Reproducible efficacy of loading oral propafenone in restoring sinus rhythm in patients with paroxysmal atrial fibrillation

This is the first study to demonstrate the reproducibility of an oral propafenone loading dose in converting paroxysmal atrial fibrillation in patients without significant cardiac disease or hypertension. This finding may support the development of the "pill-in-the-pocket" treatment strategy in this group of patients.     

Medikamentöse Rhythmuskontrolle bei Vorhofflimmern

Medicinal antiarrhythmic therapy is either used in the acute setting to convert atrial fibrillation to sinus rhythm or as chronic medication to preserve sinus rhythm if a rhythm control strategy is followed. The choice of the antiarrhythmic agent is based on the presence or absence of structural heart disease. In addition, oral anticoagulation should be established according to current guidelines. In the acute setting the armamentarium comprises flecainide, propafenone, vernakalant and amiodarone. Usually, combination therapy with an atrioventricular (AV) node slowing drug (a beta blocker or verapamil) is used. For chronic rhythm control a class IC drug, such as sotalol, dronedarone and amiodarone is given depending on the comorbidities. In the absence of structural heart disease, rare episodes of paroxysmal atrial fibrillation can be treated by a pill-in-the-pocket strategy, i.e. self-administered pharmacological cardioversion with flecainide or propafenone. Despite recent advances in catheter ablation of atrial fibrillation, medical rhythm control continues to play an important role due to its ubiquitous availability and relatively easy use. The risk for proarrhythmia has to be evaluated in all patients.     

Relation between atrioventricular pathways and ventricular response during atrial fibrillation and flutter.

We have analysed the ventricular response as seen on the surface electrocardiogram in patients with paroxysmal atrial fibrillation and flutter in relation to the electrophysiological properties of the corresponding atrioventricular pathways. In 15 patients who had atrial fibrillation with conduction solely through the atrioventricular node, there was a significant correlation between th shortest and mean RR intervals during atrial fibrillation and the functional refractory period, "pre-Wenckebach cycle length", and the shortest ventricular cycle length that resulted from 1:1 atrioventricular conduction. In 18 patients with conduction through an accessory atrioventricular pathway the only good correlation was between the shortest and mean ventricular rate during atrial fibrillation and the "pre-Wenckebach cycle length" and shortest ventricular cycle length during 1:1 atrioventricular conduction. In 12 patients with an atriofascicular bypass tract or rapidly conducting atrioventricular node there was no significant correlation between the RR intervals during atrial fibrillation and the electrophysiological indices; the same lack of correlation was evident in all 11 patients with atrial flutter, all of whom had atrioventricular nodal conduction. The response of atrioventricular pathways to electrophysiological testing, particularly the use of incremental atrial pacing, provides useful guidance in the further management of these atrial arrhythmias.     

A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory

OBJECTIVE: The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND: Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS: The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricular" (A-V) or "atrial-atrial-ventricular" (A-A-V). RESULTS: The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS: In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.     

射频消融房室交界区慢、快经区域对犬和人心房颤动时心室率的影响

本文观察经导管射频消融房室交界区慢、快径区域对大和人心房颤动时心室率的影响.方法 杂种犬4条,体重11±1.2kg.房室结折返性心动过速患者7例,年龄29～65岁.阵发性房颤患者4例,年龄62～70岁,其中2例为短P-R间期综合征.均先采用“下位法”消融慢径区域后,若房室结有效不应期或房颤时平均R-R间期无明显变化,则加行“快径”区域消融.房颤诱发采用猝发脉冲电刺激(人)或静滴氯化乙酰胆碱后猝发脉冲电刺激(犬).结果 7例房室结折返性心动过速患者中5例经下位法射频消融阻断慢径,房室结前传有效不应期及诱发房颤时平均R-R间期明显延长(222±33ms vs 285±42ms和539±44ms vs 656±53ms P<0.01),无并发症.4条大及4例阵发性房颤患者经心内电生理检查证实均无房室结双径路表现,选择性消融“慢径区域”后,房室结有效不应期和房颤时平均R—R间期无明显变化,加行“快径区域”消融后,房室结有效不应期和房颤时平均R—R间期明显延长(犬145±16ms vs 185±22ms和305±13ms vs 403±17ms P<0.01,人220ms vs 490ms和367ms vs 690msP<0.01),1例房颤患者术后3天出现Ⅲ°AVB,2周后恢复为Ⅰ°AVB.本文还在动物实验中观察到消融快径区域时,房侧靶点(A/V>1)较室侧靶点(A/V<1)更易于造成Ⅲ°AVB.结论 选择性射频消融慢径区域对减?     

Extreme tachycardia complicating the use of disopyramide in atrial flutter.

A 59-year-old man presented with atrial flutter and a 2:1 atrioventricular response, which, after intravenous disopyramide, became 1:1. A mechanism of slowed atrial flutter rate and improved atrioventricular nodal conduction, similar to that recognised with quinidine, is suggested.     

Limitation of tachycardia zone resulting from longitudinal dissociation of the atrioventricular node in concealed pre-excitation.

Two cases with a concealed left-sided accessory atrioventricular bypass tract are described. In both, functional longitudinal dissociation of the atrioventricular node narrowed the range of atrial premature beat coupling intervals which could initiate re-entry using the accessory pathway. In case 1 early premature atrial beats were followed by an atrioventricular nodal re-entrant echo. The atrial echo pre-empted retrograde conduction over the Kent bundle and thus limited the development of paroxysmal supraventricular tachycardia. In case 2 atrioventricular nodal conduction showed typical features ascribed to dual atrioventricular nodal pathways. In addition there was a bradycardia-related retrograde block in the concealed accessory pathway. Early premature atrial beats, because of exclusive "slow pathway" anterograde conduction, arrived at the ventricles during the period of bradycardia-dependent retrograde block and failed to initiate a macro re-entrant tachycardia. This study shows that (1) longitudinal dissociation within the atrioventricular node may limit the ability to initiate tachycardia in patients with concealed pre-excitation; and (2) discontinuous atrioventricular nodal conduction curves occasionally help to reveal bradycardia-related retrograde block in a concealed accessory pathway.     

Fetal tachyarrhythmia with 1:1 atrioventricular conduction. Adenosine infusion in the umbilical vein as a diagnostic test

This is the report of a case of fetal tachyarrhythmia with 1:1 atrioventricular conduction detected by pre-natal echocardiography in a fetus at 25-weeks gestation. Adenosine infusion via cordocentesis was performed as a diagnostic test to differentiate between atrioventricular nodal reentrant supraventricular tachyarrhythmia and atrial flutter. After infusion, transient 2:1 atrioventricular dissociation was obtained and the diagnosis of atrial flutter was made. Transplacental therapy with digoxin and amiodarone was then successfully used.     

Electrocardiographic manifestations and clinical significance of atrioventricular nodal alternating Wenckbach periods

Atrioventricular nodal alternating Wenckebach periods were defined as episodes of 2:1 atrioventricular block in which there was a gradual increase in transmission intervals of conducted beats ending in two or three consecutively blocked atrial impulses. This is one of the mechanisms whereby 2:1 atrioventricular block progresses into 3:1 or 4:1 atrioventricular block. Alternating Wenckebach periods appear during rapid atrial pac,ng (even in the absence of depressed atrioventricular nodal function), provided that the atria can be captured at a rate fast enough to allow for the occurrence of this phenomenon. Treatment of atrial flutter with digoxin and quinidine produces alternating Wenckebach's periods, with associated electrocardiographic changes specific for the type of drug given. In patients with "atrial tachycardia with atrioventricular block" due to digitalis intoxication or with primary disease of the conducting system or with acute myocardial infarction, there are coexisting severe arrhythmias and clinical symptoms requiring almost immediate pharmacologic or electrical therapy. We conclude that atrioventricular nodal alternating Wenckebach's periods are common and frequentyly transient and that they occur in a variety of clinical conditions, most of which are benign; however, contrary to what is commonly accepted, some episodes appear in clinical settings requiring prompt pharmacologic or electrical treatment.     

Die Behandlung von Vorhofflimmern im Alltag

Atrial fibrillation is the most common arrhythmia in the adult. During recent years the therapeutic strategy has markedly changed. Some of these changes can be summarized as follows: Basis therapy includes betablockers and – in patients with structural heart disease – ACE-inhibitors and AT₁-Blockers respectively. Class 1C-antiarrhythmic agents (flecainide or propafenon) should be restricted to patients with no or minimal left ventricular impairment. Amiodaron is the drug of choice in patients refractory to class 1C-agents and in those with already reduced left ventricular function. The “pill-in-the-pocket” regime can be used successfully in patients without structural heart disease and rare episodes of atrial fibrillation. Catheter ablation for paroxysmal and short lasting chronic atrial fibrillation was introduced into the clinical practice in 2006. The European and US-American guidelines recommend this technique for patients with no or minimal structural heart disease who are highly symptomatic and refractory or intolerant to antiarrhythmic agents. Decisions for curative catheter ablation in patients with long standing atrial fibrillation, heart failure or valvular heart disease should be individualized but are to date not generally recommended.     

Role of adenosine as mediator of bradyarrhythmias during hypoxia in isolated guinea pig hearts

Tissue concentrations of adenosine, an endogenous metabolite with negative chronotropic and dromotropic actions, are known to increase when myocardial oxygen supply is reduced. In this study the concentrations of endogenous adenosine released during a period of hypoxic perfusion were measured to determine whether they are sufficient to account for the effect of hypoxia on atrioventricular conduction in isolated perfused guinea pig hearts. In addition, the efficacy of competitive adenosine antagonism in reversing the effect of hypoxia on atrioventricular conduction and atrial automaticity were compared. Effluent samples for adenosine were collected at the onset of spontaneous and atrial pacing induced second degree atrioventricular block during hypoxic perfusion (PO2 3.07 kPa) and during the combined infusion of adenosine plus the nucleoside transport blocker, dipyridamole (PO2 71.1 kPa). The mean (SEM) atrial cycle lengths associated with the onset of atrioventricular block were 333(10) and 297(2) ms respectively. Effluent concentrations of adenosine associated with atrioventricular block during hypoxia (2342(160) pmol X min-1 X g-1 heart weight) were approximately equal to those obtained during the infusion of adenosine plus dipyridamole (2538(256) pmol X min-1 X g-1 heart weight) (no statistically significant difference). During hypoxic perfusion, among hearts showing spontaneous atrioventricular block and those in which atrial slowing prevented the onset of spontaneous block, the competitive adenosine antagonist aminophylline (60 mumol X litre-1) reversed either spontaneous or atrial pacing induced block without any effect on spontaneous atrial cycle length.(ABSTRACT TRUNCATED AT 250 WORDS)     

An unusual ventricular loop associated with right juxtaposition of the atrial appendages

We report two autopsied cases of an unusual ventricular loop in hearts with right-sided juxtaposition of the atrial appendages. Case 1 showed usual atrial arrangement, a concordant atrioventricular connexion with a disharmonious ventricular loop showing left-hand topology and double outlet right ventricle with normally related arterial trunks. The atrioventricular connexions were crossing, with the inlet to the left-sided morphologically right ventricle being posterior to that of left ventricle. Mitral hypoplasia and coarctation of the aorta were the associated lesions. The second case showed usual atrial arrangement, a discordant atrioventricular connexion with an imperforate left atrioventricular orifice and double outlet right ventricle with the aorta in the right-sided position. A large right atrium was connected to right-sided morphologically left ventricle. A prominent dimple in the left atrial floor was firmly attached to the hypoplastic right ventricle which was left-sided and anterior. A small but discrete inlet portion of the right ventricle could be traced towards the anteriorly located left atrial dimple. Thus, despite the presence of a discordant atrioventricular connexion with the usual atrial arrangement, there was righ-hand ventricular topology. In each case the inlet component of the ventricular septum was displaced, being to the right in case 1 and anteriorly in case 2. We suggest that the embryologic mechanism producing disharmony between the atrioventricular connexion and the segmental combinations be interpreted on the basis of posterior ventricular looping, since they are best explained on the basis of a hypothetical heart with posteriorly located outflow tracts.     

Effects of atrioventricular interval on left ventricular diastolic filling assessed with pulsed Doppler echocardiography

Effects of changes in atrioventricular interval on left ventricular diastolic filling were studied using pulsed Doppler echocardiography in 14 patients with programmable dual chamber pacemakers. Peak early diastolic filling velocity (E) and peak atrial filling velocity (A) were measured from the transmitral flow velocity pattern at three different atrioventricular intervals under the same pacing rate of 80 beats.min-1 in each patient. When the atrioventricular interval was switched from intermediate [148(SD10) ms] to short [68(11) ms], stroke volume did not change significantly [60(14) to 58(13) ml], but E increased from 39(12) to 44(11) cm.s-1 (p less than 0.05), and A decreased from 48(8) to 38(9) cm.s-1 (p less than 0.05). At the short atrioventricular interval, incomplete atrial emptying by the atrial contraction seemed to cause a reciprocal increase in the early diastolic filling. When the atrioventricular interval was switched from intermediate to long [234(16) ms], stroke volume, E and A did not change significantly [57(14) ml, 37(13) cm.s-1, 51(8) cm.s-1 respectively]. At the short and long atrioventricular intervals, atrial filling always changed in the direction opposite to that of early diastolic filling. Changes in stroke volume as well as peak early diastolic filling velocity caused by altering atrioventricular interval were pronounced in aged patients and patients with decreased early diastolic filling. In conclusion, left ventricular diastolic filling patterns can be affected by atrioventricular interval even without any concomitant pathological changes in the left atrial or ventricular function. These effects should not be taken lightly, especially in patients with decreased left ventricular early diastolic filling.     

Antiarrhythmic drugs in patients with recurrent atrial fibrillation: where are we?

In patients with recurrent atrial fibrillation (AF), the hallmark of treatment has long been the use of antiarrhythmic drugs. The following strategies are available: a) any antiarrhythmic treatment; b) out-of-hospital episodic treatment ("pill-in-the-pocket" approach); c) prophylactic antiarrhythmic therapy; and d) hybrid therapy. The following patients with recurrent AF should not undergo any antiarrhythmic therapy: after the first AF episode; patients with rare, hemodynamically well-tolerated and short-lasting (a few hours) AF episodes; patients with perioperative AF, without history of recurrent AF; patients with AF during acute myocardial infarction or other acute diseases, without history of recurrent AF; and "holiday heart" syndrome. In patients with infrequent AF episodes (< 1 per month) and hemodynamically well-tolerated, but long enough to require emergency room intervention or hospitalization, a good treatment might be the "pill-in-the-pocket" approach, consisting of a single-dose oral ingestion of flecainide or propafenone at the time and place of palpitation onset. A recent Italian study has shown that this treatment is effective and safe. When AF episodes are frequent and/or hemodynamically badly tolerated, the treatment of choice is the prophylactic therapy with antiarrhythmic drugs. When these drugs fail (ineffective or not tolerated) a non-pharmacological treatment or a hybrid therapy may be indicated.     

Catheter ablation by low energy DC shocks for successful management of atrial flutter.

OBJECTIVE--To assess the effects of low energy ablation of the substrate for atrial flutter. DESIGN--Initial retrospective analysis of patients undergoing low energy ablation of the atrioventricular node for refractory atrial flutter (group 1) was followed by a prospective assessment of low energy ablation in the posterio-inferior right atrium for the same condition (group 2). SETTING--Tertiary referral centre for management of cardiac arrhythmias. PATIENTS--Seven men (aged 50-67 years) with refractory atrial flutter. INTERVENTIONS--Multiple (3-10) low energy DC shocks with a cumulative energy of 100-245 J in the region of the atrioventricular node in group 1 and 12-15 low energy DC shocks (cumulative energy 110-235 J) guided by the anatomical landmarks of the triangle of Koch and applied directly to the atrial wall. MAIN OUTCOME MEASURE--Freedom from recurrence of atrial flutter. RESULTS--In group 1 despite initial complete atrioventricular block in three patients, atrioventricular conduction had resumed in all by one month. All four, however, were in sinus rhythm at follow up six to 13 months later. Two of the three patients in group 2 were free of atrial flutter at follow up three to four months after ablation. CONCLUSION--Ablation of the atrial flutter substrate with low energy DC shocks is feasible. Precise electrophysiological mapping is not necessary.     

Catheter ablation by low energy DC shocks for successful management of atrial flutter.

OBJECTIVE--To assess the effects of low energy ablation of the substrate for atrial flutter. DESIGN--Initial retrospective analysis of patients undergoing low energy ablation of the atrioventricular node for refractory atrial flutter (group 1) was followed by a prospective assessment of low energy ablation in the posterio-inferior right atrium for the same condition (group 2). SETTING--Tertiary referral centre for management of cardiac arrhythmias. PATIENTS--Seven men (aged 50-67 years) with refractory atrial flutter. INTERVENTIONS--Multiple (3-10) low energy DC shocks with a cumulative energy of 100-245 J in the region of the atrioventricular node in group 1 and 12-15 low energy DC shocks (cumulative energy 110-235 J) guided by the anatomical landmarks of the triangle of Koch and applied directly to the atrial wall. MAIN OUTCOME MEASURE--Freedom from recurrence of atrial flutter. RESULTS--In group 1 despite initial complete atrioventricular block in three patients, atrioventricular conduction had resumed in all by one month. All four, however, were in sinus rhythm at follow up six to 13 months later. Two of the three patients in group 2 were free of atrial flutter at follow up three to four months after ablation. CONCLUSION--Ablation of the atrial flutter substrate with low energy DC shocks is feasible. Precise electrophysiological mapping is not necessary.     

Atrioventricular Nodal Response to Retrograde Activation in Atrial Fibrillation

Atrioventricular Nodal Reset. Retrograde (ventriculoatrial) conduction that reaches the atrioventricular node simultaneous with, or just before an atrial impulse ean facilitate subsequent anterograde conduction. However, a spontaneous or programmed ventricular extrasystule during atrial nbrillation is generally followed by a compensatory pause indicating subsequent delayed anterograde transmission. This characteristic response was used as a model to study the mechanism of atrioventricular nodal behavior during atrial fibrillation. In eight medically-treated patients with chronic atrial fibrillation and a relatively slow but random ventricular response, single premature right ventricular stimuli were delivered after every eighth spontaneous R wave during at least 1 hour. A fixed coupling interval of the ex-trastimulus, considerably shorter than the shortest spontaneous RR interval, was used. The histograms of the postextrasystolic intervals were compared with those of the spontaneous noninterrupted RR intervals. The average postextrasystolic interval was 180 to 300 msec longer than the mean control RR interval, and in six of eight patients, the shape of the histogram of the postextrasystolic cycles was insignificantly different from that of the spontaneous RR intervals. This suggests that In those six patients, the retrograde impulse had reset the random timing cycle of atrioventricular nodal discharge during atrial fibrillation. This observation is compatible with the hypothesis that electrotonically-mediated propagation across a weakly coupled junctional area within the atrioventricular node, rather than decremental conduction and extinction of anterograde atrial impulses at different levels within the node, may be the mechanism of atrioventricular transmission in atrial fibrillation. (J Curdiovasc Electrophysiol, Vol. 1, pp. 437–447, October 1990)     

房室同时激动的房性心动过速的电生理特征

目的:探讨在腔内心电图上表现为房室同时激动的房性心动过速(AT)的电生理特征.方法:对4例房室同时激动的AT患者的电生理资料进行分析.结果:AT并发房室结缓慢前传时,A波可与滞后的V波融合,使腔内心电图表现为房室同时激动,易误诊为典型房室结折返性心动过速.结论:AT时房室也可同时激动,规范、细致的电生理检查是避免误诊的关键所在.