Invasive electrophysiologic testing: a critical appraisal.
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Arrhythmias, Cardiac↗
Biomedical subjects
M M Scheinman
Publications and source records attributed to M M Scheinman.
Recordings of basal ventricular preexcitation from electrode catheters in patients with accessory atrioventricular connections.
To determine the effects of ventricular preexcitation via accessory atrioventricular connections (ACs) on the sequence of basal ventricular activation, electrophysiologic study records of 22 patients with AC were reviewed. In each, AC site was confirmed by mapping done at operation. Local ventricular preexcitation (VP), defined as earlier timing of a local ventricular electrogram relative to the surface electrocardiographic QRS onset in preexcited compared with in normal QRS complexes, was assessed at the coronary sinus and at the ventricular septal summit recorded from the His bundle site. Five patients with concealed AC did not have VP. VP patterns with manifest AC were similar during average fusion QRS complexes and maximum ventricular preexcitation. Left free wall and left crux AC produced VP apparent on the ventricular electrogram recorded at the coronary sinus alone. With anteroseptal AC, VP was noted only at the ventricular septal summit. Posteroseptal AC produced VP that was apparent on the ventricular electrogram recorded at the coronary sinus and on the electrogram of the ventricular septal summit. Right free wall AC preexcited neither of these basal ventricular regions. The observation of VP patterns may help in localizing AC and may be particularly useful in patients without retrograde AC function at electrophysiologic study.
Adolescent↗
A prospective comparison of triple extrastimuli and left ventricular stimulation in studies of ventricular tachycardia induction.
One hundred and one patients with sustained unimorphic ventricular tachycardia underwent programmed ventricular stimulation with one of two protocols. Fifty patients underwent programmed stimulation with protocol A, which consisted of burst overdrive pacing, single, double, and triple extrastimuli at the right ventricular apex, right ventricular outflow tract, or septum, and then at the left ventricular apex. Fifty-one patients underwent programmed stimulation with protocol B, which consisted of burst overdrive pacing, single and double extrastimuli at the right ventricular apex, right ventricular outflow tract or septum, and at the left ventricular apex, followed by triple extrastimuli at these sites. The stimulation protocol was continued until sustained ventricular tachycardia or rapid, polymorphic ventricular tachycardia greater than 10 sec in duration was induced. With protocol A, clinical and nonclinical ventricular tachycardia was induced in 76% and 36% of patients, respectively; with protocol B, clinical and nonclinical ventricular tachycardia was induced in 85% and 38% of patients, respectively. Direct-current countershock for sustained polymorphic ventricular tachycardia was required in 10% of patients studied under protocol A, compared with in 2% of patients studied under protocol B. With protocol A, near-maximal yield of induced clinical (72%) and nonclinical ventricular tachycardia (30%) was attained after the use of triple extrastimuli at the first stimulation site. The yield of stimulation at a second right ventricular site and of left ventricular stimulation was only an additional 2% each. With protocol B, triple extrastimuli increased the yield of induced clinical ventricular tachycardia from 61% to 85%.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Efficacy of left cardiac sympathectomy in the treatment of patients with the long QT syndrome.
Ten patients with the long QT syndrome and recurrent syncope and/or cardiac arrest caused by ventricular arrhythmias underwent left stellate (one patient) or left cervicothoracic sympathectomy (nine patients) after failing to respond to high-dose beta-blocker therapy. The syndrome was familial in four and idiopathic in six. All patients had a prolonged resting QT interval (548 +/- 51 msec, mean +/- SD) and corrected QT interval (QTc) (556 +/- 43 msec). After sympathectomy the mean QTc shortened significantly from 556 +/- 43 to 508 +/- 65 msec (p less than .05) but the QTc remained abnormal in all but one patient. Over a mean follow-up period of 38.6 +/- 19 months, eight patients developed recurrent symptoms that included cardiac arrest in three (one fatal, two nonfatal), syncope in four, and presyncope in six. The addition of beta-blockers was ineffective in suppressing the recurrent symptoms. The control of symptoms required more extensive sympathectomy (three patients), chronic atrial pacing (three patients), and implantation of an automatic internal defibrillator (one patient). Only one patient has remained asymptomatic without drug or pacemaker therapy. In conclusion, left cervicothoracic sympathectomy proved inadequate for long-term control of symptoms in most patients with the long QT syndrome. These patients usually required concomitant drugs, more extensive surgery, or long-term cardiac pacing for symptomatic relief.
Adolescent↗
Catheter ablation of the atrioventricular junction: a report of the percutaneous mapping and ablation registry.
An international registry was formed to collate data for patients undergoing attempted catheter ablation of the atrioventricular (AV) junction and insertion of a permanent pacemaker. Over the past 2 years, data was submitted for 127 patients who were followed for a mean of 9.9 +/- 8.2 months. The most common arrhythmia treated was chronic or paroxysmal atrial fibrillation or flutter (78 patients, 61%); the remainder had supraventricular tachycardia due to AV node reentry, ectopic atrial tachycardia, or incorporated an accessory pathway. A single shock of 150 to 400 J was effective in producing chronic third-degree AV block in 45 patients while two or more shocks were used in an additional 45 patients. There was no significant difference in the total cumulative energy used in successful and unsuccessful procedures. Immediate complications related to the shock included ventricular fibrillation (one patient), pericardial tamponade (one patient), and transient hypotension (one patient). No chronic sequelae occurred as a result of these complications. Late complications (1 day to 1 month) included ventricular tachycardia (three patients), sepsis involving the pacemaker pocket (two patients), staphylococcal sepsis from temporary pacing catheter (one patient), thrombophlebitis (one patient), thrombosis of the left subclavian vein (one patient), and hemothorax (one patient). Follow-up evaluation revealed chronic third degree AV block in 90 (71%) and AV conduction resumed but no drugs were required for arrhythmia control in eight (6.5%) and arrhythmia control was achieved with previously ineffective drugs in 16 (13%). Thirteen patients (10%) had no improvement and five of these patients underwent cardiac electrosurgery for direct His bundle ablation.(ABSTRACT TRUNCATED AT 250 WORDS)
Anti-Arrhythmia Agents↗
Frequent neurologic toxicity associated with amiodarone therapy.
Fifty-four consecutive patients were treated with amiodarone for symptomatic ventricular tachycardia or ventricular fibrillation refractory to treatment with conventional antiarrhythmic drugs. A reversible neurologic syndrome of tremor, ataxia, and occasionally peripheral neuropathy without nystagmus, dizziness, encephalopathy, or long-tract signs developed in 54% of the patients and was the most common reason for altering or discontinuing drug therapy. Neurologic side effects improved or resolved within 2 days to 4 weeks of decreasing or discontinuing amiodarone. Frequent neurologic toxicity is a hitherto undescribed complication of amiodarone therapy. Wider recognition of this syndrome will avoid unnecessary and costly diagnostic evaluation.
Amiodarone↗
Personnel and equipment required for electrophysiologic testing. Report of the Committee on Electrocardiography and Cardian Electrophysiology, Council on Clinical Cardiology, the American Heart Association.
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American Heart Association↗
Electrophysiologic effects of theophylline in young patients with recurrent symptomatic bradyarrhythmias.
In this study, both acute electrophysiologic actions of intravenously administered theophylline and clinical effects of chronic oral theophylline therapy were assessed in 10 young patients (aged 9 to 41 years) without clinically significant cardiac disease, in whom recurrent symptoms of syncope and dizziness were attributed to transient bradyarrhythmias (sinus pauses, marked sinus bradycardia or paroxysmal atrioventricular [AV] block). Intravenous theophylline infusion (serum concentration range 9.5 to 12.0 mg/liter) shortened means sinus cycle length (control 973 +/- 285 ms versus theophylline 880 +/- 226 ms, p less than 0.005) and decreased both the estimated sinoatrial conduction time (control 169 +/- 56.0 ms versus theophylline 143 +/- 55.3 ms, p less than 0.05) and the maximum corrected sinus node recovery time (control 442 +/- 251.0 ms versus theophylline 255 +/- 146.2 ms, p less than 0.05). In addition, theophylline infusion shortened the minimum atrial paced cycle length with sustained 1:1 AV conduction (control 414 +/- 86 ms versus theophylline 379 +/- 97 ms, p less than 0.05) and consistently reduced AV node functional refractory periods. Subsequent chronic oral theophylline therapy (serum levels 9 to 12 mg/liter) was tolerated in 8 patients (80%). During a follow-up of 5 to 24 months, suppression of symptoms was achieved in 6 of the 8 patients. Thus, theophylline exhibits positive chronotropic and dromotropic effects in man at serum concentrations in the usual therapeutic range (10 to 15 mg/liter). Furthermore, suppression of symptoms during follow-up suggests that theophylline treatment may be a useful therapeutic consideration in some patients with recurrent symptomatic bradyarrhythmias.
Adolescent↗
Unusual features of bypass conduction in Wolff-Parkinson-White syndrome and atrial fibrillation.
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Adult↗
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.
Aged↗
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.
Adult↗
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.
Adult↗
Ventricular tachycardia: newer insights.
Electrophysiology has provided insights into our understanding of ventricular tachycardia. The techniques of electrophysiology which were useful as a research tool have only recently come to be appreciated in clinical practice. As a result, we have expanded our knowledge of the mechanisms of ventricular arrhythmias; we can distinguish among tachycardias masquerading as ventricular tachycardia; we can predict the response to drug and pacemaker treatment, and we can select out those who require surgical management.
Diagnosis, Differential↗
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.
Adolescent↗
Acute changes in infranodal conduction time following left ventriculography and sublingual nitroglycerin administration in man.
During diagnostic cardiac catheterization for the evaluation of chest pain, His bundle electrograms were obtained in 32 male patients before and 2 to 5 minutes after each of two interventions known to acutely affect left ventricular volume and left ventricular end-diastolic pressure (the injection of 40 to 60 cc of contrast medium during left ventriculography and the administration of 0.4 mg of sublingual nitroglycerin). Changes in left ventricular end-diastolic pressure (18 +/- 6 vs 30 +/- 7 mm Hg, p less than 0.001 following ventriculography and 32 +/- 8 vs 19 +/- 8 mm Hg, p less than 0.005 following nitroglycerin administration) were accompanied by parallel alterations in HQ (48 +/- 8 vs 54 +/- 10 msec, p less than 0.005 following ventriculography and 57 +/- 10 vs 53 +/- msec, p less than 0.005 following nitroglycerin administration), but there were no significant changes in atrioventricular (AV) nodal conduction (AH). Significantly greater changes in HQ were seen in patients with triple-vessel coronary artery disease than in the remainder of the population, although there was clinical and/or ECG evidence of ischemia in only one patient. We conclude that factors other than progression of intrinsic conduction system disease may affect infranodal conduction. HQ should be interpreted cautiously in situations with rapidly changing hemodynamics, especially in patients with severe coronary artery disease.
Bundle of His↗
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 less than 200 beats/min and a shortest preexcited R-R interval of greater than 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.
Adolescent↗
Treatment of cardiac arrhythmias in patients with acute myocardial infarction.
Cardiac arrhythmias and conduction disturbances are commonly observed in patients with myocardial infarction. The available data suggest the administration of prophylactic lidocaine, either through a large intramuscular dose (300 mg), which is particularly suited for out-patient situations, or through intravenous loading doses followed by a constant lidocaine infusion. Patients with ventricular arrhythmia should be treated with direct-current countershock if hemodynamic deterioration is present. Drug therapy for patients with ventricular arrhythmias who are resistant to lidocaine include procainamide, bretylium, or intravenous amiodarone (experimental drug). Treatment of atrioventricular block in acute infarction depends on the site of atrioventricular block, the infarct location, and the hemodynamic status. Generally, atrioventricular block associated with inferior infarction and normal hemodynamic states generally does require insertion of a pacemaker. In contrast, patients with anterior myocardial infarction and Mobitz II or third degree atrioventricular block should be treated with emergent temporary insertion of a pacemaker. In addition, prophylactic pacing is clearly indicated for those with acute myocardial infarction complicated by the bifascicular block pattern of first degree atrioventricular block and new onset bundle branch block.
Arrhythmias, Cardiac↗
New antiarrhythmic drugs.
Great advances have been made in our understanding of cardiac arrhythmias and the effect of drugs on these arrhythmias. Several new types of antiarrhythmic drugs have been introduced. For example, encainide, flecainide, or lorcainide are new type I drugs that exert their major effects on depressing cardiac conduction. These drugs appear to be very effective for suppression of premature ventricular contractions. The introduction of verapamil (a calcium antagonist) allows for rapid control of supraventricular arrhythmias by virtue of its effects on the slow-channel (predominately Ca++) receptors. New beta-blocking drugs have been introduced which may prove beneficial in certain clinical situations since they exert more selective blockade of the cardiac receptors (beta1) as opposed to smooth muscle receptors (beta2). Amiodarone is an extremely potent drug which is effective for both supraventricular as well as ventricular arrhythmias. The major cellular electrophysiologic effect of this drug is to prolong the action potential duration. Its major clinical drawback is the rather formidable long-term side effects which include corneal opacities, thyroid dysfunction, neurologic toxicity, and pulmonary fibrosis.
Amiodarone↗