Transvenous Electrode Catheter Research Articles

Abstract 15127: Isorhamnetin Reverses Angiotensin Ii-induced Atrial Fibrillation Vulnerability Through Electrophysiological and Structural Reverse Remodeling in Mice

Background: Isorhamnetin (ISO), a natural flavonoid compound, has been shown to have strong antioxidant and antifibrotic effects in vivo and in vitro; however, no report has been shown on the effect of ISO on arrhythmic disorders. This study aimed to investigate the effect of ISO on angiotensin-II (Ag-II) induced atrial fibrillation (AF) in mice. Methods: Wild-type male mice (C57BL/6J, 8 weeks old) were assigned in 3 groups as follows: control group (Cont), Ag-II group treated with Ag-II and Ag-II & ISO group treated with Ag-II and ISO. Ag-II (1000 ng/kg/min) was continuously administered using an implantable osmotic pump for 2 weeks, and ISO (5 mg/kg) was administered intraperitoneally one week before starting Ag-II administration. We performed AF induction and electrophysiologic study via transvenous electrode catheter and Ca 2+ imaging with isolated cardiomyocyte. We also assessed the gene expression levels of AF-related molecules, and histological examination of atrial fibrosis. Results: Compared with Cont, AF inducibility was dramatically increased by Ag-II and significantly decreased by ISO. AF duration was also remarkably prolonged by Ag-II and significantly reduced by ISO. Atrial effective refractory period (A-ERP) (BCL=150msec) was reduced by Ag-II and recovered by ISO. Incidences of diastolic intracellular Ca 2+ abnormal activities (sarcoplasmic reticulum [SR] Ca 2+ leakage) was observed in Ag-II group; however, ISO treatment eliminated these abnormalities. Ag-II induced elevated expression of fibrosis-related molecules (Col1a1, Tgfb1 and Tgfb2) and Ca 2+ -handling related molecules (Camk2 and Ryr2), those were partially normalized by ISO. Histological examination revealed that cell size and the fibrosis ratio were increased by Ag-II, and significantly attenuated by ISO. Conclusion: These results suggest that ISO prevented against Ag-II induced AF vulnerability through both electrophysiological and structural reverse remodeling.

Age‐Related Increase in Atrial Fibrillation Induced by Transvenous Catheter‐Based Atrial Burst Pacing: An In Vivo Rat Model of Inducible Atrial Fibrillation

Large animal models of atrial fibrillation (AF) are well established, but limited experimental reports exist on small animal models. We sought to develop an in vivo rat model of AF using a transvenous catheter and to evaluate the model's underlying characteristics. Echocardiogram, surface electrocardiogram (ECG), and atrial effective refractory period (AERP) were recorded at baseline in young (3 months) and middle-aged (9 months) Wistar rats. AF inducibility and duration were measured through transvenous electrode catheter in young (n = 11) and middle-aged rats (n = 11) and middle-aged rats treated with either pilsicainide (1 mg/kg iv, n = 7) or amiodarone (10 mg/kg iv, n = 9). Degrees of interstitial fibrosis and cellular hypertrophy in the atria were assessed histologically. The P-wave duration and AERP were significantly longer and echocardiographic left atrial dimension significantly larger in middle-aged versus young rats. AF was inducible in >90% of all procedures in both untreated rat groups, whereas AF inducibility was reduced by the antiarrhythmic drugs. The AF duration was significantly longer in middle-aged than in young rats and was significantly shortened by treatment with either pilsicainide or amiodarone. Histologic analysis revealed significant increases in atrial interstitial fibrosis and cellular diameter in middle-aged versus young rats. Transvenous catheter-based AF is significantly longer in middle-aged than in young rats and is markedly reduced by treatment with antiarrhythmic drugs. This rat model of AF is simple, reproducible, and reliable for examining pharmacologic effects on AF and studying the process of atrial remodeling.

Surgical management and problems of heart pacing.

Experience with 40 patients and 150 pacemakersss is reviewed. In 13 patients the initial pacing was by epicardial electrodes and in 27 by transvenous catheter electrodes. When epicardial systems were used, two electrodes were always fixed to the heart, the additional electrode being provided for temporary pacing and as a spare in case of future need. The battery unit was usually buried behind the rectus abdominis muscle. Vacuum drainage of the pacemaker pocket was used and was considered helpful in avoiding some complications. The right cephalic vein was preferred for transvenous pacing but existing venous abnormalities sometimes required use of the external jugular vein. Five patients had epicardial systems changed to transvenous ones, and in 5 the reverse procedure was needed. Pacemaker battery problems included inadequate soft tissue protection for the unit, epoxy resion fracture, titanium case leak and problems relating to design change and the special needs for overseas travel. While the danger from diathermy and radiofrequency is now recognized, similar dangers exist for those paced by 'demand' units in large electromagnetic fields.

Low‐Energy Transvenous Cardioversion of Atrial Fibrillation Using a Single Atrial Lead System

Clinical studies have shown that electrical conversion of atrial fibrillation (AF) is feasible with transvenous catheter electrodes at low energies. We developed a single atrial lead system that allows atrial pacing, sensing, and defibrillation to improve and facilitate this new therapeutic option. The lead consists of a tripolar sensing, pacing, and defibrillation system. Two defibrillation coil electrodes are positioned on a stylet-guided lead. A ring electrode located between the two coils serves as the cathode for atrial sensing and pacing. We used this lead to cardiovert patients with acute or chronic AF. The distal coil was positioned in the coronary sinus, and the proximal coil and the ring electrode in the right atrium. R wave synchronized biphasic shocks were delivered between the two coils. Atrial signal detection and pacing were performed using the proximal coil and the ring electrode. Eight patients with acute AF (38 +/- 9 min) and eight patients with chronic AF (6.6 +/- 5 months) were included. The fluoroscopy time for lead placement was 3.5 +/- 4.3 minutes. The atrial defibrillation threshold was 2.0 +/- 1.4 J for patients with acute AF and 9.2 +/- 5.9 J for patients with chronic AF (P < 0.01). The signal amplitude detected was 1.7 +/- 1.1 mV during AF and 4.0 +/- 2.9 mV after restoration of sinus rhythm (P < 0.001). Atrial pacing was feasible at a threshold of 4.4 +/- 3.3 V (0.5-msec pulse width). Atrial signal detection, atrial pacing, and low-energy atrial defibrillation using this single atrial lead system is feasible in various clinical settings. This system might lead to a simpler, less invasive approach for internal atrial cardioversion.

927-32 Effects of Digoxin and Sotalol on Atrial Defibrillation Thresholds via Implanted Transvenous Catheter Electrodes

It has been documented in animal models that a synchronized shock delivered to the atria through transvenous catheter electrodes is a feasible method to terminate atrial fibrillation (AF). Because digoxin and sotalol are frequently used in the management of patients with AF, we studied the effect of these drugs on atrial defibrillation thresholds (ADFTs). Sterile pericarditis was created using standard methods in 17 mongrel dogs. Two catheter electrodes with a 6 cm coil tip were inserted through the right external jugular vein and placed in the distal coronary sinus and in the right atrial appendage, respectively. They were subsequently used for delivery of atrial shocks. On the second postoperative day, AF was induced by rapid atrial pacing, and ADFT was determined in the drug free state and after administration of 1) a therapeutic dose of digoxin (50 μg/kg; 6 dogs); 21 a toxic dose of digoxin (increased dose, mean 106 μg/kg, associated with a digitalis toxic rhythm; 6 dogs); or 3) sotalol (1 mg/kg followed by a continuous infusion of 0.375 mg/kg/hr; 5 dogs). ADFT was determined in a 10 V step-up manner, with 20 shocks delivered at the lowest intensity that converted AF to determine % success. ADFT was defined as the lowest defibrillation energy which achieved successful atrial defibrillation between 10% and 90% of the time. Data are shown in mean ± SD. Digoxin Voltage (V) Energy (J) Impedance (Ω) %Success (%) Drug free 85 ± 21 0.27 ± 15 40 ± 7 40 ± 17 Therapeutic dose 77 ± 29 0.28 ± 18 36 ± 3 30 ± 19 Toxic dose 77 ± 29 029 ± 0.16 36 ± 8 42 ± 16 Sotalol Drug free 64 ± 5 013 ± 04 45 ± 7 30 ± 23 Sotalol 52 ± 8 * 0.10 ± 03 44 ± 7 29 ± 18 * p &lt; 005 Digoxin did not significantly affect the voltage, energy, or impedance of the shock, butsotalol significantly decreased the mean ADFT voltage required. In the sterile pericarditis model of AF: 1) ADFT was very low (1&lt;03 J) through transvenous catheter electrodes; and 2) digoxin did not significantly affect ADFTs, although sotalol decreased ADFTs determined using transvenous catheter electrodes.

901-44 Effects of the Preceding R-R Interval on the Safety of Atrial Defibrillation via Transvenous Catheter Electrodes in the Sterile Pericarditis Model

A synchronized shock delivered to the atria through transvenous catheter electrodes will terminate atrial fibrillation (AF). We evaluated the effects of the preceding R-R interval on the relative risk of inducing ventricular arrhythmias (VT/VF) during synchronized atrial defibrillation shocks delivered between implanted transvenous catheter electrodes. The sterile pericarditis model was created in 15 dogs. Two customized transvenous catheter electrodes with a 6 cm coil tip were placed, one in the distal coronary sinus and one in the right atrial appendage, respectively, to deliver atrial defibrillation shocks. Variable preceding R-R intervals were simulated systematically with 3 protocols: 1) single ventricular stimulation (PVC protocol); 2) rapid ventricular stimulation (8 stimuli, SlSl protocol); and 3) double ventricular stimulation (long-short intervals) following 8 basic stimuli (S1S2S3 protocol). The ventricular coupling interval (VCI) was shortened by 10 ms until refractoriness occurred at the pacing site. After sensing the last paced ventricular beat, an atrial shock was delivered with a 2 ms delay at a shock intensity of 300 V (maximal intensity of the device). Atrial shocks were delivered 4 times at each VCI in each protocol. VCI was norrnalized by subtracting the QT interval from the VCI. The relationship between VCI and induction of VT/VF was compared between protocols. To calculate a 99% probability of sinus rhythm (SR) after an atrial shock, logistic regression analysis was used. For all 15 dogs, the mean QT interval was 231 ± 21 ms. protocol VT/VF induction 99% probability of SR (ms) PVC 10/522 QT + 15 S1S1 13/522 QT + 28 S1S2S3 40/435 QT + 84 The incidence of VT/VF induction was significantly higher for the S1S2S3 than for the PVC or the SlSl protocol (p &lt; 0.05). The 99% probability of SR was achieved at a significantly longer VCI for the SlS2S3 than for the PVC or the SlSl protocol (p &lt; 0,05). The long-short R-R interval increases the incidence of VT/VF induction and shortens the safety zone of the VCI for synchronized atrial shocks. However, a large safety zone (VCI &gt; 315 ms) is still present, and is predictable from the QT interval.

Effects of Digoxin on Ventricular Vulnerability During Atrial Defibrillation via Implanted Transvenous Catheter Electrodes in the Sterile Pericarditis Model

Because digoxin is often used in patients with atrial fibrillation, we evaluated its effects on the relative risk of inducing ventricular tachyarrhythmia (VT/NF) during synchronized atrial defibrillation shocks delivered through implanted transvenous catheter electrodes. Sterile pericarditis was created in 10 mongrel dogs. Two catheter electrodes with a 6 cm coil tip were inserted through the right external jugular vein and placed in the distal coronary sinus and in the right atrial appendage. To systematically achieve variable preceding ventricular coupling intervals (VCls). the ventricles were paced during sinus rhythm before delivery of the atrial shock in two protocols: 1) rapid pacing (8 stimuli, S 1 S 1 protocol); and 21 double extra stimuli (long-short intervalsl following 8 basic stimuli (S 1 S 2 S 3 protocol). The VCI (S 1 S 1 or S 2 S 3 )was shortened by 10 ms until the ventricular effective refractory period was achieved. After sensing the last paced ventricular beat. an atrial shock was delivered with a 2 ms delay at a shock intensity of 300 V (3.2–3.6 J), i.e., maximum shock intensity ofthe device. Atrial shocks were delivered 4 times at each VCI in each protocol. VCI was normalized by subtracting the OT interval in the surface ECG from the actual VCI. The relationship between the VCI and induction of VT/NF was evaluated in the drug free state and after administration of a therapeutic (50 μ g/kg. 5 dogs) or toxic (to obtain toxic arrhythmia. 5 dogs) dose of digoxin. Data are shown in mean ± SD, for each protocol (S 1 S 1 or S 1 S 2 S 3 ). To calculate a 99% probability of sinus rhythm (SR) after an atrial shock.logistic regression was used. No significant difference was observed before and after digoxin administration. The longest VCI that preceded VTNF induction was QT + 50 ms (290 ms) before digoxin and QT + 50 ms (310 ms) after digoxin. digoxin QT (ms) VTNF induction 99% probability of SR (ms) control 226 ± 22 6/377 (S 1 S 1 ) 27/303 (S 1 S 2 S 3 ) QT – 4 (S 1 S 1 ) QT + 71 (S 1 S 2 S 3 ) therap 237 ± 44 8/178 (S 1 S 1 ) 16/151 (S 1 S 2 S 3 ) QT + 1 (S 1 S 1 ) QT + 73 (S 1 S 2 S 3 ) toxic 220 ± 8 8/177 (S 1 S 1 ) 15/142 (S,S 2 S 3 ) QT + 1 (S 1 S 1 ) OT + 63 (S 1 S 2 S 3 ) Digoxin did not significantly change the risk of VT/NF induction during atrial defibrillation shocks delivered through transvenous catheter electrodes at maximum shock intensity. Shocks delivered at VCls longer than 310 ms resulted in no VT/NF induction.

Rapid bedside temporary pacing by the right supraclavicular subclavian vein approach

Although the techniques of permanent cardiac pacing have been advanced, the current status of transvenous emergency ventricular pacing is still unsatisfactory. The insertion of a standard transvenous electrode catheter requires expert skill and roentgenography. Attempting to insert a flotation electrode or a standard electrode catheter to pace the right ventricle while monitoring the intracardiac electrocardiogram may be successful, but it is also time-consuming. Currently, external noninvasive temporary cardiac pacing is more reliable, but may be uncomfortable and intolerable in conscious patients, or unsuccessful in some cases. 1 Emergency ventricular pacing using a J-electrode catheter without fluoroscopy is reported to be a rapid inserting method; however, most pacing sites are in the right ventricular outflow tract, which is an unstable pacing position. Later, standard transvenous catheter pacing is still needed with roentgenography. 2 Recently, we developed a bedside transvenous right ventricular pacing method that can be performed rapidly through the right supraclavicular subclavian vein with a J-tipped guide introducer.

CARDIAC TAMPONADE DUE TO RIGHT VENTRICULAR PERFORATION BY A TRANSVENOUS ELECTRODE CATHETER : A CASE REPORT

Acute cardiac tamponade secondary to perforation of the right ventricle during a transient transvenous electrode catheter insertion, occurred in a 79-year-old man. This perforation may have occurred because the apexical tissue of the right ventricle was fragile. Prompt recognition and treatment of this potentially lethal complication of pacemaker electrode catheter insertion are essential.

Emergency ventricular pacing using a J‐electrode catheter without fluoroscopy

The initiation of emergency ventricular pacing may be delayed by a lack of facilities for immediate fluoroscopy or staff members who are skilled in positioning a transvenous electrode catheter. Techniques have been developed to overcome these problems but have been unreliable, expensive and/or uncomfortable for patients. In each of 20 consecutive haemodynamically unstable patients (13 patients with asystole or high-grade atrioventricular block and seven patients with ventricular tachycardia), an attempt was made to pace the ventricle with a Cordis 5-FG (1.67-mm) "atrial J"-electrode catheter, which was inserted transvenously without fluoroscopic guidance. Pacing was initiated successfully in 19 cases within 40 seconds to 30 minutes (median, two minutes) of skin puncture, and in 16 cases within three minutes. Fifteen procedures were performed by operators with experience of less than 10 previous pacing catheter insertions. This study demonstrates that emergency transvenous ventricular pacing can be initiated rapidly and reliably by means of a catheter with a "J" configuration, which is inserted without the use of fluoroscopy. The method can be employed successfully by operators with little experience in pacing techniques. Standard inexpensive equipment is used; the technique is safe and well-tolerated by patients.

Clinical efficacy of dual electrode systems for endocardial cardioversion of ventricular tachycardia: A prospective randomized crossover trial

In order to eliminate the need for epicardial electrodes, two large transvenous catheter electrodes or one catheter and one extrathoracic patch electrode have been proposed as alternative electrode configurations for defibrillation and ventricular tachycardia cardioversion by implantable cardioverter/defibrillators. We compared the efficacy and safety of endocardial shocks delivered through these two electrode systems in man in a prospective randomized crossover study. Twelve patients with sustained ventricular tachycardia and heart disease undergoing electrophysiologic study were evaluated. A transvenous tripolar cardioversion electrode catheter with a large distal defibrillation electrode (surface area, 400 mm2) and proximal defibrillation electrode (surface area, 800 mm2) was positioned in the right ventricular apex with a cutaneous patch electrode placed on the cardiac apex. Sustained ventricular tachycardia was induced at electrophysiologic study. Shocks were delivered using two catheter electrodes only (right ventricular cathode and right atrial anode = method I), and one catheter electrode and cutaneous patch (right ventricular cathode and cutaneous apical patch anode = method II). Synchronized monophasic shocks were delivered using three preselected protocols based on ventricular tachycardia cycle length and morphology. Initial shock energies were 25 joules for polymorphic ventricular tachycardia and ventricular fibrillation, 15 joules for monomorphic rapid ventricular tachycardia (cycle length less than or equal to 300 msec), and 5 joules for monomorphic slow ventricular tachycardia (cycle length greater than 300 msec). Ventricular tachycardia was reinduced and shock energies titrated until cardioversion threshold was obtained. Identical ventricular tachycardia episodes were treated with both methods at each energy level.(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic and right atrial systolic pressures during cardiopulmonary resuscitation: A potential indicator of the mechanism of blood flow

The absolute difference between aortic and right atrial systolic pressure (systolic pressure gradient) and the difference between the aortic diastollic and right atrial diastolic pressure (coronary perfusion pressure) were evaluated in a series of 63 adult mongrel dogs undergoing five different methods of cardiopulmonary resuscitation (CPR). Fluid-filled pressure monitoring catheters were placed in the ascending aorta and right atrium in each of the animals after induction of anesthesia with morphine sulfate and 1% halothane and oxygen. The animals were then fibrillated with a transvenous electrode catheter that had been introduced into a ventricle. After a “down time” of 3 minutes during which no CPR was performed, the animal's lungs were ventilated, and one of five methods of CPR was initiated. The systolic pressure gradient and coronary perfusion pressure were measured in all animals 1 minute after CPR was begun, and in all but the group undergoing open-chest cardiac massage after 7 minutes and 17 minutes of CPR. The systollic pressure gradient and coronary perfusion pressure were greatest during open-chest cardiac massage (true cardiac compression), intermediate in external mechanical CPR (Thumper) and standard CPR (greater in small dogs than large dogs), and lowest in CPR performed with a combined thoracic and abdominal vest apparatus (predominantly thoracic pump). The observation that the systolic pressure gradient between intrathoracic chambers is largest in open-chest cardiac massage and smallest in vest CPR suggests that similar measurements recorded during the performance of human cardiac resuscitation may be useful in determining the mechanism of blood flow.

Implantation of a Cardioverter/ Defibrillator Without Thoracotomy Using a Triple Electrode System

This article describes the implantation of an automatic implantable cardioverter/defibrillator in a 69-year-old man with coronary artery disease and recurrent sustained ventricular tachycardia without the need for a thoracotomy/sternotomy and epicardial electrodes. The patient underwent serial electrophysiological evaluation that revealed drug-refractory ventricular tachycardia. Surgical ablation was considered and rejected due to advanced, severe, pulmonary disease. A triple electrode system using two transvenous catheter electrodes and a submuscular patch electrode in the left midaxillary line was employed. A single shock was delivered simultaneously over two spatially distinct current pathways and reproducibly defibrillated ventricular fibrillation with energies less than or equal to 10 J. The automatic implantable cardioverter/defibrillator was implanted in the anterior abdominal wall and demonstrated reproducible termination of ventricular tachycardia and ventricular fibrillation.

Bidirectional transvenous/subcutaneous defibrillation of ventricular fibrillation in dogs: success rates, energy requirements, currents, voltages and impedance

Four hundred and thirteen defibrillations of alternating current-induced ventricular fibrillation were performed in 10 halothane-anaesthetized dogs (body weight: 24.5-30.5 kg). Success rates, energy demands, currents, peak voltages and impedance were determined. A transvenous catheter electrode system (Medtronic 6880, right ventricular apex and superior vena cava, distance 100 or 150 mm) and subcutaneous patch electrodes (Intec 67 L, 2nd/3rd and/or 3rd/4th left intercostal space) were used for bidirectional defibrillation. Loading voltages ranged from 600 to 850 V. With an electrode distance of 100 mm and a pulse duration of 2 ms separated by 1 ms, success rates were 100%, 40% and 0% for 850.650 and 600 V, respectively. With a 3-ms pulse duration, the corresponding rates were 100%, 60% and 50%. With a 2-ms pulse duration, successful defibrillation was achieved with energies lower than 15 J in 27%, with energies between 15 and 20 J in 77%, and 100% with energies higher than 20 J. Defibrillation currents were 4.4-9.3 A for pulse 1 (superior vena cava/ventricular apex) and 6.3-13.4 A for pulse 2 (patch/ventricular apex), respectively. Effective peak voltages ranged from 510 to 787 V and from 514 to 777V and averaged 89.6% of the loading voltages. Impedance values (peak voltage/current) were 75.5-117.7 (pulse 1) and 51.7-94.9 Ohms (pulse 2). Fifty consecutive defibrillations in one animal resulted in a decrease of impedance (114.6 to 84.9 Ohms, pulse 1:75.4 to 53.0 Ohms, pulse 2). Defibrillation of ventricular fibrillation can be achieved with acceptably low energies using a bidirectional transvenous/subcutaneous system, avoiding thoracotomy and general anaesthesia for implantation of the defibrillation system.

Nonthoracotomy internal defibrillation in dogs: Threshold reduction using a subcutaneous chest wall electrode with a transvenous catheter electrode

The efficacy of truncated exponential waveform shocks using a cardioverter-defibrillator catheter with and without a 13.9 cm2 subcutaneous thoracic patch electrode was examined in 10 pentobarbital-anesthetized dogs. The cardioverter-defibrillator catheter was positioned through the external jugular vein with the distal 4 cm2 shocking electrode located in the right ventricular apex and the 8 cm2 proximal electrode located in the superior vena cava. Four electrode configurations were tested: 1) distal electrode (cathode) to proximal electrode and chest wall patch (common anodes), 2) distal electrode (cathode) to chest wall patch (anode), 3) distal electrode (cathode) to proximal electrode (anode), and 4) chest wall patch (cathode) to proximal electrode (anode). The lowest randomized energy resulting in termination of alternating current-induced ventricular fibrillation on four trials at that energy was 20.2, 21.3, 27.4 and greater than 40 J, respectively, for configurations 1 through 4. The energy requirements for configurations 1, 2 and 3 were significantly lower than for configuration 4 (p less than 0.001). Additionally, configurations incorporating the distal electrode and the patch electrode (configurations 1 and 2) were significantly better than the catheter alone (configuration 3; p less than 0.05). There was no significant difference between configurations 1 and 2. In conclusion, the addition of a subcutaneous chest wall electrode to the cardioverter-defibrillator catheter significantly lowered energy requirements for defibrillation, suggesting that a nonthoracotomy approach for the automatic implantable cardioverter-defibrillator is feasible.

Internal Cardiac Defibrillation Threshold: Effects of Acute Ischemia

The influence of myocardial ischemia on defibrillation success was studied using two different lead orientations in halothane-anesthetized pigs. Ischemia was induced by ligating the left anterior descending artery in its distal third. Controls had loosely tied ligatures placed around the artery at the same site. Ventricular fibrillation was induced by electrical stimulation 30 minutes after coronary artery ligation. Defibrillation used a single truncated pulse of approximately 6 ms duration passed to either: a transvenous electrode catheter (Medtronic, 6880) with the cathode in the apex of the right ventricle and the anode in the superior vena cava-atrial junction region, or the cathode in the apex of the right ventricle and a mesh plaque on the epicardium of the basal lateral left ventricle as anode. Ten seconds after the onset of ventricular fibrillation, defibrillation was attempted with increasing incremental energies until defibrillation was achieved. Fibrillation episodes were repeated at 15-minute intervals until the minimum first shock was successful in defibrillating the animal (i.e., defibrillation threshold). The number of animals successfully defibrillated with a minimum energy above or below 30 J was not different between normal and ischemic animals for either electrode configuration (i.e., 3 out of 20 vs 1 out of 13 for the catheter and 5 out of 6 vs 6 out of 7 for the epicardial plaque, respectively). Also, the cumulative percent success as a function of defibrillation energy was similar in both the normal and ischemic groups. There was a significant reduction in the minimum energy necessary for defibrillation when passing current between the right ventricular apex and the left ventricular epicardial plaque. The present results indicate that, despite differences in lead orientations, acute ischemia in the anesthetized pig does not appear to influence defibrillation success.

Termination of atrial flutter during DDD pacing by rapid overdrive stimulation using the implanted pacemaker lead system

DDD pacing is not suitable in the presence of chronic atrial flutter or fibrillation. 1 However, patients with the bradycardia-tachycardia syndrome who mostly are in sinus rhythm may be considered for DDD pacing, although bradycardia control does not completely prevent further paroxysms of atrial tachyarrhythmia. 2 Even in patients without a history of attacks, future episodes of atrial flutter or fibrillation cannot be excluded at the time of implantation. 3,4 Atrial flutter may then be terminated by rapid overdrive stimulation, 5 which usually has to be performed through an additional temporary transvenous electrode catheter. However, in some dual chamber pacemakers the atrial and ventricular asynchronous modes (AOO and VOO) can be programmed to very high rates on a temporary basis “for use in clinical diagnostic settings to control and terminate episodes of tachycardia.” 6 This approach may also be suitable for converting atrial flutter to sinus rhythm without the need for additional transvenous lead insertion.

Sinus node electrogram in patients with the hypersensitive carotid sinus syndrome

Sinus node electrograms were obtained in two patients with unexplained syncope and the cardioinhibitory form of the hypersensitive carotid sinus syndrome. Direct recordings of sinus node potentials were obtained using a transvenous electrode catheter. Sinus node function was normal in both patients during standard electrophysiologic evaluation. Carotid sinus massage was performed in both patients and the sinus node electrogram was continuously recorded. After the onset of carotid sinus massage, prolongation of sinoatrial time, slowing of sinus rate of depolarization, sinoatrial exit block and finally sinus node arrest were recorded. After termination of carotid sinus massage, sinus node potentials did not precede the first atrial impulse; subsequent beats showed markedly prolonged sinoatrial times as well as changes in the P wave on the surface electrocardiogram. Sinus rate and sinoatrial time returned to control values gradually, as did the P wave configuration. Intravenous atropine (1.0 mg) abolished the abnormal response to carotid sinus massage. It is concluded that the application of carotid sinus massage in patients with the hypersensitive carotid sinus syndrome produces profound changes in sinoatrial conduction including sinoatrial exit block, as well as shifts in primary pacemaker site and sinus node arrest. These alterations in conduction and automaticity are reversible with atropine and may be secondary to denervation sensitivity to acetylcholine.

Changes in pacing threshold and R wave amplitude after transvenous catheter countershock

Transvenous electrode catheter countershock in patients with recurrent ventricular tachyarrhythmias may be followed by transient bradycardia and require temporary pacing with a catheter. The serial changes in R wave amplitude and stimulation threshold after catheter countershock in 11 halothane-anesthetized open chest dogs ranging in weight from 11.8 to 24 kg were studied. Ventricular fibrillation was electrically induced and followed by catheter defibrillation using nonsynchronized trapezoidal waveform (65% tilt) current discharge in incremental doses (5 to 50 J). Significant decreases in bipolar R wave amplitude (8.3 +/- 1 versus 2 +/- 0.2 mV, p less than 0.001) and increases in stimulation threshold (1 +/- 0.1 versus 2.3 +/- 0.4 V, p less than 0.001) were observed using the countershock catheter 15 seconds after countershock; these changes persisted for up to 10 minutes. To determine whether these changes were localized to the defibrillating catheter and whether they were species-specific, a second electrode catheter was positioned in the right ventricle distant from the countershock catheter in five pigs. Increases in stimulation threshold were observed only at the countershock catheter, suggesting that changes were secondary to local changes at the catheter-myocardium interface. No significant change in R wave amplitude or stimulation threshold was observed at the countershock catheter in three pigs given transthoracic shocks (60 to 250 J). It is concluded that current discharge through the countershock catheter results in a significant temporary reduction in R wave amplitude and an increase in pacing threshold. This may make pacing through the countershock catheter unreliable after shock delivery.

Persistent sinus nodal electrograms during abnormally prolonged postpacing atrial pauses in sick sinus syndrome in humans: sinoatrial block vs overdrive suppression.

A transvenous electrode catheter technique was used for direct recording of bipolar sinus node electrograms during postpacing atrial pauses. Multiple repetitive local sinus node electrograms during atrial quiescence validate sinus node electrograms. Such atrial pauses with sinus node electrograms are due to sinoatrial block; atrial pauses without sinus node electrograms are due to overdrive suppression or improper recording. Eight consecutive patients were prospectively selected on the basis of a corrected sinus node recovery time greater than 1500 msec during diagnostic electrophysiologic evaluation. Six patients had atrial pauses with sinus node electrograms; three patterns of sinus node electrograms during atrial pauses were observed. We conclude that (1) sinus node electrogram recording is of value in understanding the mechanism underlying postpacing atrial pauses; (2) atrial pauses are usually (6/8) caused by sinoatrial block; (3) three patterns of sinus node electrograms are observed, thus making indirect interpretation unreliable.