Electrophysiologic drug testing in patients with malignant ventricular arrhythmias: Importance of stimulation at more than one ventricular site

Sixty-four patients with symptomatic ventricular tachycardia or ventricular fibrillation underwent right ventricular apical programmed stimulation and had no inducible ventricular tachycardia during drug testing. Thirty patients (Group I) did not undergo left ventricular stimulation. Left ventricular stimulation in 38 drug trials induced no ventricular tachycardia in 50% (Group HA), nonsustained ventricular tachycardia in 26% (Group IIB), and sustained ventricular tachycardia In 24% (Group IIC).Patients in Groups I, IIA, and IIB received chronic antiarrhythmic drug therapy based on the results of electrophysiologic drug testing. Patients in Group IIC underwent further drug testing until sustained ventricular tachycardia was no longer inducible and were then entered into Group IIA or IIB; 4 patients in whom the induction of sustained ventricular tachycardia could not be suppressed by any drug regimen tested were excluded from long-term follow-up. The duration of follow-up (mean ± standard deviation) was 15.8 ± 11.5 months in Group I, 13.6 ± 3.7 months in Group IIA, and 12.1 ± 4.9 months in Group IIB. Recurrence rates of symptomatic ventricular tachycardia or sudden death were 27% in Group I, 0% in Group IIA, and 20% in Group IIB (p < 0.02 for Group IIA versus Group I and p > 0.05 versus Group IIB).If only right ventricular apical stimulation is performed during electrophysiologic drug testing in patients with malignant ventricular arrhythmias, approximately 50% of drug trials may be Incorrectly judged as suppressing the induction of ventricular tachycardia. Drug therapy that suppresses ventricular tachycardia induction with both right and left ventricular programmed stimulation results in a significantly better clinical response than therapy based on the results of only right ventricular apical stimulation.     

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 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.     

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.     

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.     

Clinical characteristics and results of electrophysiologic testing in young adults with ventricular tachycardia or ventricular fibrillation

Thirty-one patients 16 to 40 years of age (mean +/- SD = 30.7 +/- 7 years) had one or more episodes of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Underlying cardiac abnormalities consisted most commonly of cardiomyopathy (nine), long QT syndrome (LQTS) (five), and mitral valve prolapse (five); no identifiable heart disease was found in four patients. Programmed ventricular stimulation induced VT in only one of four patients with the LQTS but induced VT in 64% of 22 patients with other abnormalities. Chronic drug treatment was based either on serial electropharmacologic testing or was empiric when electrophysiologic testing failed to provoke an arrhythmia. Using this approach, we found a 13% incidence of recurrent VT and a 10% mortality over a follow-up period of 18.1 +/- 13.9 months. In young adults with VT or VF, an underlying cardiac abnormality can usually be found. Extensive evaluation should be performed to uncover the underlying cardiac abnormality as this may influence chronic management.     

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.     

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.     

Dobutamine in chronic ischemic heart failure: Alterations in left ventricular function and coronary hemodynamics

Changes in cardiac performance and coronary hemodynamics were evaluated during dobutamine infusion in patients with chronic heart failure associated with ischemic heart disease. At the maximal administered dose (10 μg/kg per min) cardiac index increased by 54 percent and stroke work index by 65 percent, indicating improved left ventricular function. Coronary sinus flow and myocardial oxygen consumption increased concomitantly, but myocardial lactate production occurred in only one of eight patients. These findings suggest that improved left ventricular function with dobutamine is associated with increased myocardial oxygen consumption; however, overt myocardial ischemia occurs infrequently.     

An accurate means of detecting and characterizing abnormal patterns of ventricular activation by phase image analysis

The ability of scintigraphic phase image analysis to characterize patterns of abnormal ventricular activation was investigated. The pattern of phase distribution and sequential phase changes over both right and left ventricular regions of interest were evaluated in 16 patients with normal electrical activation and wall motion and compared with those in 8 patients with an artificial pacemaker and 4 patients with sinus rhythm with the Wolff-Parkinson-White syndrome and delta waves. Normally, the site of earliest phase angle was seen at the base of the interventricular septum, with sequential change affecting the body of the septum and the cardiac apex and then spreading laterally to involve the body of both ventricles. The site of earliest phase angle was located at the apex of the right ventricle in seven patients with a right ventricular endocardial pacemaker and on the lateral left ventricular wall in one patient with a left ventricular epicardial pacemaker. In each case the site corresponded exactly to the position of the pacing electrode as seen on posteroanterior and left lateral chest X-ray films, and sequential phase changes spread from the initial focus to affect both ventricles. In each of the patients with the Wolff-Parkinson-White syndrome, the site of earliest ventricular phase angle was located, and it corresponded exactly to the site of the bypass tract as determined by endocardial mapping. In this way, four bypass pathways, two posterior left paraseptal, one left lateral and one right lateral, were correctly localized scintigraphically. On the basis of the sequence of mechanical contraction, phase image analysis provides an accurate noninvasive method of detecting abnormal foci of ventricular activation.     

Influence of short-term oral hydralazine therapy on exercise hemodynamics in patients with severe chronic heart failure.

Changes in left ventricular performance were evaluated in 14 patients with functional New York Heart Association class III or IV chronic heart failure before and after the addition of oral hydralazine to conventional therapy. With conventional therapy, cardiac output increased from 3.4 +/- 0.8 (mean +/- 1 standard deviation) at rest to 4.7 +/- 1.4 liters/min during exercise. This increase in cardiac output on exercise during conventional therapy was mainly due to an increase in heart rate. After the addition of hydralazine, cardiac output at rest increased to 5.0 +/- 1.4 liters/min. The increase in cardiac output was essentially due to an increase in stroke volume. This enhanced stroke volume after hydralazine therapy was maintained during exercise. Hydralazine therapy did not change either the left ventricular filling pressure at rest or the magnitude of increase in left ventricular filling pressure during exercise. Nevertheless, increased cardiac output and stroke volume with similar changes in left ventricular filling pressure during exercise indicated improved left ventricular performance after hydralazine therapy. After short-term hydralazine therapy, symptom-limited peak exercise work load, duration of exercise and maximal oxygen consumption during exercise did not increase. Clinical follow-up at 2 months after long-term therapy revealed subjective improvement in exercise tolerance in 13 of the 14 patients.     

Comparison of M-mode echocardiographic measurement of right ventricular wall thickness obtained by the subcostal and parasternal approach in children

Right ventricular (RV) wall thickness was measured from M-mode echocardiograms at end-diastole from both the parasternal and subcostal approaches in 50 children of various body surface areas (0.24 to 1.68 m2). The measurements were obtained from M-mode recordings generated from sector scans to ensure precise location and position. Twenty-three children had normal hearts, and 27 had various congenital heart defects that may be associated with RV hypertrophy. Corresponding measurements of the RV wall thickness at end-diastole from the 2 approaches were similar. Subcostal echocardiographic measurement of RV wall thickness was found to be a reliable alternative to parasternal measurement in children with normal hearts and in those with congenital heart disease and RV hypertrophy.