Gaps in anterograde conduction in patients with the short PR interval, normal QRS complex syndrome.

Of 8 patients with the short PR interval, normal QRS complex syndrome studied recently, 3 reported here displayed gaps in anterograde conduction. Atrial premature beats at decreasing coupling intervals conducted with minimal AH prolongation until a zone within the cardiac cycle was reached where conduction failed at a supra-Hisian level. Conduction resumed at earlier atrial coupling intervals and was associated with a sudden increase in the AH interval and the appearance of atrial echo beats with earliest atrial activation on the proximal coronary sinus electrogram. It is suggested that the failure of anterograde conduction at relatively late atrial coupling intervals was caused by a short AH functional refractoriness produced by the pre-excitation of the lower AV junction by a partial AV nodal bypass. Conduction resumed only when early atrial premature beats found the extranodal pathway refractory and were transmitted with decremental delay through the AV node.     

Characteristics of atrio-His conduction in the short PR interval, normal QRS complex syndrome. Evidence for enhanced slow-pathway conduction

This study confirms the existence of accelerated conductionvia a fast atrio-His pathway in patients with the so-calledLown-Ganong-Levine (LGL) syndrome. Additional slow AH pathwayconduction was detected in about 50% of patients. Comparisonof slow pathway conduction characteristics in the LGL syndromewith AH conduction in age-matched normals and patients withdual AV nodal pathways revealed that the ‘slower’of dual AH pathways in LGL patients also exhibits relativelyenhanced conduction. This finding cannot be explained by thepresence of an anomalous AH pathway (‘James’ fibre')bypassing a normal A V node. It is suggested that a non-specificand as yet unknown effect causes enhanced conduction throughoutthe A V junction in patients with the LGL syndrome.     

Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex

Eighteen subjects with a short P-R interval (<0.12 second) and normal QRS complex were studied by means of His bundle recordings and programmed atrial premature depolarizations. Eight subjects had a history of supraventricular tachycardia. During sinus rhythm, the A-H interval was less than or at the lower limits of normal values (45 to 80 msec), and the H-V interval was normal (30 to 50 msec). Atrial pacing at rates of up to 160/min produced 3 types of responses. Thirteen subjects showed a progressive increase in A-H interval similar to that of normal subjects but to a lesser degree. Three subjects showed an initial increase at low pacing rates, followed by a plateau response and further increase at higher rates. Two subjects showed no significant increase in the A-H interval. In 6 of 8 subjects with supraventricular tachycardia, atrial premature depolarizations produced atrial echo beats and sustained supraventricular tachycardia in 4, indicating atrioventricular (A-V) nodal reentry as the mechanism for the supraventricular tachycardia. In 10 subjects, refractory periods of the various components of the A-V conducting system were found to be similar to those of subjects with a normal P-R interval. The data suggest the following possible explanations for the short P-R interval: (1) total or partial bypass of the A-V node; (2) an anatomically small A-V node; (3) a short or rapidly conducting intranodal pathway; or (4) isorhythmic A-V dissociation.     

Sotalol in supraventricular tachycardia. Electrophysiologic measurements in Wolff-Parkinson-White syndrome and AV node re-entry tachycardia

The electrophysiologic effects of sotalol were studied in 11 patients with Wolff-Parkinson-White syndrome and 9 patients with AV nodal reentrant tachycardia. Electrophysiologic studies were performed before and after intravenous infusion of 80 mg sotalol over a period of 5 minutes. Sotalol prolonged the effective refractory period of the right atrium and the right ventricle. Both AV node and accessory pathway conduction were depressed by sotalol in antegrade and retrograde directions. Induction of reentrant tachycardia was prevented in 6 of 18 patients. The rate of reentrant tachycardia decreased from 182 +/- 29/min to 153 +/- 14/min (p less than 0.01) and the ventricular rate during atrial fibrillation from 148 +/- 14/min to 112 +/- 12/min (p less than 0.05). Sotalol exhibited a depressant effect on all parts of the reentrant circuit: atrium, ventricle, AV node, and accessory pathway. Thus, sotalol is effective in the therapy of patients with recurrent supraventricular tachycardias.     

Aberrant atrioventricular conduction in a patient with paroxysmal tachycardia,a short P-R interval and a normal QRS complex

A case of anomalous atrioventricular conduction is described which does not conform to the usual criteria.A mechanism is suggested to explain the observed phenomena.     

Intermittent AV conduction disturbances in patients with AV nodal bypass tracts. Possible mechanisms of unusual variant of tachycardia-bradycardia syndrome.

His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent AV conduction disturbances occurring below the site from which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent AV block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachcardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block.     

Slow pathway ablation in patients with atrioventricular node reentrant tachycardia and a prolonged PR interval

Objectives. We sought to assess the safety and efficacy of selective slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with a prolonged PR interval and atrioventricular (AV) node reentrant tachycardia.Background. Although both fast and slow AV node pathways can be ablated in patients with AV node reentrant tachycardia, slow pathway ablation, by obviating the risk of AV block, appears to be safer. However, the safety and efficacy of selective slow pathway ablation using transcatheter radiofrequency energy in patients with a prolonged PR interval during sinus rhythm are unclear.Methods. The seven study patients with a prolonged PR interval (mean ± SD 237 ± 26 ms) comprised three women and four men with a mean age of 31 ± 15 years. The slow pathway was targeted in all seven patients at the posterior/inferior interatrial septal aspect of the tricuspid annulus. Two patients presented with the uncommon variety of AV node reentrant tachycardia after initial fast pathway ablation; in the remaining five patients, the AV node reentrant tachycardia was of the common variety.Results. A single radiofrequency pulse at 30 W successfully abolished the slow pathway in both the anterograde and the retrograde direction in the two patients with uncommon AV node reentrant tachycardia. A mean of 5 ± 3 radiofrequency pulses were required in the remaining five patients with reentrant tachycardia of the common variety. The postablation PR interval and AH interval remained unchanged. The shortest cycle length of 1:1 AV conduction was prolonged significantly (from 327 ± 31 to 440 ± 59 ms, p < 0.01, as was the AV node effective refractory period (from 244 ± 35 to 344 ± 43 ms, p < 0.01). During a mean follow-up interval of 20 ± 6 months, no patient developed symptoms suggestive of AV node reentrant tachycardia or had evidence of second- or third-degree AV block.Conclusions. These data suggest that the AV node slow pathway can be ablated in patients with AV node reentrant tachycardia who demonstrate a prolonged PR interval during sinus rhythm.     

Familial occurrence of sinus bradycardia, short PR interval, intraventricular conduction defects, recurrent supraventricular tachycardia, and cardiomegaly.

Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.     

Prolonged PR interval despite a programmed short sensed AV delay: the role of intra-atrial conduction time.

Intracavitary electrogram (IEGM) is a useful tool in the interpretation of difficult pacemaker electrograms. A case of 320 ms P-V spike interval on the surface ECG despite a 110 ms programmed sensed AV delay is presented. Atrial IEGM revealed atrial tachycardia with a significant atrial conduction delay.     

短P—R综合征合并室上性心动过速的电生理观察

为探讨短Ｐ－Ｒ综合征合并室上性心动过速的电生理机制,对７例短Ｐ－Ｒ综合征合并室上性心动过速的患者进行心内电生理检查。结果发现：随着心房负扫描程序刺激,６例Ａ－Ｈ间期逐渐延长,１例间歇性延长,６例有Ａ－Ｈ间期跳跃现象;室上性心动过速时６例最早心房激动部位在希氏束,Ｖ－Ａ间期〈７０ｍｓ,１例在左后游离壁,Ｖ－Ａ间期〉７０ｍｓ。提示短Ｐ－Ｒ综合征合并室上性心劝过速的电生理机制是房室结加速传导合并房室结双     

Supraventricular tachycardia with PR interval shorter than RP interval. Electrogenetic mechanisms and diagnostic criteria

The Authors report their experience on the different clinical-electrocardiographic patterns of tachycardias with P'R interval shorter than RP'. The electrocardiographic criteria, in basal conditions and after autonomic stimulation, and the role of electrophysiologic study, particularly in transesophageal way, are discussed. Finally the Authors propose a noninvasive diagnostic algorithm for a correct clinical approach.