Focal origin of atrial tachycardia in dogs with rapid ventricular pacing-induced heart failure

Mapping and Ablation of Atrial Tachycardia in Heart Failure. INTRODUCTION: Dogs with rapid ventricular pacing-induced congestive heart failure (CHF) have inducible atrial tachycardia (AT), with a mechanism consistent with delayed afterdepolarization-mediated triggered activity. We assessed the hypothesis that AT has a focal origin. METHODS AND RESULTS: Twenty-one CHF dogs undergoing 3 to 4 weeks of ventricular pacing at 235 beats/min were studied. Biatrial epicardial mapping of 20 sustained AT episodes (cycle length [CL], 175 +/- 53 msec) in 5 dogs revealed an area of earliest activation in the right atrial (RA) free wall (13 episodes), RA appendage (4 episodes), or between the pulmonary veins (3 episodes). Total epicardial activation time during AT (73 +/- 19 msec) was similar to that during sinus rhythm (72 +/- 13 msec) and on average was <50% of the AT CL. Higher-density mapping of the RA free wall during 30 sustained AT episodes (163 +/- 55 msec) in 9 dogs identified a site of earliest activation along the sulcus terminalis most frequently as a stable, focal activation pattern from a single site. Endocardial mapping of 49 sustained AT episodes (156 +/- 27 msec) in 10 dogs revealed multiple sites of AT origin arising along the crista terminalis and pulmonary veins. Right and left ATs were terminated with discrete radiofrequency ablation, but other ATs remained inducible. A rapid, left AT generating an ECG pattern of atrial fibrillation was ablated inside the pulmonary vein. CONCLUSION: AT induced in this CHF model after 3 to 4 weeks of rapid ventricular pacing has an activation pattern consistent with a focal origin. Sites of earliest activation are distributed predominately along the crista terminalis and within or near the pulmonary veins.     

Electrical Remodeling and Atrial Dilation During Atrial Tachycardia are Influenced by Ventricular Rate: Role of Developing Tachycardiomyopathy

INTRODUCTION: Atrial fibrillation (AF) and congestive heart failure (CHF) are two clinical entities that often coincide. Our aim was to establish the influence of concomitant high ventricular rate and consequent development of CHF on electrical remodeling and dilation during atrial tachycardia. METHODS AND RESULTS: A total of 14 goats was studied. Five goats were subjected to 3:1 AV pacing (A-paced group, atrial rate 240 beats/min, ventricular rate 80 beats/min). Nine goats were subjected to rapid 1:1 AV pacing (AV-paced group, atrial and ventricular rates 240 beats/min). During 4 weeks, right atrial (RA) and left ventricular (LV) diameters were measured during sinus rhythm. Atrial effective refractory periods (AERP) and inducibility of AF were assessed at three basic cycle lengths (BCL). After 4 weeks of rapid AV pacing, RA and LV diameters had increased to 151% and 113% of baseline, whereas after rapid atrial pacing alone, these parameters were unchanged. Right AERP (157+/-10 msec vs 144+/-16 msec at baseline with BCL of 400 msec in the A-paced and AV-paced group, respectively) initially decreased in both groups, reaching minimum values within 1 week. Subsequently, AERP partially recovered in AV-paced goats, whereas AERP remained short in A-paced goats (79+/-7 msec vs 102+/-12 msec after 4 weeks; P < 0.05). Left AERP demonstrated a similar time course. Inducibility of AF increased in both groups and reached a maximum during the first week in both groups, being 20% and 48% in the A-paced and AV-paced group, respectively. CONCLUSION: Nature and time course of atrial electrical remodeling and dilation during atrial tachycardia are influenced by concurrent high ventricular rate and consequent development of CHF.     

The Response of Paroxysmal Supraventricular Tachycardia to Overdrive Atrial and Ventricular Pacing:

Pacing During Supraventricular Tachycardia. Introduction: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal Supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal Supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. Methods and Results: Fifty-three patients with paroxysmal Supraventricular tachycardia were studied. Twenty-two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal Supraventricular tachycardia was induced, 15-beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal Supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relting the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal Supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. Conclusions: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal Supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal Supraventricular tachycardia.     

不同方式起搏后人心房压力和心房有效不应期的变化

目的:32例接受导管射频消融治疗后的阵发性室上性心动过速患者,均无器质性心脏病。分别进行高位右心房(HRA)部位快速右心房起搏(AP)、右心室心尖部(RVA)快速心室起搏(RVP)、HRA+RVA部位房室同步起搏(SAVPHRA+RVA)以及冠状窦远端(CSd)+RVA部位房室同步起搏(SAVPCSd+RVA),起搏周长均为400 ms,持续时间各5 min。分别测量不同起搏方式起搏前后心房压力和HRA与CSd部位的心房有效不应期(ERPA)(ERPHRA、ERPCSd)。结果:与窦性节律(SR)时比较,AP对心房压力无明显影响[(9±4)cmH2Ovs.(7±3)cmH2O,1 cmH2O=0.098 kPa];与SR及AP比较,RVP、SAVPHRA+RVA、SAVPCSd+RVA使心房压力升高[(14±4)、(13±4)、(15±4)cmH2O,均P0.01];RVP和SAVPHRA+RVA、SAVPCSd+RVA等不同起搏方式升高心房压力作用基本相当。AP、RVP及SAVPHRA+RVA、SAVPCSd+RVA等不同起搏方式均使ERPA(ERPHRA、ERPCSd)较起搏前缩短(均P0.05)。SAVPHRA+RVA使ERPHRA较单纯AP/单纯RVP均有进一步缩短[(24±14)msvs.(15±11)/(13±9)ms,均P0.05]。SAVPCSd+RVA使ERPCSd较单纯AP/单纯RVP均有进一步缩短[(23±15)msvs.(15±12)/(14±11)ms,均P0.05]。结论:单纯RVP及SAVP均升高心房压力,且作用相当;而单纯RVP是替代SAVP研究心房机械电反馈(MEF)的理想方法。不同方式起搏可导致HRA与CSd部位的ERPA缩短。     

Atrial Pacing in Ventricular Tachycardia and Supraventricular Tachycardia with Aberrant Intraventricular Conduction: Diagnostic and Therapeutic Implications*

Summary: The diagnostic and potential therapeutic value of rapid right atrial pacing in ventricular tachycardia and supraventricular tachycardia with aberrant intraventricular conduction, was examined. The effect of right atrial pacing at incremental rates beginning 10 bpm above the rate of the tachycardia was studied in five patients with ventricular tachycardia, and in four patients with supraventricular tachycardia with rate-related bundle branch block aberration, the mechanism of tachycardia having been demonstrated at electrophysiology study. Atrial pacing resulted in persistent (four) or occasional (one) normalisation of the QRS complexes to that seen in sinus rhythm in those five patients with ventricular tachycardia. The intraventricular conduction pattern persisted with atrial pacing in those patients with supra-ventricular tachycardia and aberrant intraventricular conduction. This confirms that atrial pacing is a useful and simple diagnostic test in wide QRS tachycardia, which does not require sophisticated electrophysiological facilities. In three of the patients with ventricular tachycardia, atrial pacing terminated the arrhythmia, suggesting potential therapeutic use of rapid atrial pacing in such patients.     

The contribution of artificial pacemaking to understanding the pathogenesis of arrhythmias

Right atrial or ventricular pacing was performed on 36 occasions in 26 patients in an attempt to terminate a variety of tachyarrhythmias. Of 16 episodes of atrial flutter, 13 were terminated successfully; in 9 of the 13, sinus rhythm or the patient's pre-flutter rhythm was restored immediately, whereas in 4 patients, intervening atrial fibrillation or unstable atrial flutter occurred. Pacing terminated paroxysmal atrioventricular junctional or paroxysmal atrial tachycardia on 3 occasions; in a fourth patient, this tachyarrhythmia terminated during catheter manipulation. Six episodes of pacemaker-induced ventricular tachycardia were abolished by ventricular pacing. In 2 patients, atrial tachycardia was only transiently suppressed, and in 1 of these patients, d-c cardioversion produced a similar effect. Atrial fibrillation, spontaneously converting to atrial flutter, resulted during pacing for atrial tachycardia with block; the latter arrhythmia returned when the atrial flutter was terminated. Atrial fibrillation in 7 patients remained unaffected by atrial pacing. Based on the different electrophysiologic mechanisms responsible for reentrant excitation and automatic pacemaker discharge, an attempt has been made to determine the pathogenesis of the tachyarrhythmia by its response to pacing.     

Unequal Atrial Stretch in dogs Increases Dispersion of Refractoriness Conducive to developing Atrial Fibrillation

Atrial Stretch Precipitates Atrial Fibrillation. Introduction: We have shown previously that acute atrial dilation prolonged atrial refractoriness. We hypothesized that this increase in refractoriness might be heterogeneous and could create an electrophysiologic substrate leading to atrial fibrillation. The purpose of the present study was to test that hypothesis. Methods and Results: We studied 23 anesthetized open chest dogs. Bipolar plunge electrodes were placed in the medial free wall of the right atrium (thin region) and in the lower crista terminalis of the right atrium (thick region). Two bipolar plunge electrodes were also placed in the left ventricular apex to stimulate and record. Atrial effective refractory period (ERP) was measured in a group of nine dogs using the atrial extrastimulus method (A1A2) in two ways: during atrial pacing (AP) and during simultaneous atrioventricular (AV) pacing that achieved an AV interval of 0 msec (AV = 0). One liter/hour of normal saline was infused intravenously to elevate right atrial pressure and produce right atrial stretch. Atrial ERPs were measured before and after the normal saline infusion. To compare the extent of atrial stretch produced by volume overload, two pairs of sonomicrometer transducers were implanted in the thick and thin regions in a separate group of six dogs. The area encompassed by sonomicrometers was measured before and after saline infusion. The inducibility of atrial fibrillation was compared before and after saline infusion using rapid AP in another group of five dogs. Atrial pressure during sinus rhythm increased from 5.1 ± 0.96 mmHg to 6.3 ± 0.93 mmHg after normal saline infusion (P < 0.01). ERP increased in the thin free wall from 151 ± 14.3 to 172 ± 14.7 msec (AV = 0), and from 149 ± 12.0 to 170 ± 14.3 msec (AP). ERP increased in the thick crista terminalis from 134 ± 9.9 to 147 ± 10.2 msec (AV = 0), and from 133 ± 7.9 to 146 ± 9.8 msec (AP) (P < 0.01). The increase in ERP in the thin free wall exceeded that in the thick crista terminalis (P < 0.01), increasing the dispersion of atrial ERP. After 500-mL saline infusion for 30 minutes, the increase of area in the thin region was 12.8%± 3.7%, and that in the thick was 3.5%± 3.2%. The increase of the area in the thin region after 1000 mL for 1 hour was 18.8%± 6.2%. and that in the thick region was 6.3%± 5.1% (P < 0.01). Atrial fibrillation was not induced in any dog before saline infusion, hut induced in all five dogs after saline infusion. Conclusions: Atrial ERP in the thin right atrial free wall exceeds the ERP of the thick cristaterminalis, and an increase in atrial pressure produced by saline infusion exaggerates this ditterence by stretching thin segments of the atrial myocardium more than it stretches thick regions. Thus, atrial stretch, by increasing the dispersion of atrial ERP, may be conducive to the development of atrial fibrillation.     

螺内酯对心力衰竭犬心房颤动的影响

目的探讨螺内酯对心力衰竭犬心房颤动（房颤）的影响及其作用机制。方法21只犬随机分为3组：假手术组（n=7）、起搏组（n=7）和螺内酯组（n=7）。采用心室快速起搏建立心力衰竭犬模型。假手术组植入起搏器后不起搏;起搏组和螺内酯组以220次／min快速起搏心室6周;螺内酯组起搏前1周给予螺内酯至起搏后6周。通过缝置于左、右心房的4对电极测定房颤诱发次数及持续时间,超声心动图测定心房、心室结构和功能变化,Masson染色测定心房胶原容积分数,Westernblot半定量分析心房肌基质金属蛋白酶．9（MMP-9）、转化生长因子-β1（TGF-β1）及血小板衍生生长因子（PDGF）蛋白含量。结果（1）心室快速起搏6周后,起搏组犬房颤诱发率和持续时间显著增加（P〈0．01）,螺内酯组房颤诱发率显著降低、持续时间显著缩短（P〈0．05）。（2）与假手术组相比,起搏组犬左心室最大容积（LVVmax）及左心房最大容积（LAVmax）显著增加（P〈0．01）,左心房射血分数（LAEF）及左心室射血分数（LVEF）显著降低（P〈0．01）,螺内酯组犬LVVmax、LAVmax显著缩小（P〈0．01）,LAEF及LVEF显著升高（P〈0．01）。（3）与假手术组相比,起搏组犬心房胶原容积分数显著升高（P〈0．01）,TGF-β1、PDGF、MMP-9蛋白质表达量显著增加（P〈0．05）;与起搏组相比,螺内酯组胶原容积分数显著降低（P〈0．01）,TGF-β1、PDGF、MMP-9蛋白表达量显著减少（P〈0．01）。结论螺内酯可以减少心力衰竭后房颤的发生,其机制可能与抑制心房肌PDGF、TGF-β1表达有关。     

Right atrial versus left atrial echo zones: A proposed new criterion for determining the atrial site of retrograde preexcitation

In a patient whose electrocardiogram (ECG) initially (1966) showed a Type A Wolff-Parkinson-White pattern, recurrent supraventricular tachycardia (SVT) developed but never subsequently showed antegrade bypass conduction. Intracardiac pacing studies (1975) revealed that premature high right atrial (induced 250–450 msec after atrial depolarization) or coronary sinus depolarization (250–550 msec) resulted in SVT. Late coronary sinus depolarization resulted in SVT without A-H prolongation. During SVT, P wave morphology changed and the coronary sinus atrial electrogram preceded that from the low right atrium; retrograde ventriculoatrial conduction time was 240 msec. Neither pacing the high right atrium or coronary sinus up to rates of 200 beats/min nor progressive atrial premature depolarizations from the high right atrium or coronary sinus resulted in antegrade bypass conduction. Failure of antegrade bypass conduction does not preclude SVT due to retrograde pre-excitation and must be distinguished from atrioventricular (A-V) nodal reentry. Atrial effective refractory period (200 msec) was shorter than the minimal time required for an atrial impulse to return to the atrium (380 msec), suggesting concealed antegrade bypass conduction. Stimulation of the atrium linked to the A-V bypass results in earlier bypass activation and recovery and explains the differing high right atrial vs coronary sinus echo zones.     

Sinus node re-entrant tachycardia in man.

Sinus node re-entry (SNR) usually appears as a single beat. Tachycardias (SNRT) consistent with sustained SNR were seen in six patients and were initiated by premature stimulation of the high right atrium (six patients) and coronary sinus (four patients), and after continuous pacing from the high right atrium (four patients) or right ventricle (one patient) at rates of 130 to 200 per minute. During SNRT: (1) atrial beats exhibited a high-to-low atrial activation sequence, (2) the P-waves were similar in morphology to P-waves during sinus rhythm, and (3) re-entry in the A-V node or at the site of stimulation could be excluded. The cycle length of SNRT ranged from 625 to 320 msec. and SNRT either terminated spontaneously (six patients) or after premature atrial capture and/or vagal maneuvers (two patients). The electrophysiologic characteristics of SNRT and differentiation of SNRT from A-V nodal re-entry are discussed.     

“Paradoxical” AH Shortening Caused By Proximal Coronary Sinus Stimulation During Orthodromic Reciprocating Tachycardia

AH Shortening During ORT. Introduction: During extrastimulation or entrainment of orthodromic atrioventricular (AV) reciprocating tachycardia (ORT), the atriuni-His (AH) interval as measured at the His-bundle recording site is expected to lengthen due to extrastimu-Lation-dependent or pacing rate-dependent slowing of AV nodal conduction by impulses that penetrate the tachycardia circuit. We report 6 patients in whom the AH interval “paradoxically” shortened during ORT in response to extrastimulation and rapid pacing from the proximal coronary sinus. Methods and Results: Accessory pathway location was right anterior (1 patient), right anteroseptal (1 patient), and left anterior (4 patients). Cycle length of ORT was stahle (variation ≤ 5 msec) and ranged from 325 to 410 msec. During ORT, extrastimulation and rapid pacing were performed from the proximal coronary sinus and the right atrium. Extrastimulation from the proximal coronary sinus late in diastole caused significant shortening of AH interval in all patients hy a mean of 18 ± 3 msec (range 15 to 20 msec). AH shortening was demonstrated without a change of either the timing or morphologic appearance of the low septal right atrium at the H is-bundle recording site. This phenomenon was not ohserved during right atrial extrastimulation. Rapid pacing from the proximal coronary sinus at cycle lengths of 305 to 390 msec (i.e., 15 to 20 msec shorter than the cycle length of each ORT) again demonstrated shortening of AH interval in all patients by a mean of 15 ± 3 msec (range 10 to 20 msec). By contrast, rapid pacing from the right atrium demonstrated classical AH prolongation at any paced cycle length. Conclusion: AH shortening without a change of either the timing or morphologic appearance of the low septal right atrium at the His-handle recording site confirms the existence of a distinct posterior atrial input to the AV node. In this setting low septal right atrial activation is not requisite for AV nodal conduction. Whether activation of the low septal right atrium is essential for. or contributes to, AV nodal conduction of atrial impulses from locations other than the proximal coronary sinus needs to he determined.     

Comparison of Atrial-His Intervals During Tachycardia and Atrial Pacing in Patients with Long RP Tachycardia

Long RP Tachycardia. Introduction : The purpose of this study is to describe a simple and reliable diagnostic maneuver that allows for the rapid differentiation of atypical AV nodal reentrant tachycardia (AVNRT) from other causes of long KP tachycardia. Long RP tachycardias may he caused by atypical AVNRT, orthodromic reciprocating tachycardia (ORT) involving a slowly conducting retrograde accessory pathway, or atrial tachycardia. The differentiation of atypical AVNRT from ORT or atrial tachycardia may be difficult, especially when the differential diagnosis includes a posteroseptal accessory pathway or an atrial tachycardia arising in the posteroseptal right atrium.
Methods and Results : Twelve patients with atypical AVNRT, 21 with ORT, and 12 with an atrial tachycardia diagnosed using conventional criteria were enrolled In this study. The atrial-His (AH) interval was measured at the His-bundle position during the tachycardia and during atrial pacing from the high right atrium at the tachycardia cycle length in the setting of sinus rhythm. In patients with atypical AVNRT, the mean AH interval was 69 msec ± 50 msec (± SD) longer during high right atrial pacing than during the tachycardia (P < 0.001). In 10 of 12 patients with atypical AVNRT, the AH interval during atrial pacing was more than 40 msec longer than the AH interval measured during the tachycardia. In contrast, in patients with ORT or atrial tachycardia, the differences in AH interval between atrial pacing and tachycardia were never more than 20 and 10 msec, respectively.
Conclusion : The difference in the AH interval between atrial pacing and the tachycardia allows a simple and rapid means of differentiating atypical AVNRT from other types of long RP tachycardias.     

Atrial tachycardia without P waves masquerading as an A-V junctional tachycardia.

Two patients who presented by scalar ECG with an A-V junctional tachycardia were demonstrated during an electrophysiologic evaluation to have an atrial tachycardia without P waves in the surface ECG. Case 1 had an atrial tachycardia that conducted through the A-V node with a Wenckebach block. Atrial activity was recorded only from the proximal portion of the coronary sinus and from right atrial areas near the tricuspid valve. Case 2 had an atrial tachycardia that abruptly began and terminated following carotid sinus massage. Atrial activity was recorded only in the coronary sinusos, and pacing at that site resulted in atrial capture, with Wenckebach conduction to the ventricles. These observations demonstrate that an atrial tachycardia without P waves can simulate A-V junctional tachycardia with or without Weckebach block. Such findings may have a bearing on some important electrophysiologic concepts such as the origin of A-V junctional rhythms and the need for atrial participation in A-V nodal re-entry.     

Selective aldosterone blockade suppresses atrial tachyarrhythmias in heart failure

INTRODUCTION: Renin-angiotensin-aldosterone system activation may be involved in the pathogenesis of atrial arrhythmias in congestive heart failure (CHF). The effects of aldosterone blockade on atrial tachyarrhythmias have not been evaluated. This study's aim was to determine whether selective aldosterone blockade suppresses atrial tachyarrhythmia inducibility and modifies atrial electrical and/or structural remodeling in a canine model of rapid ventricular pacing (RVP)-induced CHF. METHODS AND RESULTS: Dogs were assigned randomly to treatment with oral placebo or eplerenone (50 mg/day) and divided into four groups: two sham-operated (no RVP) and two RVP groups. After 5 weeks of no RVP or RVP at 230 beats/min along with concurrent placebo or eplerenone treatment, dogs underwent electrophysiologic and echocardiographic studies. Sustained atrial tachyarrhythmia inducibility (>10-minute duration), atrial effective refractory periods (ERPs), systolic and diastolic function, and left atrial and left ventricular (LV) chamber sizes were assessed. Placebo-treated RVP dogs developed CHF with LV systolic and diastolic dysfunction, left atrial and LV enlargement, increased atrial ERPs, and inducible sustained atrial tachyarrhythmias. Eplerenone treatment in RVP dogs significantly suppressed sustained atrial tachyarrhythmia inducibility, nonuniformly prolonged atrial ERPs and attenuated LV diastolic dysfunction without modifying left atrial or LV dilation or ejection fractions in CHF. Isoproterenol (2-4 microg/min) reversed eplerenone's atrial antiarrhythmic and ERP prolonging effects in CHF. Eplerenone did not alter atrial ERPs in sham (no RVP) dogs without CHF. CONCLUSIONS: Eplerenone suppresses inducibility of sustained atrial tachyarrhythmias, selectively prolongs atrial ERPs, and attenuates LV diastolic remodeling in RVP-induced CHF. Aldosterone blockade may be a promising new approach for atrial tachyarrhythmia prevention in CHF.     

Effects of Azimilide Dihydrochloride on Circus Movement Atrial Flutter in the Canine Sterile Pericarditis Model

Azimilide and Atrial Flutter. Introduction: The effects of a Class III agent, azimilide di-hydrochloride, on atrial flutter circuits were studied in a functional model of single loop reentrant atrial flutter using dogs, 3 to 5 days after production of sterile pericarditis. Methods and Results: A computerized mapping system was used to construct activation maps from 138 to 222 epicardial sites in the right atrium. Doses of 3, 10, and 30 mg/kg IV azimilide dihydrochloride were analyzed in 8 dogs in which sustained atrial flutter lasting more than 30 minutes was induced by burst pacing. Atrial flutter was always due to a single loop circus movement reentry in the lower right atrium. At 3 mg/kg, azimilide dihydrochloride terminated atrial flutter in 2 dogs; however, atrial flutter was reinduced. At 10 mg/kg, atrial flutter was terminated in all 8 dogs but was reinduced in 4 dogs with slower rate. At 30 mg/kg, atrial flutter was terminated in the remaining 4 dogs and could not be reinduced. Atrial flutter cycle length always increased prior to termination. Isochronal activation maps showed that the increase in cycle length was due to additional conduction delays in the slow zone of the reentrant circuit. The site of termination was always located within the slow conduction zone situated in the lower right atrium between the line of functional conduction block and the AV ring. effective refractory periods (ERPs) were measured at selected sites in the slow zone and normal zone at twice diastolic threshold for the 10 mg/kg dose. Azimilide preferentially prolonged ERP in the slow zone (42.4 ± 20.l msec, mean ± SD) compared with (he normal zone (23.3 ± 15.4 msec, P < 0.0001). The increase in cycle length corresponded with the increase in ERP in the slow zone. Conclusions: In a functional model of circus movement atrial flutter, azimilide dihydrochloride terminates and prevents reinduction of atrial flutter by a preferential increase in refractoriness leading to further conduction delay and conduction block in the slow zone of the functional reentrant circuit.     

Conduction Velocity in the Tricuspid Valve-Inferior Vena Cava Isthmus is Slower in Patients With Type I Atrial Flutter Compared to Those Without a History of Atrial Flutter

Slower Conduction in the TV-IVC Isthmus. Introduction : In human type I atrial flutter, the electrophysiologic substrate is unclear. In order to determine if slow conduction is mechanistically important, we evaluated conduction velocity in the tricuspid valve-inferior vena cava (TV-IVC) isthmus, right atriai free wall, and interatrial septum in patients with and without a history of atrial flutter undergoing electrophysiologic study.
Methods and Results : Nine patients with (group 1) and nine without a history of type I atrial flutter (group 2) were studied. Conduction time (msec) in the right atrial free wall. TV-IVC isthmus (bidirectional), and interatrial septum was measured during pacing in sinus rhythm at cycle lengths of 600, 500, 400, and 300 msec from the low lateral right atrium and coronary sinus ostium. Conduction velocity (cm/sec) was calculated by dividing the distance between pacing electrodes and sensing electrodes (cm) by the conduction time (sec). Conduction velocity was slower in the TV-IVC isthmus in group 1 (range 37 ± 8 to 42 ± 8 cm/sec) versus group 2 (range 50 ± 8 to 55 ± 9 msec) at all pacing cycle lengths (P < 0.05). However, conduction velocity was not different in the right atrial free wall or interatrial septum between groups 1 and 2. Conduction velocity was also slower in the TV-IVC isthmus than in the right atrial free wall and interatrial septum in group 1 patients, at all pacing cycle lengths (P < 0.05). Atrial flutter cycle length correlated with total atrial conduction time (r ≥ 0.832, P < 0.05).
Conclusion : Slow conduction in the TV-IVC isthmus may be mechanistically important for the development of human type I atrial flutter.     

Influence of tachycardia cycle length and antiarrhythmic drugs on pacing termination and acceleration of ventricular tachycardia

We examined the influence of ventricular tachycardia (VT) cycle length and antiarrhythmic drugs on the frequency of VT termination and acceleration by single and double extrastimuli and right ventricular burst pacing. In 57 patients, 89 episodes of sustained VT (32 control, 57 drug) were induced by programmed electrical stimulation. Overall, 60 of 89 (67%) episodes of ventricular tachycardia were terminated by means of programmed electrical stimulation. In patients with relatively slow ventricular tachycardia (VT cycle length greater than or equal to 350 msec) pacing terminated 37 of 44 (84%) episodes but terminated only 24 of 45 (51%) episodes of more rapid VT (VT cycle length less than or equal to 349 msec, p less than 0.005). Pacing successfully terminated VT in nine of 49 (18%) episodes using a single extrastimulus, 22 of 52 (42%) episodes using double extrastimuli, and 40 of 66 (61%) episodes using burst right ventricular pacing. VT acceleration occurred in none of 49 attempts with a single extrastimulus, in eight of 52 (15%) attempts with double extrastimuli, and in 12 of 66 (18%) attempts using burst right ventricular pacing. During therapy, the frequency of either ventricular tachycardia termination or acceleration did not change regardless of the pacing termination method used. However, by prolonging the mean VT cycle length from 311.1 +/- 82.2 msec to 401.9 +/- 103.5 msec (p less than 0.01), drugs increased the overall frequency of VT termination. We conclude that: (1) pacing terminates VT more frequently if the VT cycle length is long and if right ventricular bursts are used, (2) burst right ventricular pacing increases the risk of VT acceleration, and (3) drugs increase the frequency of ventricular tachycardia termination by prolonging VT cycle length but do not affect frequency of VT acceleration.     

Entrainment of atrioventricular nodal reentrant tachycardias during overdrive pacing from high right atrium and coronary sinus: With special reference to atrioventricular dissociation and 2:1 retrograde block during tachycardias

Entrainment was attempted during electrophysiologic evaluation of 8 patients with atrioventricular (AV) nodal reentrant tachycardia. Entrainment could be performed while pacing from the high right atrium in 35 of 35 episodes, from proximal coronary sinus in 9 of 21 episodes and from distal coronary sinus in 10 of 20 episodes. The minimal rates required were 8 to 40 beats/min faster than those of the tachycardias. That the atria (as defined in electrophysiologic studies) were not a necessary component of the reentry circuit was suggested by the occurrence, during tachycardia, of short episodes of AV dissociation and of 1 episode of 2:1 retrograde block. For the tachycardia to be interrupted, the pacing rate usually had to be slightly faster than that required to entrain, as well as sufficiently rapid to produce anterograde block of an atrial impulse in the slow AV nodal pathway. Moreover, termination of tachycardia apparently was a function of the pacing site. In some episodes, either because of a proximity effect or because of a preferential input into the upper common pathway, coronary sinus pacing terminated the tachycardia at slower rates or with fewer stimuli than high right atrial pacing. Thus, patients with drug-resistant AV nodal reentrant tachycardias may benefit from recently introduced pacing techniques for termination of tachycardia through entrainment.