The role and limitations of electrophysiologic testing in patients with unexplained syncope.
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Bundle-Branch Block↗
Biomedical subjects
M M Scheinman
Publications and source records attributed to M M Scheinman.
Electrophysiologic mechanism of exercise-induced sustained ventricular tachycardia.
To elucidate electrophysiologic mechanism of exercise-induced ventricular tachycardia (VT), electrophysiologic studies were performed in 12 patients in whom sustained VT had developed during treadmill exercise testing. Six patients had arteriosclerotic coronary heart disease, 3 had cardiomyopathy, and 3 had no clinical evidence of organic heart disease. All patients had had documented episodes of sustained VT related to exertion and had experienced dizziness, syncope, or both. In addition, 3 patients had had nonfatal cardiac arrest. Electrophysiologic studies provoked paroxysms of sustained VT identical to those observed during treadmill exercise testing in 10 patients and provoked ventricular flutter/fibrillation in 1. Seven patients had VT suggestive of a reentrant mechanism, as the VT could be readily initiated with programmed ventricular extrastimulation or terminated by ventricular overdrive pacing, or both. Three patients had VT suggestive of catecholamine-sensitive automaticity. The VT could not be initiated with programmed electrical stimulation, but it could be provoked by intravenous isoproterenol infusion; furthermore, the VT could not be terminated with ventricular overdrive pacing, but it could be abolished by discontinuing isoproterenol infusion. Reproduction of VT in these 10 patients allowed serial pharmacologic testing in selecting an effective antiarrhythmic regimen. Thus (1) exercise-induced VT can be caused by either reentry or catecholamine-sensitive automaticity, and (2) electrophysiologic studies are of use in defining the underlying mechanism of exercise-induced sustained VT.
Adolescent↗
Long-term follow-up of patients with recurrent unexplained syncope evaluated by electrophysiologic testing.
Electrophysiologic testing was performed in 53 patients with recurrent syncope that remained unexplained despite a thorough neurologic and noninvasive cardiac evaluation. Fifteen patients had no structural heart disease, 9 had mitral valve prolapse and 29 had structural heart disease other than mitral valve prolapse. Nonsustained ventricular tachycardia was induced in 15 patients (28%), sustained ventricular tachycardia was induced in 9 (17%), ventricular fibrillation was induced in 4 (8%) and sinus node function was abnormal in 2 (4%). Female sex and lack of structural heart disease were independently associated with a negative electrophysiologic study (p less than 0.001). Patients with inducible ventricular tachycardia or ventricular fibrillation were treated with drugs selected on the basis of the results of electropharmacologic testing. The recurrence rate of syncope was 43% over a 31 +/- 10 month period (mean +/- standard deviation) of follow-up in patients with a negative electrophysiologic study, 40% over a 22 +/- 6 month period in patients with inducible nonsustained ventricular tachycardia, 0% over a 30 +/- 12 month period in patients with inducible sustained ventricular tachycardia and 25% over a 21 +/- 10 month period in patients with inducible ventricular fibrillation. In patients with recurrent unexplained syncope undergoing electrophysiologic testing, a potential cause of syncope is least likely to be found in women without structural heart disease. The results of programmed ventricular stimulation must be interpreted with regard to the method of induction of ventricular tachycardia and the type of ventricular tachycardia induced. The excellent response rate in patients with inducible sustained ventricular tachycardia whose therapy is guided by the results of electropharmacologic testing suggests that sustained ventricular tachycardia is a clinically significant response.(ABSTRACT TRUNCATED AT 250 WORDS)
Amiodarone↗
Electrophysiologic studies in patients with bundle branch block.
A total of 401 patients with chronic bundle branch block underwent electrophysiologic studies and were followed for a mean of approximately 30 months. Patients with an infranodal conduction time (H-Q) greater than or equal to 70 ms had a significantly higher incidence of progression to spontaneous second-degree or third-degree atrioventricular (AV) block (12%) compared with those with H-Q less than 70 ms (3.5%). The incidence of AV block was 25% for those with H-Q greater than or equal to 100 ms. Although the incidences of all deaths and cardiac deaths were higher for the H-Q greater than or equal to 70 ms group, there was no statistically significant difference in the incidence of sudden deaths in the two groups. A subgroup of 77 patients underwent prophylactic pacemaker insertion based on the presence of transient neurologic symptoms and/or a prolonged H-Q interval. We found no significant difference in the incidence of relief of symptoms or incidence of cardiac or sudden deaths between paced and unpaced groups. A subgroup of 25 patients with syncope underwent ventricular stimulation studies and ventricular tachycardia was induced in 14. We conclude that a markedly prolonged H-Q interval (greater than or equal to 100 ms) may be of value in detection of spontaneous AV block. Prophylactic pacing is of no value in either relief of symptoms or prolongation of life. Complete electrophysiologic studies, including ventricular stimulation studies, are indicated for patients with bundle branch block and syncope.
Aged↗
Amiodarone in the management of patients with ventricular tachycardia and ventricular fibrillation.
Fifty-eight patients with symptomatic ventricular tachycardia (VT) or ventricular fibrillation (VF) were treated with amiodarone. All had clinical episodes of VT/VF or inducible VT during electropharmacologic testing despite treatment with maximum-tolerated doses of conventional antiarrhythmic agents. Chronic treatment with amiodarone was begun at a dose of 800-1000 mg per day. Thirty-two patients were also treated with a previously ineffective conventional agent. Thirty patients underwent programmed ventricular stimulation after 2.6 +/- 1.7 months (mean +/- S.D.) of treatment with amiodarone at a mean daily dose of 588 +/- 155 mg. VT was induced in 25 patients (sustained in 20, nonsustained in five). Seventeen patients had a recurrence of VT or VF after 0.5-9 months of treatment with amiodarone (fatal in seven, non-fatal in 10). Forty-one patients (71%) had no recurrence of symptomatic VT or VF while being treated with amiodarone (mean follow-up period, 17.1 +/- 12.4 months). Among the 25 patients who had inducible VT with programmed ventricular stimulation while being treated with amiodarone, 19 patients (76%) have had no recurrence of symptomatic VT or VF over a follow-up period of 21.5 +/- 7.3 months. Ambulatory electrocardiographic recordings obtained after one week of treatment with amiodarone were not helpful in predicting clinical response. Twenty-two patients (38%) developed ataxia and/or an intention tremor which improved with a decrease in the amiodarone dose. Amiodarone, either by itself or in combination with conventional antiarrhythmic drugs, has a significant therapeutic effect in high risk patients with refractory VT. The finding of inducible VT during electropharmacologic testing in patients taking amiodarone does not preclude a favorable clinical response. Neurologic toxicity is common in patients treated with 600-800 mg per day of amiodarone.
Amiodarone↗
Extent of atrial participation in atrioventricular-reciprocating tachycardia.
Twenty-one patients with atrioventricular (AV) bypass tracts underwent electrophysiologic studies. The bypass tract was left-sided in 15 patients, septal in five and right-sided in one patient. Orthodromic AV-reciprocating tachycardia was induced in all 21 patients, with a mean tachycardia cycle length of 342 +/- 59 msec. The introduction of single stimuli in the high right atrium during tachycardia resulted in simultaneous dissociation of the high right atrial and low septal atrial electrograms in nine patients. In six patients, high right atrial overdrive pacing during tachycardia resulted in simultaneous dissociation of the high right atrial and low septal atrial electrograms for two to five consecutive beats. All patients in whom the low septal atrial electrogram was dissociated from the tachycardia had a left-sided bypass tract. In no patient was the coronary sinus atrial electrogram dissociated from the tachycardia by high right atrial pacing. Dissociation of the low septal atrial electrogram (as recorded in the His bundle electrogram) from AV-reciprocating tachycardia suggests that the portion of the right atrium adjacent to the AV node may not be a necessary link in the tachycardia circuit. This observation suggests that the site of entry of left-sided impulses into the AV node may be different from that of right-sided impulses.
Cardiac Pacing, Artificial↗
Invasive cardiac electrophysiologic testing: the current state of the art.
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Arrhythmias, Cardiac↗
Interventional electrophysiology.
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Atrioventricular Node↗
Catheter-induced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias.
Five patients with recurrent bouts of supraventricular tachycardia proved resistant or became intolerant of both conventional and experimental drugs. These patients were subjected to a new procedure involving delivery of DC shocks to an electrode catheter positioned adjacent to the His bundle. Complete atrioventricular (AV) block was produced in all, one patient died suddenly six weeks after shock therapy, and the remainder had complete AV block with follow-up intervals ranging from four to 12 months. Shock therapy was associated with mild elevations of creatine phosphokinase MB (31 +/- 18 units), but there was no hemodynamic evidence of tricuspid insufficiency. If this new technique proves safe and effective, it should supplant the need for open heart surgical procedures for His-bundle ablation.
Adult↗
Phase image characterization of ventricular contraction in left and right bundle branch block.
The phase image is a computer-derived functional image, based on the analysis of the time versus radioactivity curve in each pixel location of the multiple gated blood pool scintigram. Within the ventricular regions of interest, the phase angle is roughly equivalent to the time of onset of counts reduction or to the time of onset of ventricular contraction and is expressed in degrees from 0 to 360 degrees. A gray scale-coded image of such a regional phase angle, the phase image, can be looked on as a map of sequential contraction. This method was applied in 33 patients without severe contraction abnormality including 16 patients with normal conduction, 9 with right bundle branch block and 8 with left bundle branch block. In patients with normal conduction the pattern of phase angle distribution, representing the pattern of ventricular contraction, was homogeneous and symmetric in both the left and right ventricles. Analysis in this normal group indicated a slight but significant difference between the mean (+/- standard deviation) phase angle of the left ventricle (8.5 +/- 11.8 degrees) and that of the right ventricle (13.6 +/0 12.9 degrees, p = 0.01). There was a slight, but nonsignificant difference between mean intrapatient left and right ventricular phase angle onset (1.9 +/- 6.5 degrees). The mean phase angle of the right ventricle in patients with right bundle branch block (27.6 +/- 14.2 degrees) and of the left ventricle in those with left bundle branch block (21.9 +/- 14.0 degrees) was delayed compared with that in patients with normal conduction (p less than 0.05 for both). The mean intrapatient difference between left and right ventricular mean phase angles in patients with normal conduction (-5.2 +/- 6.8 degrees) was significantly different from that in patients with right (-21.8 +/- 10.3 degrees, p less than 0.001) or left (21.8 +/- 6.8 degrees, p less than 0.001) bundle branch block. The mean intrapatient difference between onset of left and right ventricular phase angles was also significantly different from normal in patients with right (-10.6 +/- 7.5 degrees, p less than 0.005) or left (18.7 +/- 8.3 degrees, p = 0.01) bundle branch block. Although phase imaging is not without artifactual error, this study demonstrates that the phase image can characterize familiar conduction abnormalities. It presents the potential for application as a general noninvasive tool in the investigation of the timing and sequence of ventricular contraction in patients with normal or abnormal ventricular activation.
Adult↗
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 IIA), nonsustained 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 +/- 1.5 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 less than 0.02 for Group IIA versus Group I and p greater than 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.
Adult↗
Electrophysiologic testing in the evaluation of patients with syncope of undetermined origin.
Thirty-two patients were prospectively evaluated for syncope (recurrent in 26 patients) with conventional neurologic and cardiovascular testing without elucidation of a cause. All patients underwent invasive electrophysiologic studies to assess sinus nodal function, atrioventricular conduction, and the inducibility of supraventricular and ventricular tachycardia (VT). Eleven patients (34%) were found to have laboratory-induced VT, 5 patients (15%) had evidence of sinus nodal dysfunction, 1 patient (3%) had infra-His atrioventricular block during atrial pacing, and 1 patient (3%) had probable quinidine-related VT. The remaining 14 patients had no detectable abnormalities during electrophysiologic study. After a mean follow-up period of 21.3 +/- 1.2 months, 10 of the 11 patients with inducible VT were asymptomatic while receiving laboratory-directed antiarrhythmic therapy, and 1 patient died from ventricular fibrillation after discontinuing the chosen antiarrhythmic regimen. Five of the remaining 7 patients with an electrophysiologic abnormality were asymptomatic after implantation of a permanent pacemaker or alteration of previous drug therapy, or both. The 14 patients with a normal electrophysiologic study were treated empirically, with recurrent syncope occurring in 4 of these patients during the follow-up period. Invasive electrophysiologic studies provided a presumptive diagnosis in 56% of patients with syncope of undetermined origin. Previously unsuspected VT accounted for 61% (11 of 18) of the detected abnormalities. Therapy specific for the electrophysiologic abnormality was usually successful in preventing recurrent syncope.
Adult↗
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 less than 55 ms in 97 patients (Group I), 55 to 69 ms in 99 patients (Group II), and greater than or equal to 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 less than 0.01, respectively). High degree block was found in 4 of 17 (24%) patients with an H-Q interval (H-Q) greater than or equal to 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 greater than or equal to 70 ms was an independent risk factor for progression to HDB, (2) H-Q greater than or equal to 100 ms identified a subgroup at particularly high risk, and (3) prophylactic pacemakers relieved neurologic symptoms but did not prolong life.
Aged↗
Effects of reduced PO2 on rapid-drive-induced hyperpolarization of diastolic transmembrane potential in feline cardiac Purkinje strands.
Using standard microelectrode techniques, we evaluated effects of diminished oxygen tension on the magnitude and time course of frequency dependent changes in maximum diastolic transmembrane potential (MDP) and on alteration of action potential duration (APD) in feline Purkinje fibers. MDP was recorded continuously during a control period (cycle length (CL) = 1000 ms), during a 5-min period of rapid drive (CL = 400 ms) and following return to pacing CL = 1000 ms. Rapid drive resulted in hyperpolarization of MDP from control value; and after return to pacing CL = 1000 ms. MDP gradually depolarized, eventually attaining a steady state value within +/- 0.5 mV of the control value. The difference between hyperpolarized MDP value and final steady-state value was designated VH, and the decline of MDP towards steady-state value approximated an exponential function (time constant = tau VH). Exposure to reduced PO2 (75 +/- 2.1 mmHg vs. control 473 +/- 39.1 mmHg) (1 mmHg = 133.322 Pa) resulted in reduction in the magnitude of VH (6.2 +/- 3.43 mV vs. 7.8 +/- 2.73 mV, mean +/- SD, p less than 0.005) and shortening of APD within 0-24 min, while measurable prolongation of tau VH (75 +/- 18.5 vs. 54 +/- 9.0 s, p less than 0.005) began at 25-49 min following onset of reduced PO2. These observations suggest that rate-related changes of MDP in cardiac tissues are oxygen dependent, and they support previously reported analagous observations in nerve which suggested that frequency dependent potential changes may in part reflect alterations of electrogenic Na-K pump activity.
Action Potentials↗
The potentiation of warfarin anticoagulation by amiodarone.
The potentiation of the anticoagulant effect of sodium warfarin by amiodarone is reported in 10 patients. Amiodarone appears to augment the depression of vitamin K-dependent coagulation factors caused by warfarin by an uncertain mechanism, and may lead to serious bleeding. The maintenance dose of warfarin should be halved when amiodarone and warfarin are prescribed together.
Aged↗
Serial electrophysiologic studies in patients with chronic bundle branch block.
Serial His bundle recordings were obtained during 1:1 atrioventricular (AV) conduction in 90 patients with chronic bundle branch block over a mean interval of 30 months. Atrioventricular conduction time (AH) increased greater than or equal to 10 msec in 25 (28%) and infranodal conduction time (HV) increased greater than or equal to 8 msec in 29 (32%), but only 10 patients had parallel increases in AH and HV intervals. Increases in conduction times were independent of age, time interval between studies, cause of heart disease or initial AH or HV intervals. Women were significantly more likely than men to show an increased HV interval and spontaneous trifascicular block. Spontaneous progression to second- or third-degree AV block occurred at the AV node in seven patients and below the node in 12 patients. The initial AH interval was prolonged in five of seven patients (71%) with AV nodal block and had increased further in only two at restudy. The initial HV interval was abnormal in eight of 12 patients (67%) who progressed to infranodal block and was prolonged further in eight at restudy. We conclude that in patients with chronic bundle branch block, (1) approximately 33% show progressive AV conduction system disease and AV nodal and infranodal disease progress independently; (2) progression of infranodal disease is more common in women; (3) AV nodal disease progress independently; (2) progression of infranodal disease is more common in women; (3) AV nodal disease is a common cause of AV block and can occur without further prolongation of the AH interval once a critical level of disease is attained, whereas infranodal block is usually accompanied by progressive lengthening of the HV interval; and (4) progression of AV conduction disease is not readily predictable from clinical and electrophysiologic variables.
Aged↗
Electrophysiologic effects of disopyramide in patients with atrioventricular nodal dysfunction.
Seventeen patients with first-degree or Mobitz I atrioventricular (AV) block and narrow QRS complexes underwent electrophysiologic drug testing before and after i.v. administration of disopyramide. Disopyramide did not significantly change the mean sinus cycle length (895 +/- 131 vs 877 +/- 119 msec), mean maximal sinus node recovery time (1134 +/- 160 vs 1133 +/- 13 msec), mean atrial effective refractory period (314 +/- 72 vs 307 +/- 54 msec), mean AV nodal conduction time (187 +/- 79 vs 180 +/- 73 msec) or the mean paced cycle length at which AV nodal Wenckebach conduction occurred (545 +/- 144 vs 497 +/- 130 msec) after disopyramide. The mean AV nodal effective refractory period decreased significantly (from 535 +/- 137 to 521 +/- 122 msec), and both infranodal conduction time and the paced ventricular cycle length producing ventriculoatrial block increased significantly (from 56 +/- 12 to 63 +/- 13 msec and from 625 +/- 158 to 655 +/- 157 msec, respectively). We conclude that i.v. disopyramide administered in a dose resulting in therapeutic blood levels showed no adverse effects on AV nodal conduction in patients with AV nodal dysfunction. In contrast, i.v. disopyramide depressed retrograde AV conduction.
Aged↗
Disopyramide.
Since disopyramide was introduced 5 years ago, the therapeutic spectrum of this drug in treating patients with ventricular and atrial arrhythmias has been found to be similar to that of the other type I antiarrhythmic drugs, quinidine and procainamide. Disopyramide has the potential to suppress sinus node function and, therefore, must be used cautiously in patients with the sick sinus syndrome. The available data indicate that it can be used safely in patients with bundle branch block and first-degree or type I second-degree atrioventricular block. Disopyramide has been found at times to precipitate ventricular tachycardia or ventricular fibrillation. Because this drug often causes decompensation in patients with congestive heart failure, it must be used very cautiously, if at all, in such patients.
Arrhythmias, Cardiac↗