ICD) was implanted. After implantation of the device patients were randomly assigned to oral treatment with d,l-sotalol (ICD/sotalol group, n = 46) or no antiarrhythmic medication (n = 47, ICD-only group).Results. During follow-up, 25 patients (53.2%) in the ICD-only group had a VT/VF recurrence in comparison to 15 patients (28.3%) in the sotalol group and 15 patients (32.6%) in the ICD/sotalol group (p = 0.0013). Therapy with d,l-sotalol, amiodarone or metoprolol was instituted in 12 patients (25.5%) of the ICD-only group due to frequent VT/VF recurrences or symptomatic supraventricular tachyarrhythmias. In nine patients, 17% of the sotalol group, an ICD was implanted after VT/VF recurrence, three patients (5.7%) received amiodarone. Total mortality was not different between the three groups.Conclusions. D,l-sotalol significantly reduces the incidence of recurrences of sustained ventricular tachyarrhythmias in comparison to no antiarrhythmic drug treatment.     

Sotalol for refractory sustained ventricular tachycardia and nonfatal cardiac arrest

The efficacy and safety of sotalol were assessed by electrophysiologic testing and ambulatory recordings in 16 patients with recurrent sustained ventricular tachycardia (VT) or nonfatal cardiac arrest who were refractory to an average of 4.8 conventional antiarrhythmic agents. Twenty-four-hour ambulatory recordings were performed before and after sotalol therapy. Fourteen patients underwent baseline electrophysiologic study and sustained VT was inducible in 12. Oral sotalol (320 to 960 mg/day) completely suppressed inducible sustained VT in 7 patients (58%), with modification in 3 (25%). Ventricular premature complexes were suppressed from baseline (mean +/- standard deviation) 431 +/- 616 to 60 +/- 110/hr (p less than 0.03). After a mean follow-up of 19 +/- 7 months, 12 of 14 patients receiving sotalol treatment had successful suppression of ventricular premature complexes (60 +/- 85/hr) and remained clinically free of sustained VT, except 2 who needed additional antiarrhythmic drugs to suppress the recurrent sustained VT. One patient died suddenly after 25 months of sotalol treatment. No severe side effects were noted during sotalol therapy. This study demonstrates that sotalol is a well-tolerated, effective antiarrhythmic agent in patients at high-risk for sudden death. It appears to be beneficial in patients who did not benefit from multiple drug treatment.     

Management of refractory sustained ventricular tachycardia with amiodarone: a reappraisal

We examined the value of clinical variables, chronic 24-hour ambulatory ECG monitoring, and chronic electrophysiologic (EP) testing in 49 patients with recurrent and refractory sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) treated with chronic oral amiodarone in order to develop a prospective approach to the management of these patients. All patients underwent control EP studies followed by continuous telemetric cardiac monitoring during oral amiodarone administration (mean duration 29 +/- 6 days, mean dose 739 +/- 230 mg). Follow-up 24-hour ambulatory ECG monitoring and EP studies were performed. Thirty VT recurrences occurred in the first 4 weeks of amiodarone therapy (total incidence, 61%), with the majority (55%) in the first 3 weeks of treatment. During long-term follow-up (1 to 42, mean 15 +/- 12 months), there were 12 symptomatic VT/VF recurrences (incidence 24%). There was a higher incidence of VT recurrences if patients had inducible sustained or nonsustained VT at chronic EP study (p less than 0.01), or complex ventricular arrhythmias on ambulatory ECG monitoring (p less than 0.05). The sensitivity, specificity, and predictive accuracy of chronic EP testing and 24-hour ambulatory ECG monitoring were 100%, 35%, and 51%, and 58%, 84%, and 78%, respectively. Chronic EP testing correctly identified all patients who had their arrhythmia suppressed by amiodarone on long-term follow-up, while 42% of all VT recurrences occurred in patients without complex ventricular arrhythmias on 24-hour ambulatory ECG monitor.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transvenous dual site left ventricular pacing plus biventricular pacing for the management of refractory ventricular tachycardia

This is a case report of a male patient with nonischemic cardiomyopathy who had severely depressed left ventricular systolic function and functional class III congestive heart failure (CHF). He also had left bundle branch block (LBBB) and recurrent ventricular tachycardia (VT). Though the patient’s CFH functional class improved after implantation of a transvenous biventricular ICD system, recurrent VT episodes required the initiation of amiodarone. After an improved condition for 28 months, recurrent VT episodes led to multiple consecutive ICD shocks, which constituted an electrical storm and a battery status of elective replacement indicator (ERI). The recurrent VT episodes were suppressed with intravenous amiodarone and lidocaine. As Radiofrequency ablation was declined by the patient, a new left ventricular (LV) lead was transvenously added, providing biventricular and dual site LV pacing. After this intervention the arrhythmia subsided and the intravenous antiarrhythmic medications were stopped. No episodes of sustained VT leading to ICD shocks were observed for the following 9 months. The events in this case suggest that dual site LV pacing with biventricular pacing could be an alternative strategy for the management of refractory VT.     

Drug conversion of nonsustained ventricular tachycardia to sustained ventricular tachycardia during serial electrophysiologic studies: Identification of drugs that exacerbate tachycardia and potential mechanisms

Eleven of 83 patients who had ventricular tachycardia (VT) and underwent serial electrophysiologic study (EPS) had a more severe VT induced while receiving a particular antiarrhythmic drug as compared to control study. For all patients only nonsustained VT was initiated during control study, while sustained VT occurred during drug testing with disopyramide (2 patients), quinidine (2 patients), amiodarone (4 patients), and encainide (7 patients), although spontaneous arrhythmias appeared well-controlled prior to repeat testing. Pacing techniques used to induce sustained VT were the same as those used in the control study in eight patients and “less aggressive” in three patients. Almost all episodes of sustained VT resulted in substantial hypotension, especially in patients who were taking encainide. Drugs associated with sustained VT increased the median tachycardia cycle length by 112 msec (p < 0.005) but increased the median ventricular effective refractory period by only 30 msec (p < 0.02). Assuming re-entry was responsible for VT, we postulate that drugs facilitated initiation of sustained VT by prolonging activation time but only minimally increasing refractoriness of the tachycardia circuit.