Antiarrhythmic and proarrhythmic properties of diazepam demonstrated by electrophysiological study in humans

We evaluated the electrophysiological parameters before and after the intravenous infusion of diazepam (0.2 mg/kg) in 20 cardiac patients to investigate the drug's antiarrhythmic effect. Diazepam did not significantly change the arterial pressure. After the intravenous infusion of diazepam, the sinus cycle length significantly shortened from 847 +/- 132 to 747 +/- 155 ms (p less than 0.01). No significant change in the maximal sinus node recovery time was noted. The AH interval at the atrial pacing length of 600 ms shortened significantly from 140 +/- 40 to 127 +/- 39 ms (p less than 0.05). However, there was no significant change after the administration of diazepam in the longest atrial pacing rate associated with Wenckebach conduction in the atrioventricular (AV) node, effective and functional refractory periods of the AV node, HV interval, and QRS width during ventricular pacing at the cycle length of 600 ms. The atrial and ventricular effective refractory periods remained unchanged after the administration of diazepam. Six of the eight patients who showed dual AV nodal refractory period curves in the control study did not demonstrate them after diazepam administration by increasing the atrial or AV node effective refractory period. Thus, diazepam showed significant electrophysiological effects of the heart including shortening of the sinus cycle length, improvement in AV node conduction, and no significant effect on the His-Purkinje or intraventricular conduction and refractoriness of the atrium, AV node and ventricle. On the other hand, diazepam may influence the inducibility of supraventricular reentrant tachycardia incorporating the AV node.     

Changes in atrial and ventricular refractoriness and in atrioventricular nodal conduction produced by combinations of vagal and sympathetic stimulation that result in a constant spontaneous sinus cycle length

The vagal nerves modulate adrenergic effects on sinus cycle length, atrioventricular (AV) nodal conduction, and refractoriness of atria and ventricles. We tested whether varying levels of vagal-sympathetic input could yield the same spontaneous sinus cycle length but also alter effective refractory periods of the right atrium, right ventricle, and left ventricle and AV nodal conduction times. Dogs anesthetized by alpha-chloralose were studied in the open-chest, neurally decentralized state. In 10 dogs, sinus cycle length was maintained constant during 3 levels of bilateral ansae subclaviae stimulation (4 msec, 3 mA at 1, 2, and 4 Hz) by titrating simultaneous bilateral vagal stimulation (varying pulse width and frequency). Each combination of ansae subclaviae-vagal stimulation yielded the same sinus cycle length as the control value, but refractory periods of right atrium and right and left ventricles shortened progressively as the frequency of ansae subclaviae stimulation increased. Atrioventricular nodal conduction time (AH interval) shortened in 2 dogs and lengthened in 3 dogs. His-Purkinje conduction time (HV interval) was unchanged. In 9 dogs, the effect of simultaneous unilateral ansae subclaviae stimulation at 2 Hz and ipsilateral vagal stimulation that yielded the same sinus cycle length were determined. Right-sided ansae subclaviae-vagal stimulation shortened refractoriness of right atrium and anterior left ventricle significantly. The AH interval lengthened in 1 dog. Left ansae subclaviae-vagal stimulation shortened the refractory periods of anterior and posterior left ventricle significantly and reduced the AH interval in 3 dogs. In 8 dogs, the effects of bilateral ansae subclaviae stimulation alone at 2 Hz, vagal stimulation alone at an intensity required to keep the sinus cycle length constant during ansae subclaviae stimulation, and simultaneous bilateral ansae subclaviae and vagal stimulation were tested. The right atrial refractory period was shortened significantly by ansae subclaviae stimulation alone and by vagal stimulation alone and was shortened further by simultaneous stimulation of both autonomic limbs. The right and left ventricular refractory periods were shortened by ansae subclaviae stimulation alone and by simultaneous stimulation of both limbs but tended to be prolonged by vagal stimulation alone and when added to ansae subclaviae stimulation. In 7 dogs, the effects of simultaneous stimulation of bilateral ansae subclaviae at 2 Hz and vagi at intensities that maintained the AH interval constant at an atrial pacing cycle length of 300 msec were determined.(ABSTRACT TRUNCATED AT 400 WORDS)     

The effect of atrial dilatation on the genesis of atrial arrhythmias

The effect of atrial stretching on the genesis of atrial arrhythmias was studied in 26 dogs. Left atrial dilatation was produced by inflation of a balloon catheter. Electrophysiological studies were performed by programmed electrical stimulation of the atrium and ventricle. The irritability of the atrium markedly increased when it was distended and atrial arrhythmias (sustained or non-sustained atrial tachyarrhythmias) could regularly be induced by administration of an early extrastimulus or--more rarely--by atrial burst pacing. In 10 cases spontaneous atrial tachycardia appeared during atrial balloon dilatation. The atrial effective refractory period shortened and the atrial conduction time lengthened on atrial stretching, while other electrical variables (cycle length, sinus node recovery time, atrioventricular conduction time, intraventricular conduction, ventricular refractory period, QT interval) remained unchanged. Atrial balloon dilatation was not accompanied by marked haemodynamic changes, and the left ventricular pressure curve, the contractility of the left ventricle and the central venous pressure did not change significantly on atrial stretching. The experimental data suggest that the atrial dilatation plays an important part in the pathogenesis of atrial arrhythmias.     

Transcutaneous stimulation of the heart ventricles: its effectiveness, comfort during the examination and new diagnostic possibility

An attempt of assessment of transcutaneous cardiac pacing tolerance in healthy volunteers was carried out as well as abilities of this method utilization for examination of retrograde atrioventricular conduction. Ventricles were paced through highohm electrodes positioned on the chest wall with simultaneous recordings of transoesophageal ecg at the level of the left atrium and the sphygmogram of the right common corotid artery. Pacing perception threshold, skeletal muscle stimulation threshold, cardiac pacing threshold, algesic and myo-respiratory threshold of examination tolerance were estimated. Effective ventricular pacing within the range of stimulation tolerance was obtained in 10 of 15 patients (67%). Mean ventricular pacing threshold was higher than pacing perception and skeletal muscles stimulation thresholds (42 mA; 9.4 mA and 20.2 mA). Ventricular pacing threshold was lower than algesic and muscles thresholds of examination tolerance (60-70 mA) warranting relatively good tolerance of transcutaneous cardiac ventricular pacing. In 8 of 10 persons with effective ventricular stimulation retrograde a-v nodal conduction was stated which proved that transcutaneous cardiac ventricular stimulation can be used for noninvasive assessment of retrograde a-v nodal conduction.     

Latent retrograde atrioventricular conduction in healthy persons

45 patients (13 females and 32 males; mean age-37 years) without an organic heart disease underwent the study, on condition that effective transesophageal, ventricular stimulation was achieved. The transesophageal pacemaker SP-5 made by OBR TEMED ZABRZE was used. Ventricular stimulation threshold and a lock of evident retrograde conduction was estimated during ventricular stimulation with a constant cycle length of 500 ms. To assess concealed retrograde atrioventricular conduction, programmed ventricular stimulation of a 50 ms cycle length was applied between late diastole and left ventricular refraction. Concealed retrograde atrioventricular conduction was diagnosed of a sinus impulse reached later ventricles than that during sinus rhythm preceding an examination. There was no evident atrioventricular retrograde conduction in 15 patients (33%). In 9 of them (60%) programmed stimulation revealed concealed retrograde atrioventricular conduction reaching atrioventricular node. Obtained results indicate, that the transesophageal programmed ventricular stimulation enables to examine concealed a-v conduction phenomenon and can be helpful in approximate localization of retrograde atrioventricular block.     

Effects of upright posture on anterograde and retrograde atrioventricular conduction in patients with coronary artery disease, mitral valve prolapse or no structural heart disease

To assess the effects of posture on anterograde and retrograde atrioventricular conduction, electrophysiologic testing was performed in 25 patients in both the supine and 45 degrees upright positions on a tilt table. Retrograde conduction was present during ventricular pacing in 17 patients in the supine position; all 17 continued to manifest retrograde conduction in the upright position. In all patients with absent retrograde conduction while supine, retrograde conduction could not be demonstrated while upright. Upright posture significantly (p less than 0.05) shortened the sinus cycle length (from 808 +/- 34 to 678 +/- 26 ms, mean +/- standard error of the mean), AH interval during sinus rhythm (78 +/- 6 to 69 +/- 6 ms), and AH interval during atrial pacing at cycle length 500 ms (123 +/- 13 to 91 +/- 9 ms). Total atrioventricular conduction time during atrial pacing shortened significantly (from 169 +/- 13 to 136 +/- 10 ms), as did ventriculoatrial conduction time during ventricular pacing (from 192 +/- 9 to 178 +/- 7 ms). Upright posture also significantly shortened both anterograde block cycle length (390 +/- 20 to 328 +/- 17 ms) and retrograde block cycle length (466 +/- 27 to 354 +/- 18 ms). However, the effect of upright posture on retrograde block cycle length was significantly greater than on anterograde block cycle length: a 21% decrease retrograde vs a 14% decrease anterograde (p less than 0.05). These effects may produce clinically important changes in characteristics of arrhythmias that depend on the properties of anterograde and retrograde conduction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic demonstration of concealed conduction in anomalous atrioventricular bypass tracts

To demonstrate the occurrence of concealed conduction in anomalous atrioventricular (AV) bypass tracts, 11 patients were selected for study. Two had a right-sided and nine had a left-sided bypass tract. Electrode catheters were placed in the right atrium, coronary sinus, AV junction and right ventricle. After every eighth atrial or ventricular driving beat (A1 or V1) at a constant cycle length, two successive atrial or ventricular premature beats (A2 and A3 or V2 and V3) were delivered. The A1A2 or V1V2 interval was fixed at 30 ms greater than the effective refractory period of the atrium or right ventricle, but less than the effective refractory period of the bypass tract in the anterograde or retrograde direction. This allows A2 or V2 to capture the atrium or ventricle, but not conduct in the bypass tract. The A3 or V3 was delivered from late diastole with a progressively shorter A2A3 or V2V3 interval until atrial or ventricular refractoriness was encountered. In the anterograde direction, the presence of A2 prevented A3 conduction in the bypass tract despite A1A3 intervals being longer than the anterograde effective refractory period of the bypass tract in 8 of the 11 patients. In the retrograde direction, the presence of V2 prevented V3 conduction in the bypass tract despite V1V3 intervals being longer than the retrograde effective refractory period of the bypass tract in 3 of the 11 patients. Thus, using the technique of programmed electrical stimulation, concealed conduction in anomalous AV bypass tracts can be demonstrated in both anterograde and retrograde directions.     

Ventricular echo beats during ventricular pacing or junctional bradycardia: studies in the normal canine heart

In 15 adult dogs ventricular echoes were elicited during sinus rhythm by incremental ventricular pacing and during atrioventricular (AV) junctional rhythm by depressing simultaneously AV junctional automaticity and retrograde AV nodal conduction. Concomitant slowing of AV junctional automaticity and conduction was achieved by selective intranodal administration of verapamil. In three dogs incremental pacing from either ventricle failed to retrogradely activate the atria, and in each case the site of block was found to be in the AV node. In two dogs with retrograde atrial capture there was little or no rate-dependency of retrograde ventriculoatrial (VA) conduction. During incremental ventricular pacing a single ventricular echo beat was observed in 10 of the 12 dogs that had atrial capture, and the atrium appears to be an essential link in the production of each ventricular echo. Ventricular echo occurred when the time allotted for retrograde VA conduction amounted to 70 +/- 4% of the duration of the ventricular pacing cycle length. During AV junctional rhythm, a single ventricular echo was elicited in half of the dogs and in each of those cases intranodal verapamil produced a profound depression of retrograde VA conduction. These experiments suggest that retrograde AV nodal longitudinal dissociation occurs in the slow current-dependent cells of the AV node.     

Determinants of antegrade echo zone in the Wolff-Parkinson-White syndrome

Forty-five patients with the Wolff-Parkinson-White syndrome and reciprocating tachycardia which utilized the atrioventricular (A-V) node for antegrade conduction and an accessory pathway for ventriculo-atrial (retrograde) conduction were studied. The extrastimulus technique in the right atrium and coronary sinus at multiple pacing cycle lengths was used. Three types of "echo zones" were defined by the relationship of the antegrade effective refractory period (ERP) of the accessory pathway, the longest coupling interval accompanied by an atrial echo, the ERP of the A-V node, and the functional refractory period of the atrium. Eighteen of 45 patients (40%) had more than one type of echo zone demonstrated by changing either pacing site or pacing cycle length or both. Pacing site and intraventricular conduction delay were found to have important effects on the longest coupling interval accompanied by an atrial echo in those echo zones in which the longest coupling interval accompanied by an atrial echo was less than the antegrade ERP of the accessory pathway. The echo zone is a useful concept to explain the physiology of the common reciprocating tachycardia in patients with the Wolff-Parkinson-White syndrome. However, the echo zone is profoundly affected by pacing site and pacing cycle length. When these variables are changed, many patients can be shown to have more than one type of echo zone. Studies of the echo zone have limited value as therapeutic guides.     

Surgery for Wolff-Parkinson-White syndrome interrupts efferent vagal innervation to the left ventricle and to the atrioventricular node in the canine heart

The hypothesis that cardiac surgery to interrupt accessory pathways also interrupts autonomic nerves to the canine ventricle and to the atrioventricular node was tested in four groups of dogs. Group 1 (n = 6) underwent dissection of the atrioventricular fat tissue and cryolesion created by application of a cryoprobe at -60 degrees C for 2 min along the lateral left atrioventricular groove, the same surgical procedure as carried out in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the left ventricular free wall. Group 2 (n = 6) underwent dissection of the atrioventricular fat pad alone and group 3 (n = 6) dissection and cryolesion along the posterior left atrioventricular groove as performed in patients with Wolff-Parkinson-White syndrome with accessory pathways located in the posterior paraseptal area. Group 4 consisted of 11 non-operated control dogs. Four to 13 days after surgery the ventricular effective refractory period (ERP) was determined during bilateral ansae subclaviae stimulation (4 ms pulses, 2-3 Hz, and 2-3 mA), noradrenaline infusion (0.5 micrograms.kg-1.min-1), and bilateral vagal stimulation (4 ms pulses, 20 Hz, and current strength to induce asystole or complete atrioventricular block). Atrioventricular nodal conduction (AH interval) and spontaneous sinus cycle length were also determined in group 3 dogs. Ansae subclaviae stimulation and noradrenaline infusion shortened effective refractory period significantly at each left ventricular test site. The amount of effective refractory period shortening induced by ansae subclaviae stimulation did not differ among the test sites except for the posterior left ventricle in group 1 dogs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Frequency-Dependent Electrophysiological Effect of Ibutilide on Human Atrium and Ventricle

Most of the class III antiarrhythmic agents developed in recent years blocks the rapid component of delayed rectifier potassium current (IKr). IKr blocker shows reverse use-dependency and also may cause torsades de pointes at slower heart rate. Ibutilide fumarate, a novel class III antiarrhythmic agent, increases window Na(+) current at the action potential plateau phase. We studied the rate-dependent effect of ibutilide on the electrophysiological parameters of human atrium and ventricle. Franz catheter and a pacing catheter were placed closely in the high right atrium and right ventricular apex to record monophasic action potentials (MAP) during pacing at cycle length (PCL) of 600 ms and 350 ms in eight patients who underwent electrophysiological study. MAP duration of right atrium (RA-MAPD) and right ventricle (RV-MAPD), effective refractory period of RA and RV (RA-ERP and RV-ERP), intra-atrial conduction time (IACT) and intra-ventricular conduction time (IVCT) were measured before and after intravenous administration of ibutilide (0.01 mg/kg up to 1mg). A conduction time from RA pacing spike to distal coronary sinus potential was used to measure IACT, while QRS duration of surface ECG during RV pacing was used to measure IVCT. Ibutilide prolonged RA-MAPD by 60 ms at PCL 600 ms and by 53 ms at PCL 350 ms; RV-MAPD by 48 ms at PCL 600 ms and by 55 ms at PCL 350 ms. Ibutilide did not affected RA and RV-ERP/MAPD ratio, IACT, and IVCT. Ibutilide prolongs MAPD and ERP of human atrium and ventricle without reverse use-dependency.     

Clinical electrophysiologic effects of lorcainide in patients and its effect on the conduction of accessory pathway in Wolff-Parkinson-White syndrome

The electrophysiologic effects of the intravenous administration of a new antiarrhythmic drug, lorcainide, were evaluated by programmed electrical stimulation of the heart in 20 patients with and without Wolff-Parkinson-White (WPW) syndromes. Lorcainide shortened the sinus cycle length from 721.0 +/- 125.9 to 649.5 +/- 100.1 ms (P less than 0.001), but did not influence sinus node function and AV node conduction and refractoriness, slightly increased atrial effective period (ERP) (P less than 0.02) and did not change ventricular ERP (P less than 0.2), obviously lengthened atrial conduction time, H, H-V interval and the width of V wave. Lorcainide caused complete antegrade block of the accessory pathway (AP) in six of 9 WPW patients and resulted in exclusive conduction over the AV nodal. His conduction in two patients with atrial flutter. It also prolonged the retrograde conduction time and refractoriness of AP, and prevented initiation of orthodromic atrioventricular tachycardia (O-AVRT) in six of 12 patients by blocking of the retrograde conduction of the AP, increased the cycle length of tachycardia from 321.7 +/- 43.6 to 361.7 +/- 54.9 ms (P less than 0.005) by marked prolongation of retrograde AP conduction time in 6 patients in whom O-AVRT could still be induced. It is concluded that intravenous lorcainide does not affect sinus node and AV node function, slightly influences atrial and ventricular refractoriness, obviously suppresses atrial, His bundle and intraventricular conduction, and is an effective antiarrhythmic drug for patients with WPW by blocking both the antegrade and retrograde conduction of the AP.     

Double atrial responses to a single ventricular impulse due to simultaneous conduction via two retrograde pathways

Electrophysiologic studies were performed in two patients. In one patient (Case 1) with ventricular pre-excitation and paroxysmal supraventricular tachycardia, studies after diltiazem administration showed two QRS responses to a single atrial stimulus during atrial pacing at a cycle length of 300 ms. The first QRS response with full pre-excitation and short PR interval was consistent with accessory pathway conduction, while the second QRS response with a normal duration and an atrio-His bundle interval of 350 ms was consistent with normal pathway conduction. The second QRS response was followed by initiation of supraventricular tachycardia. Studies after verapamil administration on a separate day disclosed two atrial responses to a single QRS complex during ventricular pacing at cycle lengths between 330 and 280 ms, suggesting simultaneous retrograde accessory and normal pathway conduction. In Case 2 with a supraventricular tachycardia using a fast atrioventricular nodal pathway for anterograde and a slow ventriculoatrial pathway for retrograde conduction, two atrial responses to a single QRS complex were observed during ventricular pacing at cycle lengths between 500 and 400 ms. The first atrial response showed a stimulus to atrial interval of 120 ms and an atrial activation sequence with the low septal right atrium being earlier than other atrial sites, suggesting retrograde fast pathway conduction. The second atrial response showed a stimulus to atrial interval of 505 ms and an atrial activation sequence with low septal right atrium being simultaneous with the proximal coronary sinus, suggesting retrograde slow pathway conduction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiological effects of acute ventricular dilatation in the isolated rabbit heart

We examined the effects of left ventricular dilatation on epicardial pacing threshold, conduction velocity, and effective refractory period (ERP) in the isolated, retrograde perfused rabbit heart. Left ventricular size was modified by acutely changing the volume of a fluid-filled balloon anchored within the vented left ventricle. Increases in left ventricular volume, associated with increases in left ventricular end-diastolic pressure from 0 +/- 1 to 35 +/- 2 mm Hg, were not associated with significant changes in pacing threshold or conduction velocity. The left ventricular ERP decreased significantly with an added volume of 1.5 ml (91.4 +/- 5.5 msec) compared with starting volume (117.7 +/- 3.8 msec, p less than 0.01). Right ventricular ERP did not change significantly with increases in left ventricular volume. The left and right ventricular ERPs were comparable at starting volume (117.7 +/- 3.8 and 117.6 +/- 3.5 msec, respectively; p = NS) but were significantly different with an added volume of 1.5 ml (91.4 +/- 5.5 and 112 +/- 5.6 msec, p less than 0.05). These changes were independent of coronary perfusion pressure and paced cycle length, suggesting that ischemia is an unlikely explanation for the observed effects. Changes in left ventricular volume decreased left ventricular ERP in a regionally heterogeneous manner, increasing the temporal dispersion of recovery over the left ventricle nearly twofold. Induced ventricular arrhythmias (ventricular tachycardia or fibrillation) were significantly more frequent at high (35%) than at low (3%) volumes during left ventricular pacing. We conclude that ventricular dilatation is associated with increased dispersion of refractoriness in this model, a finding that correlates with propensity for reentrant arrhythmias.     

伊布利特对人体心房与心室电生理特性的影响

探讨伊布利特对人体右房、左房及右室有效不应期(RA-ERP、LA-ERP及RV-ERP)与房间、室间传导时间的影响。测定25例射频消融术后患者于静脉推注伊布利特(0.0167mg/kg)前后在基础起搏周长为600ms时的RA-ERP、LA-ERP及RV-ERP,同时测量起搏与窦性心律时的心房、心室传导时间。其中通过起搏冠状静脉窦远端间接起搏左房。结果:①伊布利特明显延长RA-ERP、LA-ERP及RV-ERP(P均<0.001)。②使用伊布利特后,对窦性心律时的P波宽度、PR间期、QRS时限、AH及HV均无明显影响(P>0.05),对房间及室间传导时间无明显影响(P>0.05),亦对急性期的起搏阈值无明显影响(P>0.05)。③使用伊布利特后2例出现右束支阻滞。结论:伊布利特可明显延长RA-ERP、LA-ERP及RV-ERP,但不影响房间、室间传导时间。     

Effect of acute subendocardial ischemia on ventricular refractory periods

OBJECTIVES: To investigate the impact of acute subendocardial ischemia on the dispersion of ventricular refractory periods. METHODS: Acute subendocardial ischemia was induced in sheep by partial ligation of the left circumflex coronary artery and rapid pacing of the left atrium. The ventricular effective refractory period (ERP) was measured in five areas of the left ventricle by a programmed premature stimulation technique. RESULTS: The average ERP and ERP dispersion remained unchanged in the control group (n=5, P>0.05). In the study group (n=5), the ERP was shortened following subendocardial ischemia. ERP dispersion decreased significantly from 48+/-9 ms to 36+/-13 ms 30 min after the ischemia (P=0.02). There was neither spontaneous nor stimulation-induced ventricular arrhythmia after ischemia. CONCLUSION: Acute subendocardial ischemia leads to a homogenous reduction of ventricular ERP. This may partially explain why subendocardial ischemia is associated with a low incidence of ventricular arrhythmia.     

The excitation-conduction system of the heart in primary mitral valve prolapse (electrophysiological study)

Forty patients (mean age 40 yrs) with primary mitral valve prolapse (MVP) and 20 healthy controls were subjected to electrophysiologic investigation. The following measurements were performed: 1) intracardiac conduction time, 2) effective and functional refractory periods of the right atrium, a-v node and right ventricle, 3) Wenkebach point, 4) retrograde Wenkebach point. Disturbances of intracardiac conduction were detected in 13 (32.5%) patients with MVP (in 8 patients within proximal part of the conduction system, in 5 patients distally). Patients with MVP were more sensitive to ajmaline. Conduction time in the proximal part was significantly increased only in these patients. The incidence of retrograde conduction was more frequent in the patients with MVP than in the controls. In 12 (30%) patients with MVP, constant conduction time and high value of retrograde Wenkebach point were found. Mean values of effective and functional refractory periods of the right ventricle and effective refractory period of the a-v node were not significantly different in both groups. In patients with MVP, mean values of effective and functional refractory periods of the right atrium were significantly lower and functional refractory period of the a-v node significantly higher than in the controls. In 8 (20%) patients with MVP and in 2 (10%) controls, longitudinal division of the a-v node was found. Atrial hyperreactivity was detected in 14 (35%) patients and in 3 (15%) controls. In conclusion, MVP is often accompanied by electrophysiologic abnormalities, such as disturbed intracardiac conduction, retrograde preexcitation, shortening of atrial refractory periods, longitudinal division of the a-v node and atrial hyperreactivity.     

Effect of autonomic nervous system modulation on retrograde atrioventricular nodal conduction in the human heart

Although the influence of the autonomic nervous system on anterograde atrioventricular nodal conduction is well established, its effect on retrograde atrioventricular nodal conduction has not been examined systematically. Since retrograde atrioventricular nodal conduction in subjects with normal anterograde conduction may vary from intact retrograde conduction to complete retrograde block when assessed during ventricular pacing, in this study patients with (a) intact retrograde atrioventricular nodal conduction (group 1) were studied during parasympathetic (vagal) stimulation by carotid sinus pressure and during sympathetic inhibition (propranolol 0.2 mg.kg-1 intravenously) and (b) retrograde atrioventricular nodal block (group 2) were studied during vagal blockade (atropine 0.04 mg.kg-1 intravenously) and during sympathetic stimulation (isoproterenol 1-4 micrograms.min-1 infusion). In both groups changes in sinus cycle length and anterograde atrioventricular nodal conduction were measured. In group 1 vagal stimulation by carotid sinus pressure in 20 patients caused the cycle length at which retrograde atrioventricular nodal block was induced to be significantly lengthened from a mean(SD) of 375(59) to 451(51) ms in six patients; caused complete retrograde block in 10 patients; and had no effect in four patients. Sympathetic inhibition by propranolol in another 15 patients delayed the onset of pacing induced retrograde atrioventricular nodal block from a mean(SD) of 340(60) to 418(80) ms in 11 patients; caused complete retrograde atrioventricular nodal block in three patients; and had no effect in one patient. In group 2 vagal blockade by atropine caused a 1:1 retrograde response during ventricular pacing up to a mean(SD) cycle length of 470(135) ms in six out of eight patients. The infusion of isoproterenol caused the retrograde atrioventricular nodal block to be abolished and 1:1 conduction to be resumed up to a ventricular pacing mean(SD) cycle length of 364(57) ms in six out of eight patients. It is concluded that (a) the autonomic nervous system modulates retrograde atrioventricular nodal conduction in a similar manner to its anterograde counterpart and (b) that since retrograde atrioventricular nodal conduction was reversible after the administration of either atropine or isoproterenol retrograde atrioventricular nodal block may be dynamic (physiological) rather than fixed (anatomical) in nature.     

快速心房激动对心房肌电生理特性的影响

比较快速心房起搏与急性心房颤动 (简称房颤 )诱发心房电生理特性的变化。以 15 0～ 2 0 0ms起搏周长(PCL)对 4 5例成功射频消融后 (RFCA)病人右房进行S1S1刺激诱发急性房颤 ,据能否诱发急性房颤分为非房颤组和急性房颤组 ;再以 4 0 0msPCL对心房快速激动前后高位右房、低位右房、His束周围等多部位进行S1S2 扫描 ,测定心房有效不应期 (ERP)、ERP离散度 (ERPd)、右房内及房间的传导时间的变化 ;另以 35 0 ,4 0 0和 4 5 0ms三个PCL随机对RAA进行S1S2 扫描 ,观察ERP频率自适应性的变化。两组心房快速激动后 4 0 0msPCL下右房各刺激部位及三种不同PCL右心耳ERP均较心房快速激动前有明显的缩短 ,并且缩短的程度相同。两组病人心房快速激动前后房内和房间传导时间及ERPd没有明显改变。两组心房快速激动前后斜率均值均较激动后明显下降 ;心房快速激动前、后斜率均值两组间无显明差别 (P >0 .0 5 )。结论 :两种方式的心房快速激动可诱发相似的心房电重构现象。     

Electrophysiology of oral encainide

The electrophysiologic effects of oral encainide were assessed in 15 patients. Electrophysiologic studies were performed before and after 3 or more days of oral encainide therapy, 100 to 300 mg/day (mean 242 ± 66). Patients received no other cardioactive drugs during this time. Encainide significantly (p < 0.005) lengthened the following: A-H interval (74.5 ± 21.5 to 105.5 ± 39.1 ms, mean ± standard deviation), the shortest atrial pacing cycle length maintaining 1:1 atrioventricular (A-V) nodal conduction (339.0 ± 71.3 to 417.0 ± 88.6 ms), H-V interval (47.5 ± 7.8 to 67.1 ± 12.9 ms), QRS interval (103.5 ± 30.9 to 132.3 ± 35.7 ms), right atrial (233.8 ± 27.2 ms to 282.9 ± 38.6 ms) and right ventricular (235.7 ± 15.6 to 267.1 ± 36.9 ms) effective refractory periods and Q-T interval (364.4 ± 38.0 to 416.9 ± 55.3 ms). The spontaneous sinus cycle length did not change significantly. In four patients who had accessory A-V muscle connections (two manifest, two concealed) encainide abolished anterograde conduction over the accessory pathway in two patients, and increased the retrograde effective refractory period and/or lengthened retrograde conduction time or blocked retrograde conduction in the accessory pathway, or all three variables, in all four patients. There was no correlation between the plasma encainide concentration obtained at the time of study and the magnitude of change in any electrophysiologic variable.It is concluded that (1) encainide depresses conduction in the A-V node, His-Purkinje system and accessory pathway, and increases refractoriness of the atrium, ventricle and accessory pathway, and (2) differences between these results and those of earlier studies using encainide in a single intravenous dose (which found no significant effects on A-V nodal conduction or atrial and ventricular refractoriness) may be explained in part by the effects of an active metabolite of encainide.