Atrial Threshold Research Articles

A simplified approach to temporary DDD pacing using a single lead, balloon-tipped catheter with overlapping biphasic impulse stimulation.

Temporary DDD pacing offers significant hemodynamic benefits in emergency management of bradyarrhythmias but is underused because of its complexity (two leads) and unreliability. Single lead VDD pacing with atrial sensing via a floating dipole is feasible, but atrial pacing is limited by high thresholds and phrenic nerve stimulation (PNS). Overlapping biphasic impulse (OLBI) stimulation may avoid these problems. The authors designed a single lead balloon-tipped catheter for temporary transvenous DDD pacing, incorporating noncontact atrial dipoles for OLBI stimulation. This catheter was deployed using fluoroscopic guidance in 74 patients (43 men, 31 women) with mean age 56.9 +/- 17.0 years. Pacing parameters were assessed at implantation and follow-up. The median procedural time was 6.6 (range 1.2-25.0) minutes and fluoroscopy time 1.9 (range 0.2-7.8) minutes. Stable VDD pacing was achieved in all cases. Atrial capture was achieved in 73 of 74 cases with both modes at maximum output but was restricted by PNS at outputs below atrial capture threshold in 3 of 74 cases with OLBI and 10 of 74 cases with standard bipolar mode (P = 0.04). At outputs > or = 1.0 V above atrial threshold, reliable DDD pacing without PNS was achieved and maintained in 67 (91%) of 74 patients in OLBI compared to 53 (72%) of 74 patients in bipolar mode (P = 0.003). Pacing parameters were stable during follow-up (median 53 hours, range 6-168 hours). In conclusion, the single lead catheter with OLBI stimulation allows temporary VDD and DDD pacing without PNS to be achieved in > 90% of patients. This rapid and convenient approach should facilitate DDD pacing in emergency settings.

Clinical significance of the atrial fibrillation threshold in patients with paroxysmal atrial fibrillation.

AF threshold and the other electrophysiological parameters were measured to quantify atrial vulnerability in patients with paroxysmal atrial fibrillation (PAF, n = 47), and those without AF (non-PAF, n = 25). Stimulations were delivered at the right atrial appendage with a basic cycle length of 500 ms. The PAF group had a significantly larger percentage of maximum atrial fragmentation (%MAF, non-PAF: mean +/- SD = 149 +/- 19%, PAF: 166 +/- 26%, P = 0.009), fragmented atrial activity zone (FAZ, non-PAF: median 0 ms, interquartile range 0-20 ms, PAF: 20 ms, 10-40 ms, P = 0.008). Atrial fibrillation threshold (AF threshold, non-PAF: median 11 mA, interquartile range 6-21 mA, PAF: 5 mA, 3-6 mA, P < 0.001) was smaller in the PAF group than in the non-PAF group. Sensitivity, specificity, and positive predictive value of electrophysiological parameters were as follows, respectively: %MAF (cut off at 150%, 78%, 52%, 76%), FAZ (cut off at 20 ms, 47%, 84%, 85%), AF threshold (cut off at 10 mA, 94%, 60%, 81%). There were no statistically significant differences between the non-PAF and PAF groups in the other parameters (effective refractory period, interatrial conduction time, maximum conduction delay, conduction delay zone, repetitive atrial firing zone, wavelength index), that were not specific for PAF. In conclusion, the AF threshold could be a useful indicator to evaluate atrial vulnerability in patients with AF.

Temporary transvenous atrial pacing in horses: threshold determination.

The purpose of this study was to perform temporary atrial pacing and to determine the atrial strength-duration (S-D) curve which displays the minimal pulse intensity necessary to achieve atrial capture. In 7 horses, atrial pacing was applied using a temporary pacing catheter and a pacemaker as electrical pulse generator. Using the stimulus reduction method, 3 approaches for atrial threshold determination were used. With the fixed pulse width method, at several pulse widths, the corresponding minimal amplitudes to achieve capture were determined, describing an S-D curve. With the fixed amplitude method, the corresponding threshold pulse widths were determined at several fixed amplitudes. The third method proved to be the best and was a combination of both aforementioned methods to determine 2 points of the S-D curve. From these 2 points the whole S-D curve was calculated using a mathematical equation. Temporary pacing can be used to terminate atrial flutter, to induce atrial arrhythmias or to obtain more information about the electrophysiological properties of the heart, such as the atrial refractory period, atrial vulnerability and atrioventricular conduction.

Left atrial- and left ventricular-based single lead DDD pacing.

Single lead physiological pacing with right ventricular apex stimulation is feasible in patients with normal sinus node function and is associated with lower costs and a reduced complication rate. Left ventricular or biventricular pacing using the tributaries of the coronary sinus was reported to improve functional status and quality-of-life in patients with advanced congestive heart failure and intraventricular conduction delays. In addition, the proximal part of the coronary sinus has been successfully used for left atrial stimulation. The feasibility and pacing characteristics of left atrial- and left ventricular-based temporary pacing using a conventional single pass lead were studied. The tip of the lead was advanced in a distal position of the lateral or posterolateral branches of the coronary sinus, providing a stable position of the middle and proximal electrode pair in the first 2-7 cm of the coronary sinus. A successful stable position was achieved in 13 of 21 consecutive attempts. Using overlapping biphasic (OLBI) stimulation, left atrial and left ventricular pacing threshold were 2.3 +/- 0.6 and 2.5 +/- 0.5 V, respectively. Acceptable sensing values were measured for P waves (4.1 +/- 0.7 mV) and R waves (9.7 +/- 3.9 mV). There was a good correlation between the diameter of the coronary sinus as assessed by quantitative coronary angiography at the level of the middle and proximal rings and atrial pacing threshold (r = 0.92, P < 0.0001). Thus, single lead left atrial- and left ventricular-based pacing is feasible although further development is necessary to increase the success rate for stable stimulation at both sites.

Implantation of a dual chamber pacing and sensing single pass defibrillation lead.

Dual-chamber ICDs are increasingly used to avoid inappropriate shocks due to supraventricular tachycardias. Additionally, many ICD patients will probably benefit from dual chamber pacing. The purpose of this pilot study was to evaluate the intraoperative performance and short-term follow-up of an innovative single pass right ventricular defibrillation lead capable of bipolar sensing and pacing in the right atrium and ventricle. Implantation of this single pass right ventricular defibrillation lead was successful in all 13 patients (age 63 +/- 8 years; LVEF 0.44 +/- 0.16; New York Heart Association [NYHA] 2.4 +/- 0.4, previous open heart surgery in all patients). The operation time was 79 +/- 29 minutes, the fluoroscopy time 4.7 +/- 3.1 minutes. No perioperative complications occurred. The intraoperative atrial sensing was 1.7 +/- 0.5 mV, the atrial pacing threshold product was 0.20 +/- 0.14 V/ms (range 0.03-0.50 V/ms). The defibrillation threshold was 8.8 +/- 2.7 J. At prehospital discharge and at 1-month and 3-month follow-up, atrial sensing was 1.9 +/- 0.9, 2.1 +/- 0.5, and 2.7 +/- 0.6 mV, respectively, (P = NS, P < 0.05, P < 0.05 to implant, respectively), the mean atrial threshold product 0.79, 1.65, and 1.29 V/ms, respectively. In two patients, an intermittent exit block occurred in different body postures. All spontaneous and induced ventricular arrhythmias were detected and terminated appropriately. Thus, in a highly selected patient group, atrial and ventricular sensing and pacing with a single lead is possible under consideration of an atrial pacing dysfunction in 17% of patients.

Far field R wave sensing early after implantation-comparison of active and passive fixation leads

With increasing use of Mode Switch algorithms, Far Field R wave Sensing (FFRS) has again become increasingly ImportanL We compared results eady after implantation with a passive and active fixation lead in a dual chamber pacing system allowing the programming of high atrial sensitivities (up to 0.1 mV), in avoiding FFRS. METHODS: 45 patients received a dual chamber pacemaker, Biob'onik Ac~os DR. In 29 patients, an affial bipolar preshaped tined J lead (BiotTonik Synox SX 53 JBP; ring-tip distance 14 mm) was used, 16 patients received an atrial bipolar active fixation lead (Biob'onik Elox 53 BP; dng-tip distance 10 ram). The ventricular lead was a unipolar lead (Biotronik Polymx PX 60-UP) in all cases. P and R wave amplitudes, thresholds and lead impedances ware measured. FFRS threshold was defined as the highest atTial sensitivity setting without Far Field detection of the paced R wave by the atrial sensing amplifier. During FFRS testing, simultaneous recording of atrial and ventricular IEGM, marker channel (A&V) and surface ECG was performed. Measurements ware made within 2 months postimplanL RESULTS: Results are summarized in table 1. Ta~el I E~p. Pwave N d ~ d ~ d NdaJle~:llmp. FFRSunipolm i FFRS / (mv~ (v at 0.4 ms) I (n) I (mV) ~po~ (mV) I ~ 2.89 +/-1.4 0.48 +/0.42 709 +/147 I 0.37 +h 0.22 p.21 .I.h 0.07 I ActhmFtxa0on I 2.33W-1.51 1.11 +/*0.43 378+/-38 I 0.49+1-0.27 p.24+h0.13 I P value ~ 0.2 0.003 <0.001 0.2 / 0.7 (P values = comparison of measumnlents in passive and aclfve fixation lead group) Both leads showed comparable results in terms of atrial sensing, whereas the atrial threshold was significantly higher with the active fixation lead, at least in the early phase after implantation. Lead impedance was higher with the passive (high impedance) lead. Venbicular measurements ware comparable in both groups. FFRS was significantly better in both groups with bipolar sensing compared to unipolar sensing. CONCLUSION: In the early phase after implantation (< 2 months), P wave sensing was comparable with both leads, but anal threshold was higher with the active fixation lead. Far Field R wave sensing was comparable in both leads and better with bipolar compared to unipolar sensing. HIGH IMPEDANCE LATEST GENERATION VENTRICULAR LEADS: COMPARISON BETWEEN TWO STEROID AND ONE NON -STEROID ELUTING LEAD WITH ULTRASMALL PACING SURFACE. D. Cornacchia E. Tampieri, S. Silvani, Cardiology Department, Ravenna, M. Nastasi, Cardiology Department Villabianca Bad, ITALY.

SD3212, a new antiarrhythmic drug, raises atrial fibrillation threshold in isolated rabbit hearts

SD3212 is a new antiarrhythmic drug which has class I, III, and IV effects. The purpose of this study was to elucidate the electrophysiological effects of this compound on a rabbit atrial fibrillation model, and to test a hypothesis that atrial fibrillation threshold is a quantitative indicator of atrial vulnerability. Whole hearts were excised from rabbits, and the aortas cannulated to perfuse the coronary arteries. Atrial fibrillation was induced with a burst stimulation of 50 Hz for 1 s while 3 microM acetylcholine (ACh) was perfused. When the right atrial appendage was paced at 200-ms intervals, SD3212 prolonged interatrial conduction time: control 30 +/- 1.2 ms, ACh 33 +/- 1.4 ms, ACh + SD 1 microM 37 +/- 2.4 ms, ACh + SD 3 microM 52 +/- 8.1 ms. The drug also prolonged the effective refractory period: control 80 +/-3.0 ms, ACh 48 +/- 3.8 ms, ACh + SD 1 microM 65 +/- 4.7 ms, ACh + SD 3 microM 98 +/- 15 ms. The rate of induction of atrial fibrillation by rapid pacing was 26% in Tyrode's solution, 85% in the presence of ACh, and 38% in the presence of ACh + SD 1 microM. The atrial fibrillation threshold decreased from 8.6 +/- 0.8mA (control) to 2.5 +/- 0.7 mA in the presence of ACh. It increased again to 7.8 +/- 1.0 mA in the presence of SD3212 (1 microM). SD3212 prolonged both the conduction time and refractory period. A reversed use-dependency was not prominent. These features caused antifibrillatory effects. Thus, the atrial fibrillation threshold seems to be a good quantitative indicator of atrial vulnerability.

Inhibitory effects of aprindine on the delayed rectifier K+ current and the muscarinic acetylcholine receptor-operated K+ current in guinea-pig atrial cells.

In order to clarify the mechanisms by which the class Ib antiarrhythmic drug aprindine shows efficacy against atrial fibrillation (AF), we examined the effects of the drug on the repolarizing K+ currents in guinea-pig atrial cells by use of patch-clamp techniques. We also evaluated the effects of aprindine on experimental AF in isolated guinea-pig hearts. Aprindine (3 microM) inhibited the delayed rectifier K+ current (IK) with little influence on the inward rectifier K+ current (IK1) or the Ca2+ current. Electrophysiological analyses including the envelope of tails test revealed that aprindine preferentially inhibits IKr (rapidly activating component) but not IKs (slowly activating component). The muscarinic acetylcholine receptor-operated K+ current (IK.ACh) was activated by the extracellular application of carbachol (1 microM) or by the intracellular loading of GTPgammaS. Aprindine inhibited the carbachol- and GTPgammaS-induced IK.ACh with the IC50 values of 0.4 and 2.5 microM, respectively. In atrial cells stimulated at 0.2 Hz, aprindine (3 microM) per se prolonged the action potential duration (APD) by 50+/-4%. The drug also reversed the carbachol-induced action potential shortening in a concentration-dependent manner. In isolated hearts, perfusion of carbachol (1 microM) shortened monophasic action potential (MAP) and effective refractory period (ERP), and lowered atrial fibrillation threshold. Addition of aprindine (3 microM) inhibited the induction of AF by prolonging MAP and ERP. We conclude the efficacy of aprindine against AF may be at least in part explained by its inhibitory effects on IKr and IK.ACh.

Influence of active pectoral can on transvenous atrial cardioversion threshold in patients with implantable cardioverter-defibrillator

Influence of active pectoral can on transvenous atrial cardioversion threshold in patients with implantable cardioverter-defibrillator

Steroid‐Eluting Epicardial Pacing Electrodes: Six Year Experience of Pacing Thresholds in a Growing Pediatric Population

Indications for pacemaker implantation in the pediatric population often include sinus or atrioventricular node dysfunction following surgery for congenital heart defects. However, patient size, cardiac defects, and vascular and valvular concerns may limit transvenous lead utilization. Since the epicardial surface of these patients often exhibits variable degrees of fibrosis from scar tissue formation or pericardial adhesions, chronic low output (2.5/1.6 V, 0.3 ms) epicardial pacing from implant is not currently recommended in children due to frequent threshold changes and electrode exit block. As a result, pacing in children is often viewed as a less efficient system than in adults. The addition of steroid combined with newer low threshold electrode designs however stabilizes the electrode-tissue interface and eliminates postimplant changes seen with standard smooth surface electrodes potentially permitting efficient chronic pacemaker application to all patient ages. The stability of chronic low output epicardial pacing with steroid-eluting electrodes was prospectively studied in 22 patients (ages 2 days-18.5 years, median 3.5 years) for up to 6 years. Chronic pulse width thresholds were compared according to implant site and association of prior cardiac surgery. A total of 26 pacing leads were implanted. The acute implant mean pulse width threshold (2.5 V) for all the electrodes studied was 0.10 ms +/- 0.05 ms. Stable low thresholds were maintained for up to 6 years without significant variation from implant. Mean ventricular pulse width thresholds (0.12 ms +/- 0.05 ms) were significantly higher (P < 0.001) than atrial thresholds (0.06 ms +/- 0.03 ms) at implant and throughout the study period. The thresholds in the patients following cardiac surgery were comparable to those without previous cardiac surgery (P = NS). Stable low thresholds may be chronically maintained for up to 6 years for epicardial steroid-eluting electrodes irrespective of pacing site or associated cardiac surgery.

Results of electrophysiologic studies in patients with acute Chagasic myocarditis.

As the acute stage of Chagas' myocarditis is rarely detected, little is known about the electrophysiologic characteristics of that stage. This investigation was undertaken to conduct an electrophysiologic study of the properties of the heart during the acute phase of Chagasic myocarditis. We studied eight patients who had positive xenodiagnosis, positive mice culture, and positive complement fixation test for Chagas' disease. Trypanosoma cruzi were identified in all of the patients' stained blood samples. Right ventricular endomyocardial biopsies were obtained, evidencing a distinct infiltrate of lymphocytes that confirmed the diagnosis of acute myocarditis. The cardiac dimensions and the ventricular systolic and diastolic function were preserved in all patients. The electrocardiogram evidenced conduction defects in two patients. The signal-averaged electrocardiogram displayed late potentials in three patients. In the electrophysiologic study, atrial fibrillation or flutter was induced in four patients. When compared with control patients, Chagasic patients were found to have greater values of atrial threshold, A-H interval, and atrioventricular (AV) nodal effective refractory period. The H-V interval was mildly prolonged in two patients, but the dynamic AV nodal conduction was preserved (1:1 conduction during right atrial stimulation at a cycle length of 400 ms) in all the Chagasic patients. The ventricular parameters were within normal limits, and no sustained ventricular arrhythmia could be induced. Patients with mild acute Chagasic myocarditis may suffer from electrical abnormalities and arrhythmias that are more evident at the supraventricular level and the AV junction.

Toward optimizing a preshaped catheter and system parameters to achieve single lead DDD pacing.

P wave electrogram amplitudes and atrial stimulation thresholds were determined in eight Hanford miniature swine using a preshaped catheter with an "S" curve in the SVC, and a major lobe in the atrium to enhance electrode contact with the atrial wall. The catheter was designed for pacing and sensing in the DDD mode. P wave amplitudes were also ascertained with two commercially available VDD leads and compared to the data from the experimental catheters. The preshaped catheter used two 6-mm2 platinum iridium atrial electrodes with a 7-mm separation. Both atrial electrodes are on the same side of the catheter, facing outward on the major atrial lobe formed in the catheter. The P wave amplitudes were tested only in the differential bipolar configuration. For the eight preshaped catheters, the mean was 6.6 +/- 3.8 mV while for the conventional leads it was 2.9 +/- 1.6 mV. The mean atrial stimulation thresholds ranged from 1.1 +/- 0.2 V to 2.3 +/- 1.2 V, with still lower thresholds of 0.9-1.3 V when using the parallel unipolar atrial electrode configuration, in which both parts of the bipolar atrial electrode are configured as a unipolar electrode. The data suggest that bipolar simulation may be effective if sequential reverse polarity pulses are used to achieve cathodal stimulation from each electrode of the bipolar pair, on a beat-to-beat basis.

Estimulação DDD com eletrodo único usando estimulação atrial bifásica simultânea: primeiros resultados clínicos

A estimulação de dupla câmara (DDD) com eletrodo único usando eletrodo atrial flutuante está limitada em função dos altos limiares encontrados para captura atrial. Avaliamos um sistema novo de cabo eletrodo para estimulação atrial que utiliza dois anéis atriais com pulsos de onda quadrada simultâneos unipolares lançados com polaridade oposta. O primeiro pulso é aplicado ao pólo distal do eletrodo e é positivo, o segundo pulso é aplicado ao pólo proximal do eletrodo e é negativo, ambos em relação à carcaça do gerador. O atraso entre os dois pulsos é programável entre 0,0 ms e 1,0 ms. A distância entre os anéis a nível atrial é de 10 mm e a distância entre o pólo distal atrial e o eletrodo ventricular unipolar pode ser selecionado entre 11, 13 e 15 cm. O posicionamento dos anéis a nível atrial é selecionado de acordo com a medida do limiar de estimulação do pulso bifásico simultâneo, incluindo manobras respiratórias para confirmar a captura/sense contínuos. O gerador de pulso tem uma única conexão para o eletrodo e a capacidade de aplicar os pulsos programáveis de onda quadrada com polaridades opostas, com atrasos programáveis de 0,0 a 1,0 ms. O gerador pode ser programado para estimulação VDD com eletrodo único. Este sistema foi implantado em 4 pacientes com bloqueio AV total e função sinusal normal. Os limiares de estimulação atrial e diafragmático foram medidos com várias configurações do pulso, larguras e atrasos, intra e pós-operatórios. A porção média do átrio direito foi selecionada como a melhor posição para os anéis atriais com captura contínua durante inspiração profunda. As medidas intra-operatórias e pós-operatórias (48 horas) foram: Limiar Intra-operatório Pós-operatório atrial unipolar 3,2 + 0,47 V não realizada atrial (bifásico simultâneo) 1,6 + 0,37 V 3,37 + 0,84 V diafragmático acima de 7 V 5,21 + 0,3 V sense de onda P 2,35 + 1,3 mV 1,27 + 0,8 mV Os pacientes tiveram alta com o gerador programado no modo VDD. A evolução de 30 dias após o implante mostrou perda de captura atrial transitória durante inspiração em 1 paciente, apesar da ausência de outras variações no limiar, comparado com a evolução de 48 horas pós implante. Em conclusão, a estimulação bifásica simultânea reduz o limiar de estimulação atrial, ao mesmo tempo em que mantém o sense atrial adequado com uma margem de segurança em relação à estimulação diafragmática.

Dual chamber pacing with a single lead system: initial clinical results.

A new mode of biphasic pacing was used in 26 patients to assess the feasibility of atrial pacing by means of the floating atrial ring electrodes of a single lead VDD permanent pacing system. During implantation, atrial pacing was possible in 25 patients with a 1-ms total pulse duration, a mean atrial threshold of 1.70 +/- 0.60 V (range, 0.6-3.0), and a mean diaphragmatic threshold of 6.7 +/- 2.5 V (range, 2.5-10.0). At 3 months, the atrial threshold had increased beyond 4.8 V in three patients. In the 22 other patients, the mean atrial threshold was 2.2 +/- 0.5 V (range, 1.50-3.50) in the supine position and 2.5 +/- 0.8 V (range, 1.5-4.8) in the sitting position. Stable atrial capture without diaphragmatic stimulation was achieved in 76% of patients.

Unsatisfying Results in Long‐Term Atrial Pacing with a Bipolar Active Fixation Atrial Lead

A high dislodgment rate during long-term atrial pacing using the unipolar sickle-shaped active fixation lead was recently reported; therefore, the long-term results of atrial pacing in 118 consecutive patients with the bipolar sickle-shaped active fixation lead (Biotronik FH60-BP) were evaluated. Between January 1989 and September 1993, 87 leads (74%) were inserted for dual chamber pacing and 31 leads (26%) for atrial pacing only. At the time of implantation, the bipolar atrial electrogram had a mean voltage of 4.4 +/- 1.6 mV, whereas the acute atrial threshold was 0.72 +/- 0.38 V and 1.46 +/- 0.67 mA at 0.5-msec pulse duration and mean resistance 506 +/- 79 omega. Early lead dislodgment (< 1 month after implantation) occurred in 9 patients (7.6%). During a mean follow-up of 21.8 months (median 20.9 months), late dislodgment (> 1 month after implantation) occurred in 6 patients (5.1%) after a mean interval of 7.9 months (range 3-14 months). Due to the unacceptably high late dislodgment rate, which to date remains unexplained, new implants of this lead are not recommended.

Mechanism of interruption of atrial flutter by moricizine. Electrophysiological and multiplexing studies in the canine sterile pericarditis model of atrial flutter.

Moricizine is said to have potent effects on cardiac conduction but little or no effect on cardiac refractoriness. The effects of moricizine (2 mg/kg IV) on induced atrial flutter were studied 2 to 4 days after the creation of sterile pericarditis in 11 dogs. Ten episodes of stable atrial flutter before and after the administration of moricizine were studied in 9 dogs in the conscious, nonsedated state, and 7 episodes were studied in 6 dogs in the anesthetized, open chest state. In the conscious state, the effects of moricizine on atrial excitability, atrial effective refractory period, and intra-atrial conduction times were studied by recording during overdrive pacing of sinus rhythm from epicardial electrodes placed at selected atrial sites. Moricizine prolonged the atrial flutter cycle length in all the episodes, from a mean of 133 +/- 9 to 172 +/- 27 milliseconds (P < .001), and then terminated 7 of the 10 episodes. Moricizine increased the atrial threshold of excitability from a mean of 2.3 +/- 1.4 to 3.3 +/- 2.2 mA (P < .01) and prolonged intra-atrial conduction times (measured from the sulcus terminalis to the posteroinferior left atrium) from a mean of 58 +/- 6 to 64 +/- 5 milliseconds (P < .005). Prolongation of the atrial effective refractory period from 166 +/- 20 to 174 +/- 24 milliseconds (P < .05) was observed only at the sulcus terminalis site. In the open chest studies, administration of moricizine prolonged the atrial flutter cycle length from a mean of 150 +/- 15 to 216 +/- 30 milliseconds (P < .001) and then terminated the atrial flutter in all 7 episodes. As demonstrated by simultaneous multisite mapping from 95 bipolar sites on the right atrial free wall, the atrial flutter cycle length prolongation was either due to further slowing of conduction in an area of slow conduction in the reentrant circuit of the atrial flutter (5 episodes) or further slowing of conduction in an area of slow conduction plus the development of a second area of slow conduction (2 episodes). The change in conduction times in the rest of the reentrant circuit was negligible (10.9 +/- 8.7% of the total change). In all 7 episodes, the last circulating reentrant wave front blocked in an area of slow conduction. Moricizine (1) prolongs the atrial flutter cycle length, primarily by slowing conduction in an area of slow conduction in the reentrant circuit, (2) terminates atrial flutter by causing block of the circulating reentrant wave front in an area of slow conduction of the reentrant circuit, and (3) effectively interrupts otherwise stable atrial flutter in this canine model. The reason for these effects of moricizine are not readily explained by its effects on global atrial conduction times and refractoriness studied during sinus rhythm. Local changes in conduction in an area(s) of slow conduction are responsible for both cycle length prolongation and atrial flutter termination rather than the traditional wavelength concept of head-tail interaction.

P-wave morphologic analysis for automatic atrial threshold test

P-wave morphologic analysis for automatic atrial threshold test

Effect of bertosamil on atrial and ventricular threshold for fibrillo-flutter in comparison with quinidine in anaesthetized cats

Effect of bertosamil on atrial and ventricular threshold for fibrillo-flutter in comparison with quinidine in anaesthetized cats

Alternate Methods for the Determination of Atrial Capture Threshold Utilizing the Telemetered Intracardiac Electrogram

Periodic determination of pacemaker capture threshold is important to ensure appropriate pacemaker function. During dual chamber pacing, it is sometimes difficult to identify evidence of atrial depolarization on surface electrocardiography (ECG), and this can interfere with the ability to ascertain atrial capture. We describe new methods for determining atrial capture threshold using a standard telemetered endocardial atrial electrogram (AEGM). For the first method, the atrial output is decremented until loss of atrial capture is demonstrated by the appearance of native P wave activity on the AEGM. The atrial capture threshold can then be accurately determined as the point at which a stepwise increase in atrial output results in extinction of the native P wave activity. The second method uses the direct visualization of the AEGM recorded between the ring electrode and pacemaker generator during unipolar (lead tip electrode) pacing. This requires the presence of a bipolar lead. Using this method of recording, it is possible to identify a signal after the atrial stimulus artifact during atrial capture, which disappears with loss of capture. This signal is consistent with a paced "evoked atrial potential" and allows verification of atrial capture. After validating the methods in two sets of test patients with clearly identifiable atrial depolarization on surface ECG, one method was successfully applied to a patient in whom atrial depolarization could not be reliably ascertained on surface ECG. These methods promise to be useful in selected patients in whom confirmation of atrial capture would otherwise be difficult.

The Influence of Endocardial Electrode Fixation Status on Acute and Chronic Atrial Stimulation Threshold and Atrial Endocardial Electrogram Amplitude

The endocardial atrial electrogram or "P wave amplitude" (PWA) and pacemaker atrial stimulation thresholds are important parameters determining correct pacing system function. Pacemaker lead fixation mechanism and lead age may negatively influence these parameters. Therefore, we compared acute and chronic PWA and atrial stimulation thresholds in 33 patients with permanent transvenous atrial screw-in leads, follow-up 647 days +/- 297 days; and in 31 patients with nonscrew leads, follow-up 855 days +/- 512 days (P = ns). The PWA differed between the two lead types acutely (1.97 mV +/- 0.8 mV for screw-in versus 2.48 mV +/- 1.1 mV for nonscrew-in leads; P less than 0.05), but not chronically (2.21 mV +/- 0.8 mV vs 2.2 mV +/- 1.2 mV; P = ns). Acute and chronic atrial pacing thresholds did not differ between groups. We also analyzed an early interim PWA in a subgroup of patients (mean 31 days after implantation). The nonscrew fixation group interim PWA was 1.76 mV +/- 0.9 mV versus 2.7 mV +/- 1.2 mV at implant (P less than 0.001). The screw-in lead interim PWA was 2.04 mV +/- 0.9 mV versus 1.97 mV +/- 0.7 mV at implant (P = ns). (1) A significantly higher endocardial PWA occurs at the time of lead implantation in nonscrew versus screw-in lead groups, but the chronic PWA does not differ between the two groups. (2) A transient but marked early (mean approximately 31 days) attenuation of the PWA occurs only with nonscrew-in leads. (3) Atrial threshold stimulation energies do not differ between the two lead groups acutely or during follow-up.