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.     

Reentry confined to the atrioventricular node: Electrophysiologic and anatomic findings

A patient with recurrent disabling, paroxysmal supraventricular tachycardia refractory to drug treatment underwent electrophysiologic studies. The paroxysmal supraventricular tachycardia was found to be due to atrioventricular (A-V) nodal reentry. The patient died shortly after surgical His bundle section and detailed anatomic studies were performed. These showed fatty infiltration of the approaches to the sinoatrial node, atrial preferential pathways, and A-V node and common bundle. The A-V node was mechanically damaged and the common His bundle was completely severed. These abnormalities were clearly delineated and there was no evidence of an atrio-His bundle bypass tract to an accessory A-V node. Specifically, the central fibrous body and pars membranacea were defined and no atrial muscular fibers pierced these structures to join the A-V bundle. It is concluded that paroxysmal supraventricular tachycardia due to A-V nodal reentry can be confined to the A-V node.     

Unusual complications of epicardial pacemakers: Recurrent pericarditis,cardiac tamponade and pericardial constriction

Three patients with unusual complications after insertion of an epicardial pacemaker are described. In one patient pericarditis and severe cardiac tamponade developed that required emergency pericardiocentesis 8 weeks after pacemaker insertion. No evidence of myocardial perforation was observed at operation. In another patient two unusual complications developed: (1) migration of the pulse generator from the epigastric site of implantation into the pelvis, and (2) recurrent pericarditis with occult signs of constriction. In another patient recurrent pericarditis and clinical evidence of constriction developed. All three patients required pericardiectomy. Recurrent pericarditis after insertion of an epicardial pacemaker requires careful medical follow-up because either life-threatening tamponade or chronic constrictive pericarditis may develop.     

Two-dimensional echocardiographic recognition and repair of subvalvular mitral aneurysm of the left ventricle in an infant

The clinical features, diagnostic studies and surgical treatment of a subvalvular mitral aneurysm of the left ventricle are described. The infant presented at 9 weeks of age with large apical ventricular septal defects and pulmonary hypertension. The subvalvular aneurysm was an incidental finding. Both lesions were treated surgically.     

Programmed ventricular stimulation in mitral valve prolapse: analysis of 36 patients

Programmed ventricular stimulation with 3 extrastimuli was performed in 36 patients with mitral valve prolapse (MVP). Among 11 patients without transient cerebral symptoms, none had inducible ventricular tachycardia (VT) or ventricular fibrillation (VF), whether or not nonsustained VT or ventricular premature complexes (VPC) were present during ambulatory electrocardiographic recordings. These patients remained well without antiarrhythmic drug therapy for 6 to 57 months (mean 23) of follow-up. Two patients with recurrent unexplained syncope and no documented ventricular arrhythmia during electrocardiographic monitoring also had no inducible VT or VF. Among 20 patients with syncope or presyncope and documented nonsustained VT or VPCs during electrocardiographic monitoring, polymorphic nonsustained VT was induced in 8, sustained unimorphic VT in 2, and VF in 3. In 1 patient who had inducible polymorphic nonsustained VT, electrocardiographic monitoring during syncope showed sinus rhythm. Among 3 patients with a history of sustained VT or VF, unimorphic VT was induced in each. Patients with MVP who have asymptomatic ventricular ectopic activity and no inducible VT may have a benign prognosis without treatment. In patients who have transient cerebral symptoms and documented nonsustained VT or VPCs, VT or VF is inducible in 65%, most often polymorphic VT. It is unclear in which patients this finding is clinically significant and in which it is a nonspecific response to programmed stimulation.     

Value of the H-Q interval in patients with bundle branch block and the role of prophylactic permanent pacing

His bundle electrograms were obtained in 313 patients with chronic bundle branch block who were followed for a mean period of almost 3 years. The infranodal conduction time (H-Q interval) was < 55 ms in 97 patients (Group I), 55 to 69 ms in 99 patients (Group II), and > 70 ms in 117 patients (Group III). There was a higher incidence of organic heart disease in patients in Group III, but the groups were otherwise comparable. On follow-up study, mortality and the incidence of sudden death were similar among the groups, but patients in Group III had a greater incidence of progression to high degree atrioventricular block (HDB) than did those in Groups I and II (14 of 117 [12%] versus 4 of 97 [4%] and 2 of 99 [2%], p < 0.0, rmrespectively). High degree block was found in 4 of 17 (24%) patients with an H-Q interval (H-Q) ≥ 100 ms.

Sixty-two patients underwent permanent prophylactic pacemaker insertion at the discretion of the referring physician and were compared with 231 patients who did not. Paced patients had a higher incidence of transient neurologic symptoms and prolonged H-Q, but the groups were otherwise comparable. On follow-up study, mortality and the incidence of sudden death were similar among the groups, but symptom relief was significantly more common among patients with pacemakers.

In conclusion, in our population (1) H-Q ≥ 70 ms was an independent risk factor for progression to HDB, (2) H-Q ≥ 100 ms identified a subgroup at particularly high risk, and (3) prophylactic pacemakers relieved neurologic symptoms but did not prolong life.     

Electrophysiologic testing in the management of survivors of out-of-hospital cardiac arrest

Forty-five patients survived a cardiac arrest due to ventricular tachycardia (VT) or ventricular fibrillation (VF). Programmed ventricular stimulation was performed with the patients taking no antiarrhythmic medications. Sustained VT was induced in 26 patients (58%) and nonsustained VT in 8 (18%). With treatment aimed at the underlying heart disease (plus empiric antiarrhythmic therapy in 2 patients), the 11 patients who had no inducible VT have had no recurrence of symptomatic VT or cardiac arrest over a follow-up period of 19 +/- 9 months (mean +/- standard deviation). Conventional antiarrhythmic drugs suppressed the induction of VT and were used for chronic treatment in 9 of 34 patients (26%) with inducible VT. Three of these 9 patients had recurrent VT or sudden death, whereas 6 have had no recurrence over follow-up of 20 +/- 7 months. In the 25 of 34 patients in whom the induction of VT was not suppressed by conventional antiarrhythmic drugs, 23 were treated with amiodarone (daily dose 550 +/- 120 mg), and 2 underwent coronary artery bypass grafting with either aneurysmectomy or map-directed endocardial resection. One of the latter 2 patients died suddenly 12 months after surgery. Among the 23 patients treated with amiodarone, 2 had fatal VT or sudden death and 21 (91%) did not, over 18 +/- 14 months of follow-up. In survivors of a cardiac arrest, the chief value of electrophysiologic testing is in identifying patients without inducible VT, who appear to have a low risk of recurrent sudden death with treatment directed at the underlying heart disease. Serial electropharmacologic testing with conventional antiarrhythmic drugs is disappointing, with a low incidence of arrhythmia suppression.     

Electrophysiologic testing in the management of patients with the Wolff-Parkinson-White syndrome and atrial fibrillation

Twenty patients with the Wolff-Parkinson-White (WPW) syndrome and 1 or more episodes of symptomatic atrial fibrillation (AF) due to rapid anterograde bypass tract conduction underwent electrophysiologic testing. The mean ventricular rate during spontaneous AF was 242 ± 56 beats/min (± standard deviation) and the shortest preexcited R-R interval was 194 ± 40 ms. Six patients underwent surgical bypass tract ablation and 14 were treated medically, based on the results of electropharmacologic testing. Over a mean follow-up period of 35 ± 19 months (± standard deviation), only 1 patient treated medically had a recurrence of minimally symptomatic AF. The successful chemoprophylaxis of symptomatic AF was associated with the inability to induce AF and atrioventricular reciprocating tachycardia during drug testing (7 patients) or with the induction of AF with a ventricular rate < 200 beats/min and a shortest preexcited R-R interval of > 250 ms (7 patients). Electrophysiologic testing can identify a subgroup of patients with WPW and AF in whom medical therapy is a suitable alternative to bypass tract ablation.