Biomedical subjects
Publications and source records attributed to A J Greenspon.
Radiofrequency catheter ablation (RFA) has emerged as a common therapeutic option for cardiac arrhythmias. Although tremendous strides have been made to improve the efficacy and safety of this procedure, adverse outcomes are still an unfortunate reality. The goal of this review is to point out the most common pitfalls of RFA and offer guidelines on how to minimize the risks.
INTRODUCTION: Accurate analysis of the arrhythmia substrate is important for successful radiofrequency ablation of sustained ventricular tachycardia (VT) after myocardial infarction (MI). METHODS AND RESULTS: A multielectrode "basket" catheter capable of endocardial recording and pacing was inserted percutaneously into the left ventricle of post-MI swine for analysis of the mechanism of sustained VT. Sustained VT was induced in 42 of 61 pigs that survived an acute MI produced by percutaneous transluminal coronary angioplasty balloon occlusion of the left anterior descending coronary artery and injection of agarose gel beads. A multielectrode "basket" catheter (Constellation) with 64 electrodes was inserted in 35 of these animals for analysis of the VT. Induced VT had a cycle length of 179 +/- 25 msec at control and 230 +/- 43 msec after administration of intravenous procainamide. Presystolic electrical activity was recorded from at least 1 of 32 bipolar pairs of electrodes at a mean 40.7 +/- 23.6 msec prior to QRS onset. Isolated mid-diastolic potentials were recorded in 26 of 35 animals. In 22 animals, there were multiple isolated potentials recorded from adjacent electrode pairs. Isochronal maps demonstrated that these potentials returned to the systolic site of origin. Resetting of sustained VT by single premature ventricular stimuli was observed in 6 of 12 animals. Entrainment with overdrive pacing was seen in 19 of 26 animals with induced VT. Concealed entrainment was observed in ten animals. The mean stimulus to QRS interval was 45 +/- 28 msec. Concealed entrainment was observed from adjacent electrode pairs with different stimulus to QRS intervals. CONCLUSION: These data suggest that sustained VT in this model is due to reentry with an excitable gap. A multielectrode "basket" catheter is useful for analyzing the zone of slow conduction participating in the tachycardia circuit. Such analysis may provide useful information to guide successful catheter ablation of sustained VT after MI.
BACKGROUND: Endocardial mapping using standard electrode catheters is often technically limited in ventricular tachycardia and constitutes a major obstacle to successful ablation. We wished to examine the utility of a basket-shaped multielectrode mapping catheter (MMC) in the mapping and ablation of ventricular tachycardia. METHODS AND RESULTS: This study of sustained monomorphic ventricular tachycardia (SMVT) was conducted in two phases in the postinfarction pig model. In the first phase, the utility of the MMC in providing adequate localization of potential ablation site(s) of SMVT by different techniques (presystolic potentials, pace mapping, and concealed entrainment) was assessed in 21 pigs. In the second phase, ablation of induced SMVT was attempted in 10 pigs. Mapping of SMVT was performed after percutaneous introduction of the MMC to the LV. Comprehensive mapping was performed in 90 episodes of SMVT and required 2.0 to 25 seconds. Diastolic potentials were recorded during 86 episodes; good or identical pace maps (> or = 9 of 12 paced surface ECG leads identical to ventricular tachycardia surface ECG leads) were obtained in 25 of 31 maps, and entrainment was achieved during 28 of 42 SMVTs. In 10 pigs, 10 SMVTs were recorded at least twice and were considered for radiofrequency ablation. An 8-mm tip ablation catheter was advanced to potential ablation sites with a specially designed "homing" device, requiring a median time of 120 seconds. In these 10 pigs, either identical pace map (> or = 11 of 12, 6 SMVTs) or concealed entrainment (4 SMVTs) guided the ablation procedure. After ablation, 8 of 10 SMVTs were rendered noninducible, while 2 pigs died during energy application of degeneration of SMVT to ventricular fibrillation. CONCLUSIONS: The MMC allows rapid, comprehensive, and reliable endocardial mapping during SMVTs, which facilitates successful ablation in the porcine post-myocardial infarction model.
A basket shaped catheter carrying 64 electrodes was developed in the left ventricle (LV) of 53 pigs which had undergone induction of myocardial infarction. Pacing during sinus rhythm, or echocardiographic and hemodynamic measurements as well as pathological studies revealed no significant damage due to the basket catheter. Eighty one episodes of ventricular tachycardia (VT) were mapped and analyzed, requiring only several beats and less than 10 seconds to complete. We were able to successfully ablate ventricular tachycardias in four pigs.
Currently, analysis of sustained ventricular tachycardia postmyocardial infarction in man is limited by the time required for single point activation mapping and the difficulty in obtaining information during hemodynamically unstable arrhythmias. To overcome these limitations, we developed a multielectrode "basket" catheter for endocardial recording and pacing. This report describes the first clinical use of such a catheter to guide successful radiofrequency ablation of incessant sustained ventricular tachycardia postmyocardial infarction. This system may significantly shorten the time required for VT analysis and improve the results of radiofrequency catheter ablation for VT postmyocardial infarction.
BACKGROUND: Identification of critical areas within the ventricular tachycardia circuit is a prerequisite for catheter ablation. Currently, mapping during ventricular tachycardia, usually performed with standard catheters, is difficult and time-consuming and can be used only in patients with hemodynamically stable tachycardia. METHODS AND RESULTS: A total of 43 pigs underwent closed-chest induction of myocardial infarction. A basket-shaped catheter carrying 64 electrodes was deployed in the left ventricle during normal sinus rhythm. Unipolar pacing at 3 mA was successful in 78% of the basket catheter electrodes, demonstrating good electrode-tissue contact. Hemodynamic and echocardiographic measurements did not reveal any significant interference with myocardial or valvular function during or after catheter deployment. One hundred eighteen episodes of monomorphic ventricular tachycardia were induced in 28 pigs through right ventricular stimulation, 81 of which were mapped and analyzed. Ventricular tachycardia mapping was rapid, requiring only several beats and < 10 seconds to complete. Presystolic potentials, a possible target for ablation, were identified in 58% of the tachycardia episodes mapped. Pathological examination revealed only minor valvular and endocardial catheter-induced lesions immediately after mapping and none a month later. CONCLUSIONS: The multielectrode catheter enables rapid and safe percutaneous endocardial mapping of ventricular tachycardia in the swine model. Exploration of the clinical potential of the multielectrode catheter seems warranted.
Current radiofrequency (RF) ablation technology is limited by small lesion size. To enhance the size of RF-induced left ventricular (LV) endocardial lesions, we evaluated the effects of an enlarged distal electrode tip and increased RF power on lesion volume. Steerable electrode catheters with distal electrode tips of 4 to 12 mm were studied in anesthetized dogs at power settings of 20 to 100 W. Temperature was continuously monitored from a thermistor located at the tip of the catheter. RF energy (500 kHz, unmodulated) was applied between the tip of the catheter and a large skin electrode at four separate LV sites in each animal. Hearts were excised, frozen, sectioned, and stained with nitroblue tetrazolium. Lesion area was planimetered and volume was calculated. Lesion volume increased with increasing electrode size and delivered power. However, a rise in impedance limited maximal lesion size at higher power with each electrode. Maximal lesion size with an 8 mm tip was approximately twice the size of the maximal lesion with a 4 mm tip (914 +/- 362 mm3 vs 460 +/- 150 mm3, p < 0.01). Minimal lesions were seen with large tip electrodes at power < 40 W because of low tip temperature (< 55 degrees C). Average tip temperature correlated with measured lesion volume (r = 0.7). Ventricular fibrillation occurred in approximately one half of the animals studied, and was associated with larger lesion volume (p < 0.01). Catheter ablation of ventricular tachycardia may be enhanced by this technology.
BACKGROUND: Type I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug. METHODS AND RESULTS: Thirty-five patients receiving type I antiarrhythmic drugs for the treatment of sustained monomorphic ventricular tachycardia (VT) were studied before and after drug therapy. A total of 41 drug studies were performed (lidocaine, n = 10; procainamide, n = 16; flecainide, n = 15). Sustained monomorphic VT of an identical electrocardiographic morphology was induced during the control and follow-up drug studies. During the control study, there was no significant change in the VT cycle length over time. Compared with control, significant prolongation of the onset VT cycle length was observed after treatment with procainamide and flecainide (increase of 52 +/- 24 and 80 +/- 49 msec, respectively) but not after treatment with lidocaine (increase of 8 +/- 37 msec). Additional drug-induced prolongation of the VT cycle length occurred during a 40-second observation period. This secondary "use-dependent" cycle length prolongation contributed significantly to the steady-state VT cycle length during treatment with flecainide (increase of 82 +/- 34 msec; p < 0.0001). Although a use-dependent increase in VT cycle length was observed with procainamide and lidocaine, the increase was not statistically significant (increase of 12 +/- 15 and 8 +/- 8 msec, respectively). The estimated time constants for the onset of use-dependent VT cycle length prolongation were distinctly different for the three drugs. Flecainide's prolongation of the VT cycle length occurred slowly, with an estimated time constant of 12.5 +/- 5.0 seconds. In contrast, the time course of VT cycle length prolongation was rapid during treatment with lidocaine and intermediate during treatment with procainamide (time constants of 0.52 +/- 0.51 and 4.0 +/- 1.3 seconds, respectively). CONCLUSIONS: Use-dependent prolongation of VT cycle length during treatment with type I antiarrhythmic drugs was observed in humans. This effect was clinically significant during treatment with flecainide (i.e., the use-dependent slowing of the heart rate improved the hemodynamic tolerance of the arrhythmia). Finally, the estimated time constants for the use-dependent prolongation of VT cycle length by the three test drugs are similar to their reported in vitro time constants for use-dependent sodium channel blockade.
The effects of type I antiarrhythmic drugs on the signal-averaged electrocardiogram (SAECG) were analyzed in 58 patients with inducible sustained monomorphic ventricular tachycardia. SAECGs were acquired before and after drug therapy. A total of 99 drug trials were analyzed (mean 1.7 per patient). Analysis of temporal domain parameters included the duration of the QRS complex (QRSD), the high frequency total duration of the filtered QRS complex (HFTD), the duration of the signal under 40 microV (D40), initial QRS (HFTD minus D40), and the root mean square amplitude (RMSA) of the terminal 40 msec of the QRS signal. Changes in temporal parameters failed to predict drug efficacy. There were, however, type-specific drug effects on the SAECG. With the exception of type IB drugs, all drugs increased the QRSD, HFTD, and D40. Type IC drugs caused more prolongation of the QRSD and HFTD than type IA, IB, and the combination of IA+IB drugs. Prolongation of the HFTD was related to prolongation of the late potential and the initial portion of the QRS complex. A preferential effect of these drugs on the late potential was not observed. Type IC drugs also caused more prolongation of ventricular tachycardia cycle length than type IA or IB drugs. However, the increase in ventricular tachycardia cycle length did not correlate with a change in the SAECG. In summary, type I antiarrhythmic drugs cause a global slowing of ventricular activation. Although analysis of the SAECG following drug therapy was not useful for predicting drug efficacy, drug induced changes in the SAECG may be helpful for categorizing antiarrhythmic agents.
The efficacy and safety of external programmable automatic antitachycardia pacemakers (ATPs) used in the critical care setting for recurrent sustained monomorphic ventricular tachycardia (VT) was evaluated. Ten patients who had failed a mean of 4.0 +/- 1.4 antiarrhythmic medications (range 2-7) and who had previously required electrical cardioversion for VT were enrolled. Prior to ATP use, successful overdrive pacing termination of VT was demonstrated in all patients. Intertach (Intermedics, Inc.; n = 9) and Orthocor II (Cordis, Inc.; n = 1) ATPs were attached to temporary bipolar transvenous or epicardial pacing leads. Mean patient age was 66.4 +/- 11.5 years, and mean left ventricular ejection fraction was 22 +/- 7.5%. At the time of initial ATP use, mean VT cycle length was 347 +/- 88 msec (range 280-550 msec). A burst scanning antitachycardia pacing algorithm was used in each patient; one patient was also treated with a fixed rate burst adapted to VT cycle length. The duration of ATP use ranged from 2-25 days (median 5), successfully terminating greater than 3,369 VT episodes (median 3, range 0 to greater than 3,103 episodes per-patient). Two episodes of ATP induced rate acceleration occurred, each successfully terminated by the ATP. Only two patients required external cardioversion during ATP use, one for primary ventricular fibrillation and one for rapid polymorphic VT associated with antiarrhythmic drug withdrawal. ATPs also provided antibradycardia pacing and allowed for serial programmed ventricular stimulation. No complications were associated with transvenous catheter or ATP use.(ABSTRACT TRUNCATED AT 250 WORDS)
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This open-label, multicenter study was designed to assess the electrophysiological properties of intravenous recainam, an investigational Class I antiarrhythmic agent. In 25 patients undergoing electrophysiological studies for the evaluation of arrhythmias, recainam was administered intravenously in a loading infusion (0.1 mg/kg/min) for 40 minutes, followed by a maintenance infusion (0.02 mg/kg/min) until the completion of the study. Electrophysiological measurements were obtained at baseline, 30 minutes after initiation of the loading infusion, and 30 minutes after termination of the infusion during washout. Conduction intervals, refractory periods, and sinus node recovery times were measured during sinus rhythm and during atrial or ventricular pacing. Vital signs were obtained and recorded before, during, and after recainam infusion. The results showed no change in mean arterial pressure, but heart rate increased slightly by 4 beats/min following recainam infusion. Recainam produced a generalized slowing of intracardiac conduction. The mean intraatrial conduction time, measured at an atrial paced cycle length of 600 msec, increased during recainam loading infusion by 44%, from 38.8% +/- 2.8 to 53.0 +/- 5.4 msec; intranodal conduction time increased by 10%, from 102.0 +/- 5.5 to 112.1 +/- 5.2 msec; and infranodal conduction time increased by 31% from 53.1 +/- 3.0 to 70.7 +/- 3.8 msec. Slowed conduction persisted during washout. The mean right atrial effective refractory period was significantly prolonged (+7% at 600 msec cycle length and +8% at 450 msec cycle length, P less than 0.05 and P less than 0.01, respectively) during recainam loading and remained so during washout.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Concealed retrograde activation has been proposed as a mechanism for antegrade conduction block in the bundle branches and atrioventricular accessory pathways. We studied this hypothesis (linking) in 10 patients with the Wolff-Parkinson-White syndrome in whom antegrade preexcitation could be persistently blocked by overdrive atrial pacing. METHODS AND RESULTS: An atrial pacing protocol, with a decremental ramp followed by an incremental ramp, defined a range of atrial paced cycle lengths (linking window) associated with both persistent conduction and block in the accessory pathway. Within the limits of the linking window, the ability of an atrial impulse to conduct over the accessory pathway was dependent on the preceding state (i.e., conduction or block). The observed linking window ranged from 70 to 290 msec (mean, 185 +/- 68 msec) and closely approximated the measured delay in retrograde activation of the accessory pathway during persistent antegrade block. The mean antegrade effective refractory period of the accessory pathways was long (486 +/- 156 msec), and in each case, it exceeded the antegrade refractory period of the normal atrioventricular pathway. Critically timed premature ventricular extrastimuli, delivered while linking was maintained in the accessory pathway, were able to interrupt the linking and restore antegrade accessory pathway conduction. CONCLUSIONS: These observations suggest that accessory pathway linking is associated with bidirectional block in the accessory pathway. The ability to initiate linking (and the stability of the phenomenon) depends on a critical relation between antegrade accessory pathway refractoriness and the magnitude of retrograde accessory pathway activation delay.
Directed surgical intervention in patients with ventricular tachyarrhythmias who have experienced failure of amiodarone therapy is a common clinical scenario. Sixty-seven patients with malignant ventricular tachyarrhythmias received either an automatic implantable cardioverter-defibrillator (n = 43) or subendocardial resection (n = 24). Nineteen cardiothoracic procedures (automatic implantable cardioverter-defibrillator in six, endocardial resection in 13) were performed in 17 patients who received amiodarone before surgery. Eight received the drug acutely as a loading dose of 1,200 mg/day for 7-14 days; 11 patients were on chronic oral amiodarone at a mean dose of 362 +/- 74 mg/day. Eight patients were removed from amiodarone therapy a mean of 6.6 days before surgery. Adult respiratory distress syndrome (ARDS) developed after surgery in nine (50%) of 18 surgical survivors. ARDS was manifested by hypoxemia, pulmonary infiltrates, and prolonged intubation. Pulmonary capillary wedge pressure and cardiac output were measured before and after surgery and during ARDS. Pulmonary capillary wedge pressure and cardiac output remained constant after surgery at a time that the PaO2/FIO2 ratio fell significantly. By contrast, none of the remaining 44 patients who did not receive amiodarone developed ARDS despite similar preoperative and intraoperative clinical parameters. Patients with ventricular tachyarrhythmias who receive even a short course of amiodarone are at risk for postoperative ARDS.
The effects of atrial pacing on the signal-averaged electrocardiogram were studied in 14 patients with remote myocardial infarction and a history of cardiac arrest or sustained ventricular tachycardia (group I) and in 13 patients with coronary artery disease and no history of sustained ventricular tachyarrhythmia (group II). Recordings of the signal-averaged electrocardiogram were obtained at control and during atrial pacing at rates of 80, 100, and 120 beats/min. All patients had recordings analyzed from at least two paced rates. At control, the mean high frequency total duration of the QRS complex (HFTD) was significantly longer in group I versus group II patients (123 +/- 5.6 versus 111 +/- 3.5 msec, p less than 0.05). Although the duration of the QRS signal under 40 microV (D40) was higher in group I versus group II patients (42 +/- 4.7 versus 32.4 +/- 3.5 msec) and the root mean square amplitude of the terminal 40 msec QRS (RMSA) was lower in the group I patients (27 +/- 7.5 versus 38.1 +/- 8.8 microV), these differences did not achieve statistical significance. There was no effect of atrial pacing on the measured signal-averaged parameters of HFTD, D40, and RMSA. Although there was a difference between group I and group II at each paced rate analyzed, atrial pacing did not help to further stratify the groups. In patients with coronary artery disease, atrial pacing is not a useful method of stratifying high-risk patients. Changes in serial signal-averaged electrocardiograms from the same patient are not due to heart rate variability.
This report describes the cardiac conduction abnormalities, detected by invasive electrophysiological study, in two identical siblings with symptomatic congenital long QT syndrome. Both patients had evidence of intra-Hisian conduction delay in response to programmed atrial stimulation and pacing induced infranodal block was seen in one of the two patients. The response of the observed conduction delay to autonomic interventions is described. The observed electrophysiologic abnormalities are consistent with previously reported pathological findings and document the association of functional conduction system disease with congenital QT prolongation.
To test the effect of trimethoprim (an antibiotic commonly administered with sulfamethoxazole) on the disposition of the antiarrhythmic procainamide hydrochloride and its active metabolite N-acetylprocainamide, 10 healthy men received 1 g of procainamide hydrochloride orally on two occasions, coadministered with placebo or trimethoprim (100 mg twice a day for 2 days before and then 200 mg with the procainamide dose). Trimethoprim decreased the mean (+/- SD) renal clearance by 45% after the dose of procainamide was administered (487 +/- 129 vs 267 +/- 123 mL/min) and that of N-acetylprocainamide by 26% (275 +/- 78 vs 192 +/- 82 mL/min) compared with placebo. The mean area under plasma concentration--time curve 0 to 12 hours after dosing increased 39% for procainamide (19.8 +/- 4.8 vs 27.6 +/- 7.2 mg.h/L) and 27% for N-acetylprocainamide (9.1 +/- 2.1 vs 11.4 +/- 2.8 mg.h/L). The corrected QT electrocardiographic interval at 2 hours after the procainamide dose was 0.40 +/- 0.02 second with placebo and 0.43 +/- 0.03 second with trimethoprim. Trimethoprim may increase procainamide and N-acetylprocainamide plasma concentrations, resulting in increased pharmacodynamic response apparently caused by the competition for renal tubular cationic secretion.
Because of allegations that the implantation of many permanent cardiac pacemakers has been unjustified, we reviewed the indications for all new pacemakers implanted at 30 hospitals in Philadelphia County between January 1 and June 30, 1983, and paid for by Medicare. Complete chart data were evaluated for 382 implants. We determined whether the indications for implantation were appropriate and adequately documented on the basis of standard clinical practice. Implants were classified as possibly indicated primarily because of inadequate diagnostic evaluation (63 percent) or inadequate documentation of an accepted indication (36 percent). Implants were classified as not indicated primarily because a rhythm abnormality was incorrectly identified as a justifiable indication (84 percent). We found that 168 implants (44 percent) were definitely indicated, 137 (36 percent) possibly indicated, and 77 (20 percent) not indicated. Unwarranted implantation was both prevalent (73 percent of hospitals had an incidence of 10 percent or more) and independent of the type of hospital (university teaching, university-affiliated, and community hospitals). The additional tests most often required to clarify the need for a pacemaker in inadequately evaluated cases included electrophysiologic studies (37 percent) and ambulatory monitoring (31 percent). We conclude that in a large medical population in 1983, the indications for a considerable number of permanent pacemakers were inadequate or incompletely documented.