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Biomedical subjects

R Yee

Publications and source records attributed to R Yee.

At least 145 records · Page 8Linked to original sources
PubMed1993

Defibrillation shocks produce different effects on Purkinje fibers and ventricular muscle: implications for successful defibrillation, refibrillation and postshock arrhythmia.

OBJECTIVES: To understand the mechanisms of postdefibrillation arrhythmias and failed defibrillation, we studied the cellular effects of high voltage shocks on different cardiomyocytes in the dog. BACKGROUND: The causes of postdefibrillation arrhythmias and unsuccessful defibrillation are not clear. METHODS: High voltage shocks with voltage differentials of 9.3 to 97.6 V/cm were delivered to isolated canine papillary muscles with attached Purkinje fibers. Transmembrane potentials were recorded simultaneously from the Purkinje fiber and the ventricular muscle using standard microelectrode techniques. RESULTS: After delivery of high voltage shocks, significant depolarization and rapid firing were observed in Purkinje fibers. The maximal rate of the rapid firing in the Purkinje fibers correlated with shock intensity (r = 0.69, p < 0.05). In contrast, in ventricular muscle, only slight depolarization and a transient refractory state were observed after the shock. The incidence of the refractory state was correlated with both the shock intensity and the rate of the rapid firing in the Purkinje fiber (r = 0.89 and 0.74, p < 0.01 and 0.05, respectively). Propranolol at a concentration sufficient for complete beta-blockade (1 mg/liter) did not change the tissue response to shocks but suppressed or abolished the shock-induced rapid firing of Purkinje fibers at a higher concentration (3 mg/liter). Blockade of the slow calcium channel with verapamil (400 micrograms/dl) did not alter the responsiveness of the preparation to shocks. CONCLUSION: These results indicate that high voltage shocks induce different responses in Purkinje fibers and ventricular muscle. The shock-induced rapid firing in the Purkinje fiber may contribute to postshock arrhythmias and possibly refibrillation in some cases. The shock-induced transient refractory state in the ventricular muscle may prevent the ventricle from responding to the rapid firing and thus may decrease the incidence of postshock arrhythmias.

Action Potentials↗
PubMed1993

Predictors of defibrillation efficacy in patients undergoing epicardial defibrillator implantation. The Multicenter Pacemaker-Cardioverter-Defibrillator (PCD) Investigators Group.

OBJECTIVES: The objective of this study was to identify predictors of defibrillation threshold in patients undergoing epicardial defibrillator implantation. BACKGROUND: Factors that predict epicardial defibrillation efficacy are poorly defined. METHODS: The data from 375 consecutive adult patients were reviewed. After exclusion of 137 patients in whom defibrillation threshold was not obtained, 238 patients (32 women and 206 men) with a mean age of 58.9 +/- 13.3 years formed the study group. Coronary heart disease was present in 175 patients and the mean left ventricular ejection fraction was 35.8 +/- 15.4%. At device implantation, three epicardial patch sizes were available and shocks could be delivered over one current pathway (two patches) or over two current pathways (three patches with simultaneous or sequential shocks). Defibrillation threshold was defined as the lowest programmed energy that successfully defibrillated the heart, provided there had been an unsuccessful shock at a lower energy level or successful defibrillation at < or = 5 J. RESULTS: The mean defibrillation threshold was 8.6 +/- 5.3 J. With univariate analysis, female gender, sequential shocks with three patches, higher left ventricular ejection fraction and lower New York Heart Association functional class predicted a lower defibrillation threshold. In the multivariate analysis, female gender (coefficient -3.9; 95% confidence interval [CI] -1.9 to -5.0 J), ejection fraction (coefficient -0.6; CI -0.1 to -1.0 J/decile) and sequential shocks (coefficient -2.5; CI -1.0 to -4.0 J) were independently associated with a lower defibrillation threshold. Total epicardial patch conductive surface area normalized to body surface area reached borderline significance (coefficient 0.004; CI 0 to 0.01; p = 0.10). Antiarrhythmic drug use, including amiodarone, did not predict defibrillation threshold. CONCLUSIONS: Female gender, high left ventricular ejection fraction and the use of sequential pulse shocks were important determinants of improved defibrillation efficacy.

Aged↗
PubMed1993

A placebo-controlled trial of intravenous and oral disopyramide for prevention of neurally mediated syncope induced by head-up tilt.

OBJECTIVES: A double-blind randomized trial was designed to determine the efficacy of intravenous and oral disopyramide phosphate in preventing neurally mediated syncope induced by a head-up tilt test. BACKGROUND: Neurally mediated syncope is a frequent cause of syncope and may be induced by head-up tilt testing. Recent uncontrolled trials have suggested that disopyramide may be an effective therapy in patients with neurally mediated syncope. METHODS: Twenty-two consecutive patients with recurrent neurally mediated syncope and two or more successive positive head-up tilt test responses were randomly allocated to receive either intravenous disopyramide or placebo. Head-up tilt testing at 60 degrees was performed for 15 min. If presyncope or syncope was not provoked, isoproterenol infusion was started at a rate of 1 microgram/min and the rate gradually increased until a 25% increase in heart rate was achieved. Eleven patients were subsequently randomized in crossover fashion to receive oral disopyramide (800 mg/day) or placebo during 1 week. The primary end point was prevention of syncope or presyncope provoked by head-up tilt testing. RESULTS: Head-up tilt test results were positive for syncope in 12 (75%) of 16 patients receiving intravenous placebo and in 12 (60%) of 20 patients receiving disopyramide (p = 0.55 Fisher exact test, 95% confidence interval [CI] -14% to 40%). In the intravenous phase, complete crossover was achieved in 15 patients. Head-up tilt test results during this phase were positive in 13 patients (87%) receiving placebo and in 12 patients (80%) receiving disopyramide (p = 0.50 Fisher exact test, 95% CI -19% to 32%) and were positive in all patients receiving their initially randomized drug or placebo. In the oral phase, head-up tilt results were positive in only two patients (18%) assigned to placebo and in three patients (27%) receiving disopyramide (p = 0.54 Fisher exact test, 95% CI -42% to 24%). A mean follow-up time of 29 +/- 8 months was obtained in 21 of the 22 patients. Syncope recurred in 3 (27%) of the 11 patients receiving disopyramide and 3 (30%) of the 10 patients not treated pharmacologically (p > 0.05). CONCLUSIONS: Intravenous disopyramide was ineffective for the prevention of neurally mediated syncope provoked by head-up tilt testing. No significant effect was observed after oral therapy with disopyramide. There was a striking decrease in the incidence of positive tilt test results over time regardless of intervention, thus discouraging the use of head-up tilt as the single method of assessing therapeutic efficacy. Recurrence of syncope after the investigative protocol was infrequent over long-term follow-up regardless of treatment group.

Administration, Oral↗
PubMed1993

Elimination of slow pathway conduction: an accurate indicator of clinical success after radiofrequency atrioventricular node modification.

OBJECTIVES: The purpose of this study was to determine the optimal end point of radiofrequency atrioventricular (AV) node modification using anatomically guided slow pathway approaches in patients with AV node reentrant tachycardia. BACKGROUND: The optimal end point for AV node modification using radiofrequency energy is uncertain, although elimination of inducible AV node reentrant tachycardia has been used. METHODS: We followed up 51 consecutive patients (40 women, 11 men, mean age +/- SD 41 +/- 16 years) with symptomatic AV node reentrant tachycardia for 12 +/- 6 months (range 4 to 24) after radiofrequency AV node modification using an anatomically guided slow pathway approach. Inducible AV node reentrant tachycardia was eliminated in all patients, whereas residual slow pathway conduction persisted in 12 patients (24%) after ablation. One study was complicated by complete AV block and two patients were lost to follow-up (one with and one without residual slow pathway conduction). RESULTS: Clinical recurrence of AV node reentrant tachycardia was documented in seven patients (14%) 3 days to 3 months (median 1 month) after ablation. The recurrence rate was significantly higher in patients with than in those without residual slow pathway conduction (6 [55%] of 11 vs. 1 [3%] of 37, p < 0.01). The recurrence rate was not different between patients with only residual slow pathway conduction and those with residual slow pathway conduction and inducible single echo cycles (three [60%] of five in both groups, p = NS). The number of radiofrequency energy applications was not significantly different between those without and those with recurrence (20 +/- 17 vs. 16 +/- 9, p = NS). Junctional tachycardia during application of radiofrequency energy tended to be more frequently observed in those with a successful outcome (77% vs. 57%, p > 0.05). Of the 22 patients who underwent modification before 1992, residual slow pathway conduction was present in 9 (41%) of 22 patients. Atrioventricular node reentrant tachycardia recurred in five (56%) of these nine patients. A greater effort made in 1992 to eliminate slow pathway conduction in 29 patients resulted in residual slow pathway conduction in only 3 (11%) with recurrence in 2 (4%). CONCLUSIONS: Complete elimination of slow pathway conduction is feasible in the majority of patients. Elimination of slow pathway conduction is highly predictive of long-term success after AV node modification using an anatomically guided approach.

Adult↗
PubMed1993

Supraventricular tachycardias: the role of surgery.

Because of its high efficacy and low morbidity radiofrequency energy catheter ablation techniques have toppled the hierarchy of choice in the electrophysiological intervention armamentum. This review assesses current role of surgery and its foreseeable future. Most accessory AV pathways can be attained by endocardial manipulation and ablated. Surgical dissection of accessory pathways on the beating heart had documented that most pathways were paraannular, although right-sided pathways may be distant to the annulus. Results of accessory pathway ablation have shown that right-sided pathways are difficult to approach and ablate. Surgical ablation may currently be considered after failed catheter ablation. AV nodal modification using catheter ablation also yields excellent results. Radiofrequency energy creates a discrete lesion associated with discrete electrophysiological alteration. Surgical dissection is associated with more diffuse and extensive anatomical and electrophysiological changes and is no longer used even after failed catheter ablation. The arrhythmogenic anatomical substrate associated with atrial flutter is not yet well delineated in the coronary sinus os region. How to extend tissue modification for uniform success here is not yet known. Further surgical approach combined with extensive intraoperative cardiac mapping may ultimately prove a valuable guide for subsequent catheter technique. Atrial fibrillation is the last surgical frontier unchallenged by catheter techniques. Arrhythmogenic anatomical substrate is diffuse spreading over the entire atrial myocardium without a discrete target. The associated pathology is diffuse, severe, and progressive and present even in the so-called lone atrial fibrillation. Progression of underlying pathology can nullify the best designed surgical rationale in terms of sinus node chronotropic function, and atrial contractility. Currently used surgical techniques, i.e., the corridor and the Maze operations, have contributed to a better selection of patients. Surgery is still associated with significant morbidity and relative efficacy, and may be improved before becoming the electrophysiological intervention of choice for atrial fibrillation. In conclusion, atrial fibrillation is a greater surgical challenge, but has to be met with the same standard used for other supraventricular tachycardias.

Atrial Fibrillation↗
PubMed1993

Malposition of transvenous pacing lead in the left ventricle.

Malposition of pacemaker leads has been described in several locations but rarely in the left ventricle. The incidence and clinical course of this pacemaker complication are unknown. We describe clinical, electrocardiographic, chest X ray, and echocardiographic findings in four patients in whom the transvenous pacing lead was inadvertently placed through the interatrial septum and mitral valve into the left ventricle. In these patients, lead misplacement was not recognized at the time of implantation and lead malposition was diagnosed a mean of 2 years later. All four patients had right bundle branch block configuration paced complexes. In retrospect, chest X rays suggested atypical lead position in all, but the initial posterior-anterior and lateral chest X rays were misinterpreted and contributed to the delay in diagnosis. When lead misplacement in the left ventricle was considered it was confirmed by two-dimensional echocardiography. One patient subsequently presented with a stroke and the remainder were diagnosed when they presented with other unrelated problems. Pacing thresholds were normal at the time of implantation and behaved normally during follow-up. The patient presenting with stroke was anticoagulated and the other three have been managed expectantly without anticoagulation. Diagnosis of left ventricular lead malposition is not difficult but requires a high index of suspicion. A 12-lead ECG and posterior-anterior and lateral chest X rays after implantation can be diagnostic. Patients with pacing lead in the left ventricle may remain asymptomatic with normal lead function during long-term follow-up. Anticoagulation should be considered when this problem comes to attention for the first time during follow-up.

Aged↗
PubMed1993

Comparative atrioventricular node properties after radiofrequency ablation and operative therapy of atrioventricular node reentry.

The anatomical substrate for atrioventricular (AV) node reentry is unclear. To gain insights into the mechanism of cure of AV node reentry by nonpharmacological techniques, we compared AV node properties in 53 patients undergoing operative therapy (perinodal dissection) and 43 undergoing radiofrequency ablation (28 posterior approach, 15 anterior approach). Anterior radiofrequency ablation was associated with significant AH prolongation (62 +/- 18 msec vs 136 +/- 64 msec, P < 0.0001), loss of "fast" pathway physiology, and no change in the anterograde refractory period of the AV node (273 +/- 24 msec vs 268 +/- 28 msec, P = NS). Posterior radiofrequency ablation did not change the AH interval (67 +/- 17 msec vs 68 +/- 17 msec, P = NS), prolonged AV node effective refractory period (275 +/- 48 msec vs 320 +/- 55 msec, P < 0.0001), and was associated with loss of "slow pathway" physiology. Operative treatment prolonged the AH interval (66 +/- 18 msec vs 83 +/- 37 msec, P < 0.0001) and the AV node effective refractory period (264 +/- 52 msec vs 364 +/- 112 msec, P < 0.0001), and affected dual pathway physiology inconsistently. These data support the view that the "fast" and "slow" pathways are distinct perinodal entities that can be selectively ablated. The operative approach causes more diffuse and variable injury to the AV node region.

Adolescent↗
PubMed1993

Arrhythmogenic effects of catecholamines are decreased in heart failure induced by rapid pacing in dogs.

Increased circulating catecholamines are considered to be arrhythmogenic in heart failure. It is unclear whether increased circulating catecholamines contribute directly to ventricular arrhythmias or are only markers of the severity of heart failure. The present study determined the sensitivity of the failing heart to the arrhythmogenic effect of exogenous norepinephrine in a rapid pacing-induced model of heart failure in dogs (240 beats for 4 wk, n = 14). A similarly operated, non-paced group served as controls (n = 9). Cardiac sensitivity to the arrhythmogenic effect of catecholamines was determined by measuring the minimal dose of exogenous norepinephrine that induced ventricular tachycardia (arrhythmogenic threshold dose, ATD). ATD significantly increased after development of heart failure in heart-failure group (1.62 +/- 0.32 microgram/kg at baseline vs. 16.65 +/- 3.48 micrograms/kg at restudy, P < 0.01), whereas no significant change was noted in the control group (1.08 +/- 0.36 microgram/kg at baseline vs. 2.53 +/- 0.36 micrograms/kg at restudy, P > 0.10). Action potential duration was unchanged by superfusion with 10(-7) M isoproterenol in both ventricular muscles (230.2 +/- 6.1 vs. 229.7 +/- 5.3 ms, P = NS) and Purkinje fibers (273.2 +/- 6.5 vs. 283.8 +/- 4.2 ms, P = NS) from the failing hearts, although isoproterenol induced a shortening in the control group (204.8 +/- 0.9 vs. 181.3 +/- 1.6 ms in ventricular muscles, P < 0.01; 313.8 +/- 6.5 vs. 279.5 +/- 5.7 ms in Purkinje fibers, P < 0.01). We conclude that the failing heart has a decreased sensitivity to the arrhythmogenic effect of catecholamines.

Action Potentials↗
PubMed1993

Heart transplantation after cardioverter-defibrillator implantation. A case control study.

A case control study was performed to determine whether previous implantable cardioverter-defibrillator (ICD) insertion adversely affects outcome after heart transplantation. Six male heart transplant recipients who had undergone ICD insertion 12 +/- 5 months before heart transplantation were compared to a cohort of six heart transplant recipients who were matched according to age, preoperative status and hemodynamics, date of transplantation, graft ischemic time, history of a previous cardiac operation, and duration of follow-up. There were no significant differences in operating room time, chest tube drainage, time to extubation, and the duration of intensive care unit or hospital stay between the two groups. Furthermore, there were no significant differences in the number of units of packed cells, fresh frozen plasma, platelets and cryoprecipitate transfused. The number of treated rejection episodes and the number of patients requiring intravenous antibiotics for infection in the first 90 days was identical between groups. It was concluded that heart transplantation after ICD implantation did not appear to carry more risk than heart transplantation after a previous cardiac operation. Our limited experience supports the potential use of the ICD in patients with life-threatening ventricular dysrhythmias who are awaiting transplantation.

Blood Loss, Surgical↗
PubMed1993

Classification and terminology of supraventricular tachycardia. Diagnosis and management of the atrial tachycardias.

This article describes some of the historical approaches to classifying supraventricular tachycardias and the evolution of the nomenclature as the knowledge of tachycardias improved. A classification scheme that is mechanistically based and favored by the authors, diagnostic criteria, clinical presentation, and therapy of the atrial tachycardias is also presented.

Humans↗
PubMed1992

An anatomically guided approach to atrioventricular node slow pathway ablation.

Radiofrequency ablation of the "slow" pathway of the atrioventricular (AV) node reentrant circuit may be guided by electrophysiologic ("slow pathway potential") or anatomic landmarks. Experience with a systematic, anatomically guided approach in 25 patients (20 women and 5 men, aged 38 +/- 15 years) with typical AV node reentry is described. The slow pathway is assumed to be the posterior input to the AV node, approaching the nodal region in the corridor between the tricuspid annulus and the orifice of the coronary sinus. A series of radiofrequency lesions are given to interrupt this corridor at its entrance to Koch's triangle. If this is unsuccessful, the series of lesions are repeated progressively at higher levels approaching the AV node. The major end point for success is elimination of the slow pathway as determined by extrastimulus testing. A mean of 1.2 +/- 0.2 ablative sessions (20 +/- 12 applications of energy) achieved clinical success in 24 of 25 patients (96%) at a follow-up of 8.6 +/- 2.2 months. Anterograde Wenckebach cycle length increased from 361 +/- 67 ms to 398 +/- 70 ms (p = 0.01), yet the atrio-Hisian interval in sinus rhythm did not change (69 +/- 17 ms before vs 65 +/- 15 ms after ablation), p = 0.22. Retrograde Wenckebach cycle length was not affected (348 +/- 78 ms before vs 366 +/- 82 ms after ablation). During ablation, transient third-degree AV block occurred in 6 patients with no permanent sequelae. This approach provides a systematic, expedient technique to eliminate slow pathway conduction based on anatomic landmarks.

Adult↗
PubMed1992

Alfentanil-midazolam anaesthesia has no electrophysiological effects upon the normal conduction system or accessory pathways in patients with Wolff-Parkinson-White syndrome.

The effects of alfentanil-midazolam anaesthesia upon the electrophysiologic (EP) properties of normal atrioventricular (A-V) and accessory pathway (AP) conduction were studied in eight patients with Wolff-Parkinson-White syndrome during accessory pathway surgical ablation. The presence of an AP was confirmed by preoperative EP studies. Anaesthesia was induced with alfentanil (50 micrograms.kg-1) and midazolam (0.15 mg.kg-1) and maintained with an alfentanil infusion (2 micrograms.kg-1.min-1) and intermittent boluses of midazolam (1-2 mg q 15 min, PRN). Following sternotomy, a baseline EP study was performed which consisted of effective refractory period (ERP) and shortest cycle length (SCC) measurement during antegrade conduction in the AV and AP, as well as during retrograde conduction in the AP. Comparison with preoperative EP studies indicated that the administration of alfentanil-midazolam anaesthesia had no effect upon conduction or ERP in either pathway. Haemodynamic stability occurred throughout the surgical procedure with no tachyarrhythmias. We conclude that a combination of alfentanil-midazolam is suitable for general anaesthesia in patients undergoing ablative procedures for accessory pathways.

Adult↗
PubMed1992

Differential effect of intravenous procainamide on anterograde and retrograde accessory pathway refractoriness.

Although procainamide may markedly impair or abolish anterograde conduction over an accessory atrioventricular (AV) pathway, orthodromic AV reentry may remain inducible. This difference may be related to a systemic differential effect of procainamide on anterograde and retrograde accessory pathway refractoriness. To examine this phenomenon, an infusion of procainamide producing five incremental blood levels over 75 min was administered to 15 patients with the Wolff-Parkinson-White syndrome. At each procainamide level, accessory pathway effective refractory period and accessory pathway block cycle length were determined in the anterograde and retrograde directions. At baseline, there were no significant differences between anterograde and retrograde accessory pathway effective refractory periods (282 +/- 7 vs. 266 +/- 9 ms, p = 0.08) and block cycle lengths (288 +/- 15 vs. 283 +/- 9 ms, p = 0.66). The concentration of procainamide resulting in 50% prolongation of accessory pathway refractoriness was less in the anterograde direction than in the retrograde direction (27.5 [log concentration -4.56 +/- SE 0.13] vs. 64.6 [-4.19 +/- 0.11] mumol/liter, p = 0.02). Similarly, the concentration of procainamide resulting in 50% prolongation of accessory pathway block cycle length in the anterograde direction (25.1 [-4.60 +/- 0.13] mumol/liter) was less than in the retrograde direction (52.5 [-4.28 +/- 0.07] mumol/liter, p = 0.01). The probability of persistence of accessory pathway conduction in the anterograde direction was less than in the retrograde direction by Kaplan-Meier analysis (p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Electrophysiologic substrate associated with pacing-induced heart failure in dogs: potential value of programmed stimulation in predicting sudden death.

To investigate the possible mechanisms of sudden death and the potential role of electrophysiologic testing in congestive heart failure, this study evaluated the electrophysiologic substrate in a model of heart failure induced by rapid pacing. Seventeen mongrel dogs underwent cardiac pacing at 220 to 240 beats/min for 5 weeks (paced group) and 11 other dogs served as a sham-operated control group. Rapid pacing of the right ventricle produced clinical and hemodynamic features of congestive heart failure. Dogs in the paced group had prolonged cardiac conduction time as reflected by longer epicardial activation time (36.1 +/- 2.4 vs. 30.8 +/- 0.8 ms, p less than 0.05). The ventricular effective refractory period was significantly prolonged after the development of heart failure (141 +/- 4 vs. 177 +/- 5 ms, p less than 0.01, at a basic pacing cycle length of 300 ms), whereas no significant change was found in the control group (140 +/- 4 vs. 145 +/- 4 ms, p = NS). The prolongation of the ventricular effective refractory period correlated with an increase in left ventricular end-diastolic pressure (r = 0.55, p less than 0.001) and the ventricular effective refractory period correlated inversely with cardiac index (r = -0.49, p less than 0.025). The rest membrane potential of ventricular muscle was less negative in the paced group compared with the control group (-80.7 +/- 2.2 vs. -85.6 +/- 2.2 mV, p less than 0.05). Intracellularly recorded action potential duration of ventricular muscle was longer in the paced than in the control group (236 +/- 9.8 vs. 198.9 +/- 2.6 ms, p less than 0.01), action potential duration at 90% repolarization).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Paracentral rheumatoid corneal ulceration. Clinical features and cyclosporine therapy.

Six patients with rheumatoid arthritis (eight eyes) presented with small paracentral perforating corneal ulcers in otherwise quiet eyes. Initial management in five patients (seven eyes) consisted of systemic immunosuppression and therapeutic tissue adhesive with a bandage contact lens or tectonic keratoplasty. Ulceration recurred in all of these eyes, and recurrent ulcers treated with repeat tectonic keratoplasty or therapeutic tissue adhesive and a bandage contact lens all developed recurrent ulceration. The introduction of topical cyclosporine therapy in five eyes with recurrent corneal ulceration was associated with arrest of keratolysis and rapid re-epithelialization of the ulcer in all cases. One corneal ulcer was successfully treated initially with topical cyclosporine, tissue adhesive, and a bandage contact lens. In patients with rheumatoid arthritis and small paracentral corneal ulcerations or perforations, application of tissue adhesive and a bandage contact lens and introduction of topical cyclosporine may be the preferred initial treatment.

Aged↗
PubMed1992

A unique preexcitation pattern related to an atypical anteroseptal accessory pathway.

Accessory atrioventricular pathways have traditionally been classified by anatomical location to four areas, namely anteroseptal, posteroseptal, and right and left free walls. Each of these have been associated with a relatively distinct preexicitation pattern electrocardiographically. We describe a patient with a unique ECG pattern suggesting preexicitation to the right ventricular outflow region. Preoperative and intraoperative electrophysiological testing confirmed the presence of an accessory pathway with an atrial insertion site near the His bundle, decremental anterograde conduction, and a ventricular insertion site in the upper part of the interventricular septum. Operative ablation near the atrial insertion site eliminated preexicitation.

Adult↗