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Publications and source records attributed to F Morady.
Catheter ablation techniques offer an alternative to surgical ablation of accessory pathways. These techniques make use of direct current countershocks, radio frequency energy, or laser energy. This article presents the experimental background and the clinical experience with these techniques.
The results of 206 programmed ventricular stimulation studies performed in 130 patients (100 men and 30 women, mean age 62 +/- 12 years, +/- standard deviation) were examined prospectively to determine the sequelae of nonsustained polymorphic ventricular tachycardia (VT) induced during programmed ventricular stimulation. The clinical indication for the electrophysiologic study was either documented monomorphic VT or unexplained syncope. The pacing protocol included 2 right ventricular pacing sites, 2 basic drive cycle lengths and up to 3 extrastimuli. In 111 studies, nonsustained polymorphic VT was induced and with continuation of the programmed stimulation protocol, sustained monomorphic VT was induced in 48 studies (43%) and polymorphic VT was induced in 13 studies (12%). Overall, sustained monomorphic VT was induced in 110 studies and sustained polymorphic VT in 18 studies. The incidence of nonsustained polymorphic VT preceding the induction of sustained polymorphic VT was significantly greater than the incidence of nonsustained polymorphic VT preceding the induction of sustained monomorphic VT (72 vs 44%, p less than 0.05). Nonsustained polymorphic VT is not a useful predictor of the outcome of programmed ventricular stimulation. The use of nonsustained polymorphic VT as an endpoint for stimulation would be likely to improve the specificity of programmed ventricular stimulation by limiting the induction of sustained nonclinical arrhythmias that require countershock, but at the cost of significantly impairing the yield of monomorphic VT.
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This prospective study compared the yield of programmed ventricular stimulation with single and double extrastimuli during an infusion of isoproterenol with that of programmed stimulation with triple extrastimuli. The subjects of this study were 58 patients who underwent programmed stimulation and did not have inducible ventricular tachycardia (VT) with single or double extrastimuli at two basic drive cycle lengths and at two right ventricular sites; 17 patients had a history of uniform VT unrelated to exercise, and 41 had no history of documented or suspected VT or ventricular fibrillation (VF). Programmed stimulation was performed with triple extrastimuli at both right ventricular sites. Isoproterenol was infused as a dose titrated to increase the sinus rate by 25% or to a rate of 100 beats/min, whichever was greater, and stimulation then was repeated with single and double extrastimuli. Among the 17 patients with a history of uniform VT, the clinical VT was induced by three extrastimuli in five patients (29%) and by two extrastimuli during isoproterenol infusion in six patients (35%, p greater than 0.05). Among the total study population of 58 patients, nonclinical multiform VT or VF was induced by three extrastimuli in 29 patients (50%), and by two extrastimuli during isoproterenol infusion in 15 patients (26%, p less than 0.05). Therefore stimulation with two extrastimuli during isoproterenol infusion has the same probability of inducing a clinical form of VT as does stimulation with extrastimuli, but the former has a significantly lower probability of inducing nonclinical multiform VT and VF.
The purpose of this study was to define the natural history of 99 patients with unexplained syncope who underwent an electrophysiologic test that either was entirely normal or demonstrated nonspecific abnormalities that were nondiagnostic (inducible polymorphic ventricular tachycardia or ventricular fibrillation, a mildly prolonged sinus node recovery time of less than 2 s, a His-ventricular interval of 55 to 99 ms or supraventricular tachycardia not associated with hypotension). The mean age (+/- SD) of the patients was 56 +/- 19 years; structural heart disease was present in 47 patients and absent in 52. Complete follow-up was available in 95 patients. During 20 +/- 11 months of follow-up, 2 patients (2%) died suddenly, 19 patients (20%) had recurrent syncope and 74 patients (78%) had no further episodes of syncope. Among the 19 patients who continued to have syncope after the electrophysiologic testing, the cause of syncope was established clinically in 4 and was found to be high degree atrioventricular (AV) block (2 patients) or sinus node dysfunction (2 patients). No clinical or laboratory findings distinguished patients who had sudden death or syncope during follow-up from patients who did not. In conclusion, in patients with unexplained syncope who undergo an electrophysiologic test that is nondiagnostic 1) the incidence of sudden death is low (2%); 2) the remission rate of syncope is high (80%); 3) the electrophysiologic test may be documented to have been falsely negative in greater than or equal to 20% of patients who continue to have syncope, syncope in these patients being caused by AV block or sinus node dysfunction; and 4) patients at risk of sudden death or recurrent syncope, or both, cannot be readily identified prospectively.
The purpose of this study was to determine whether concealed anterograde accessory pathway conduction occurs during the induction of orthodromic tachycardia by an atrial extrastimulus (S2). Sixteen patients with an overt (n = 9) or concealed (n = 7) accessory pathway had inducible orthodromic tachycardia by S2 during an atrial drive (S1) cycle length of 500 to 650 ms. A ventricular extrastimulus (S3) was introduced coincident with the His depolarization resulting from S2 during the longest S1S2 interval that reproducibly induced orthodromic tachycardia. The S1S3 interval was decreased in 10 ms steps until S3 reached ventricular refractoriness. Retrograde accessory pathway conduction of S3 in the presence and absence of S2 was compared at the same S1S3 intervals. In the absence of S2 there was retrograde accessory pathway conduction after S3 in each patient. In the presence of S2, in patients with overt pre-excitation, retrograde accessory pathway conduction after S3 was absent in one patient, prolonged in four patients and present only after long S1S3 intervals in three patients. Only one patient had unchanged retrograde conduction regardless of the presence or absence of S2. In patients with a concealed accessory pathway, retrograde accessory pathway conduction after S3 was absent in five patients and was prolonged in two. Thus, concealed anterograde accessory pathway conduction was present in 15 of 16 patients at the time of orthodromic tachycardia induction. In conclusion, concealed anterograde accessory pathway conduction occurs in a majority of patients with an overt or a concealed accessory pathway during induction of orthodromic tachycardia by an atrial extrastimulus.(ABSTRACT TRUNCATED AT 250 WORDS)
Supraventricular tachycardia (SVT), the most common sustained symptomatic arrhythmia of childhood, is often supported by a manifest or concealed accessory pathway. Permanent interruption of the accessory pathway usually requires surgical division. Recent experience with electrical ablation of posterior septal pathways in adults prompted us to apply the technique to children. Six children, ages 8 to 15 years, underwent a complete electrophysiological study followed by transcatheter electrical ablation. Five of the 6 children, 3 with a right posterior septal and 2 with a left posterior septal pathway, were approached with the ablation catheter at the os of the coronary sinus. In the remaining patient, a left lateral pathway was mapped with an electrode catheter in the coronary sinus and then approached with the ablation catheter through the patent foramen into the left atrium. Two patients are asymptomatic 18-24 months postablation; one patient had return of anomalous conduction between 7 and 21 days after ablation. Two patients had transient interruption of anomalous conduction, whereas one patient experienced no effect. We conclude that in carefully selected patients, transcatheter electrical ablation offers an alternative to surgery for permanent interruption of an accessory pathway.
Thirty-three patients with recurrent ventricular tachycardia (VT) underwent catheter ablation with direct-current shocks. One to four shocks of 100-300 joules were delivered to the presumed VT exit sites as identified by endocardial mapping and pace mapping. Fifteen patients (45%) had no recurrence of symptomatic VT during a follow-up interval of 15.5 +/- 10 months (mean +/- standard deviation). Five patients experienced six nonfatal complications (new VT or ventricular fibrillation, transient neurological deficit, atrioventricular block, brachial artery thrombosis). In conclusion, catheter ablation in selected patients with recurrent VT has the potential for preventing recurrences of VT over the long-term and is relatively safe.
This study compared the ventricular effective refractory periods measured by scanning diastole with an extrastimulus in incremental and decremental steps of 5 msec. The subjects of the study were 80 patients undergoing a clinically indicated electrophysiological test. Eight beat basic drive trains at a cycle length of 600 msec and an intertrain pause of 4 seconds were used to measure the ventricular effective refractory period (VERP). In the incremental method, the extrastimulus initially was positioned at a coupling interval shorter than the VERP and the coupling interval then was progressively increased until ventricular capture occurred. In the decremental method, the initial extrastimulus coupling interval was longer than the VERP and the coupling interval was progressively shortened until ventricular capture was lost. In 50 subjects, the mean VERP determined by the incremental method, 252 +/- 18 (+/- standard deviation), was significantly longer than the mean VERP determined in the same patients by the decremental method, 248 +/- 18 msec (P less than 0.0001). In ten subjects, a subthreshold stimulus (S') positioned 10 msec earlier than the VERP had an inhibitory effect that lengthened the VERP by an average of 7 msec; however, when S' was positioned after the seventh beat of an eight beat drive train, no inhibitory effect could be demonstrated. In 20 subjects, VERP's were determined by the incremental and decremental methods using intertrain pauses of 1, 4, 8, 12, and 20 seconds.(ABSTRACT TRUNCATED AT 250 WORDS)
Although "unipolar electrograms" recorded from the His-bundle position have been used to help position catheters for His-bundle ablation, the techniques used to record such electrograms have not been standardized. The effects of five anode locations (right chest wall, anterior chest wall, left chest wall, posterior chest wall, and inferior vena cava) on unipolar atrial, His bundle and ventricular electrograms recorded from the His-bundle position were examined in ten patients undergoing clinical electrophysiology studies. Electrograms were recorded at filter settings of 50-500 as well as 0.05-1000 Hz. The location of the anode had no consistent effect on the amplitude, duration or morphology of any of the electrograms at either filter setting, but signals recorded with the inferior vena cava anode had the highest signal-to-noise ratio. A filter setting of 50-500 Hz decreased the amplitude of atrial (0.72 to 0.33 mV-P less than 0.01), His bundle (0.38 vs 0.32 mV-P less than 0.01) and ventricular electrograms (3.71 vs 2.01 mV-P less than 0.001) compared to a filter setting of 0.05-1,000 Hz. The filter setting did not affect electrogram duration. We concluded that the use of an electrode catheter in the inferior vena cava as the anode when recording "unipolar electrograms" from the His-bundle position yields a better signal-to-noise ratio than a skin patch on the chest and appears to be the optimal method for recording unipolar electrograms.
The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240-480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9-18 months of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)
Forty-eight patients with a posteroseptal accessory atrioventricular (AV) connection underwent catheter ablation of the accessory AV connection with 200-400 J shocks delivered by a standard defibrillator. Cathodal shocks were delivered through the proximal pair of electrodes of a 6F quadripolar electrode catheter positioned in the coronary sinus such that the proximal electrodes straddled the ostium (12 patients) or the third electrode from the tip was at the ostium (36 patients). A 16-cm patch electrode positioned on the back or anterior chest served as the anode. Two to 4 shocks were delivered (total, 635 +/- 198 J, mean +/- SD). The cathether ablation procedure was clinically successful in eliminating symptomatic tachycardias in in 32 of 48 patients (67%) during a mean follow-up of 26 +/- 19 months. A long-term follow-up electrophysiology study was performed in 27 of the 32 patients who had a successful clinical outcome, and this showed that conduction through the accessory AV connection was completely absent in 25 patients and present but impaired in two patients. The success rate was significantly higher in patients with a concealed accessory AV connection (13 of 13, 100%) than in patients with manifest preexcitation (19 of 35, 54%; p less than 0.001). Among the 12 patients in whom the proximal electrodes of the ablation catheter straddled the ostium of the coronary sinus, one patient developed cardiac tamponade requiring needle pericardiocentesis; there were no instances of cardiac tamponade among the 36 patients in whom the third electrode from the tip was at the ostium of the coronary sinus. Other complications were AV block requiring a permanent pacemaker and transient atrial tachycardia in one patient each and an asymptomatic pericardial effusion in three patients. In conclusion, with the catheter ablation technique described in this study, a successful clinical outcome may be achieved in approximately two thirds of patients who have a posteroseptal accessory AV connection, and the risk of serious complications is low. This technique is particularly well suited to patients with a concealed posteroseptal accessory AV connection, in whom the success rate is higher than in patients with manifest preexcitation.
The purpose of this study was to determine whether physiologic doses of epinephrine reverse the electrophysiologic effects of quinidine in patients with an accessory atrioventricular (AV) connection. Eighteen patients with an accessory AV connection who had inducible sustained orthodromic tachycardia underwent an electrophysiologic study in the baseline state and after at least 2 days of treatment with 1.4 to 1.9 g/day of quinidine gluconate. The effects of epinephrine were then determined. Epinephrine infusion rates of 25 and 50 ng/kg/min were used in 9 patients each because these doses of epinephrine previously have been demonstrated to result in elevated plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. Quinidine prolonged refractoriness in the atrium and accessory AV connection and slowed conduction through the accessory AV connection. These effects were partially or completely reversed by epinephrine. Among 8 patients in whom quinidine resulted in orthodromic tachycardia becoming noninducible or nonsustained, sustained tachycardia became inducible again in 5 patients after infusion of epinephrine. After quinidine, atrial fibrillation was either noninducible or nonsustained in 8 patients; however, sustained atrial fibrillation could be induced in 4 of these patients after infusion of epinephrine. The results of this study demonstrate that the therapeutic effect of quinidine in patients who have an accessory AV connection are often reversed by physiologic increases in circulating epinephrine.
No previous studies have determined the pharmaco-dynamics of intravenous procainamide when administered in a dose of 15 mg/kg and at a rate of 50 mg/min, as is common practice during electropharmacologic testing. In this study, 30 patients received procainamide in this fashion; the right ventricular effective refractory period and the QRS duration at a ventricular pacing rate of 120/minute were then determined every minute for 20 minutes. Ten patients received no maintenance infusion of procainamide (group A), 10 received a 4 mg/min maintenance infusion (group B) and 10 received an 8 mg/min maintenance infusion (group C). Ten additional patients received no procainamide and served as control subjects (group D). The plasma procainamide concentration was measured at 1, 5, 10, 15 and 20 minutes after the loading dose was administered. A stable plasma procainamide concentration was not present in group A, B, or C until 15 minutes after infusion of the loading dose. The effective refractory period and QRS duration increased compared with baseline at 1 minute, decreased between 1 and 10 minutes and then remained essentially unchanged between 10 and 20 minutes in all 3 treatment groups. Concentration-effect relation was linear in each treatment group. The plasma procainamide concentrations in group C were significantly greater than in group A; however, the effects on refractoriness and QRS duration were similar in both groups. These findings indicate that with a procainamide dosing method commonly used during electropharmacologic testing, the plasma procainamide concentration decreases significantly during the first 15 minutes after the loading dose is administered.(ABSTRACT TRUNCATED AT 250 WORDS)
The Wolff-Parkinson-White syndrome, as originally described, includes palpitations, tachycardia, and an abnormal electrocardiogram (short PR interval and wide QRS complex). The clinical manifestations are dependent upon a reentrant tachycardia supported by an accessory connection bridging the atrioventricular junction and frequently appear during the first two decades of life. Palpitations are the usual symptoms; less frequently, severe symptoms, such as syncope and sudden death, may result from very rapid atrioventricular conduction across the accessory connection during atrial fibrillation. We report the surgical management of 30 young patients with this syndrome, including 6 with life-threatening tachycardia. Surgical interruption of the accessory connection(s) was curative in 90% (27/30) of the patients; life-threatening symptoms were eliminated in the other three. Based on the limited knowledge of the natural history of the Wolff-Parkinson-White syndrome, the individual patient symptoms, and the electrophysiologic properties of each patient's accessory pathway(s), an algorithm is presented outlining the treatment options. This experience strongly suggests that surgical treatment of the Wolff-Parkinson-White syndrome is safe, effective, and possibly the preferred treatment for this disorder in selected young symptomatic patients.
Pirmenol is an investigational type 1A antiarrhythmic drug the long-term efficacy of which has not been fully determined. Therefore the long-term efficacy of oral pirmenol in suppressing ventricular premature depolarizations (VPDs) was assessed in an open-label, dose-titration study. Twelve patients (eight men and four women; mean age 57 +/- 12 years) were treated for 24 to 36 months (mean 33 +/- 4). Seven had structural heart disease (three valvular heart disease, two ischemic heart disease, and two hypertensive heart disease) and five did not. The mean left ventricular ejection fraction was 0.63 +/- 0.13. Exclusion criteria included less than 30 VPDs/hr, greater than 15 beats of ventricular tachycardia (VT), or prior failure of more than two antiarrhythmic drugs. Drug efficacy was assessed by 24-hour ambulatory ECG monitoring performed every 3 months during the first year, every 4 months during the second year, and at 6-month intervals during the third year. The mean hourly frequency of VPDs during the placebo phase was 732 +/- 608. Seven patients (58%) were treated successfully with effective (greater than 75%) long-term suppression of VPDs. Two patients (17%) had a partial response with effective suppression of VPDs for the first 16 months and 5 months of treatment, respectively. Three patients failed to show consistent suppression of VPDs while receiving pirmenol. The daily dose of pirmenol ranged from 200 to 500 mg (mean 317 +/- 94 mg at the beginning of the study and 375 +/- 97 mg at the end). No proarrhythmic effects were identified during long-term treatment, and none of the patients withdrew from the study prematurely.(ABSTRACT TRUNCATED AT 250 WORDS)
Three patients who had incessant ventricular tachycardia and in whom a zone of slow conduction was identified are presented. Each patient's tachycardia was refractory to multiple antiarrhythmic drugs and was being treated with amiodarone at the time of the electrophysiologic study. The ventricular tachycardia cycle length was 500 to 580 ms. In Patients 1 and 2, a single site at the posterolateral wall or low septum in the left ventricle was identified at which overdrive pacing during ventricular tachycardia resulted in ventricular capture with a stimulus to QRS interval of 280 to 400 ms and with little or no change in the configuration of the QRS complexes during pacing as compared with during ventricular tachycardia. In Patient 3, the same phenomenon was observed at two areas in the left ventricle: at the inferior wall, overdrive pacing during ventricular tachycardia resulted in a stimulus to QRS interval of 440 to 470 ms, whereas at the posterolateral wall, the stimulus to QRS interval was 320 to 360 ms. Transcatheter shocks of 100 to 240 J delivered at the pacing sites have been successful in preventing recurrences of ventricular tachycardia over a follow-up period of 10 to 11 months. These observations may be explained by the pacing site being located within a reentrant circuit in a zone of slow conduction bounded by inexcitable tissue between the pacing site and the exit site of the reentrant circuit. In Patient 3, the variable stimulus to QRS intervals are explained by variable proximity of the pacing sites within the slow conduction zone to the exit site of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)
The electrophysiologic effects of circulating epinephrine in humans were examined in four study groups of 10 subjects each. In 10 subjects without structural heart disease (Group 1) and in 10 patients with coronary disease or dilated cardiomyopathy (Group 2) epinephrine infusion at 25 and 50 ng/kg body weight per min for 14 min resulted in an elevation of the plasma epinephrine concentration in the physiologic range. In both groups it produced a dose-dependent decrease in the effective refractory period of the atrium, atrioventricular (AV) node and ventricle and improvement in AV node conduction. Epinephrine facilitated the induction of sustained ventricular tachycardia in 3 of the 20 subjects. In Group 3, a beta-adrenergic blocking dose of propranolol was added to the infusion of 50 ng/kg per min of epinephrine. Propranolol not only reversed the effects of epinephrine, but also lengthened these variables compared with baseline values. In Group 4, propranolol was administered first, followed by 50 ng/kg per min of epinephrine. Propranolol alone slowed AV node conduction and mildly prolonged the refractory periods. In the presence of beta-blockade, epinephrine had no effect on AV node properties but resulted in a lengthening of the atrial and ventricular effective refractory periods. In conclusion, epinephrine in physiologic doses shortens the effective refractory period of the atrium, AV node and ventricle, improves AV node conduction and may facilitate the induction of sustained ventricular tachycardia. The overall electrophysiologic effects of epinephrine result from stimulation of beta-receptors. Stimulation of alpha-receptors by epinephrine has no effect on the AV node but prolongs the effective refractory period of the atrium and ventricle, partially offsetting the shortening of refractory periods mediated by beta-receptor stimulation.