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Second-Degree Wenckebach Type AV Block Due to Block Within the Atrium'

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Second-Degree Wenckebach Type AV Block Due to Block Within the Atrium' British Heart Journal, I972, 34, II27-II36. Br Heart J: first published as 10.1136/hrt.34.11.1127 on 1 November 1972. Downloaded from Second-degree Wenckebach type AV block due to block within the atrium' Onkar S. Narula, Manfred Runge2, and Philip Samet From the Division of Cardiology, Department of Internal Medicine, Mount Sinai Hospital of Greater Miami, Miami Beach, Florida, and the University of Miami, School of Medicine, Miami, Florida, U.S.A. Two patients with a history of paroxysmal supraventricular tachycardia were analysed by His bundle and intra-atrial recordings. The electrocardiogram showed sinus bradycardia in I patient and sinus bradycardia with sino-atrial Wenckebach in the other. The conduction times through the A V node and His Purkinje system were normal in both cases. The intra-atrial conduction time was slightly prolonged (55 msec) in one and normal (40 msec) in the other during normal sinus rhythm. In both cases with atrial pacing from high right atrium, the conduction time from the pacing impulse (PI) to atrial activation in the area of the A Vjunction (PI-A) progressively lengthened with increase in atrial pacing rate and finally classical second-degree Wenckebach type of block was manifested at cycle lengths of 460 and 465 msec. The pacing impulse to QRS interval (PI-R) showed a progressive increase before the blocked stimulus. The lengthening of the PI-R interval was due to progressive increase in the intra-atrial (PI-A) conduction copyright. time. In the dropped beats, thepacing impulse was notfollowed by an A deflection. This observation indicated Type I block within the atrium. Similarly, during induced premature atrial beats, the PI-A time progressively lengthened as the coupling interval was shortened. These findings were reproducible and were seen despite a fourfold increase in stimulus strength and changes in electrodes and site of stimulation along the lateral right atrial border. This study (I) shows second-degree Wenckebach block within the atrium; (2) supports the existence of sinoatrial http://heart.bmj.com/ Wenckebach; and (3) suggests the atrium as another possible site for re-entry and a cause for supraventricular tachycardia because of the degree of delay and block exhibited within the atrium. It is well known that block during impulse I967; Narula and Samet, I970). In contrast, transmission may occur at any site where a Wenckebach type (Mobitz I) of AV block is difference in functional refractory period is generally considered to occur in the AV present or where decremental conduction node. Recent reports have also shown that occurs (Hoffman and Cranefield, I960; the Wenckebach type of block may be ob- on September 23, 2021 by guest. Protected Cranefield, Hoffnan, and de Carvalho, 1959; served within the His bundle and bundle- Cranefield, Klein, and HofEnan, I971; branches (Narula and Samet, I970; Puech Singer, Lazzara, and Hoffman, I967). Mobitz et al., 1970). Intra-atrial conduction defects (I924) first defined the electrocardiographic have been known to cause first-degree AV criteria for the two types of second-degree block (Katz and Pick, I956; Narula et al., atrioventricular (AV) block (Type I and II). 197I). Though second-degree block within The Type II block, commonly known as the atrium has been previously proposed, it Mobitz II, has been clinically and experi- has not been documented (Phibbs, I963). mentally localized to the His-Purkinje system The purpose of this study is to present the (Donoso, Adler, and Friedberg, I964; Kauf- electrophysiological data in 2 patients who man et al., I96I; Watanabe and Dreifus, manifested the typical Wenckebach AV block secondary to blocked P waves within the Received 28 February I972. atrium itself, i.e. proximal to the AV 1 This report was presented at the 2Ist Annual Scien- node. tific Session of the American College of Cardiology, It is also shown that in these 2 cases, the I-5 March I972, Chicago, Illinois. intra-atrial conduction time was rate-depen- 2 Present address: First Medical Clinic, University of dent and progressively increased with in- Hamburg, Hamburg 20, West Germany. crease in rate. The evidence further shows II28 Narula, Runge, and Samet Br Heart J: first published as 10.1136/hrt.34.11.1127 on 1 November 1972. Downloaded from some of the potential inherent fallacies of normal axis. The next day, the ventricular rate arrhythmia interpretations based solely on was 95 a minute after digitalis therapy. Two days the duration of the PR interval in the surface after admission, an electrocardiogram revealed sinus bradycardia (45 a minute). The PR inter- electrocardiogram. val was o-i8 sec and the QRS complex remained unchanged (Fig. I, 22 April 197I). On the sixth hospital day, a cardiac conduction study was performed to help guide future drug Case reports or possible pacing therapy. His bundle recordings Case I A 69-year-old white woman was ad- and sinus node recovery time were obtained as mitted because of tachycardia. At the age of 17, described previously (Narula et al., 1970; Narula, she was told she had a heart murmur. Episodes Samet, and Javier, 1972). During the study, the of palpitations, first noted at age 52, were con- sinus cycle length ranged from I250 to I400 trolled by quinidine administration. Digoxin msec. The PR interval was I75 msec. The con- (0-25 mg daily) was started at 6i because of trol conduction times through the AV node exertional dyspnoea. Three weeks before admis- (A-H) and His Purkinje system were 75 and 45 sion, she stopped digitalis and quinidine therapy, msec, respectively. The conduction time through whereupon recurrent tachycardias developed. the atrium was slightly prolonged (55 msec) and On examination, she exhibited the typical find- suggested intra-atrial conduction delay. This was ings of mitral insufficiency and stenosis. X-ray further confirmed during induced premature atrial examination revealed cardiomegaly with left beats and atrial pacing with 2 msec pulse dura- atrial enlargement and calcified mitral valve tion. During premature atrial beats, the con- leaflets. The clinical impression was rheumatic duction time from the pacing impulse in the high heart disease, cardiomegaly, mitral stenosis and right atrium to atrial (A2) activation in the area insufficiency, pulmonary hypertension, and par- of the AV junction progressively lengthened oxysmal supraventricular tachycardia, Class II-C. (from go to i6o msec) with increase in prematurity The electrocardiogram on admission (Fig. I, of the premature atrial beats (Fig. 2, Panel A to 20 April I971) showed supraventricular tachy- D). The absolute atrial refractory period, as cardia (probably atrial tachycardia with 2: I AV measured by induced premature atrial beats at I minute. The double the diastolic threshold was 425 msec block) with a ventricular rate of I5 a copyright. QRS complex was o0og sec in duration with a (Fig. 2, Panel E). FIG. I Case i. Rhythm strip (20 April 1971) shows supraventricular tachycardia which is followed by normal sinus rhythm 2 days later (22 April 197I). The I2 standard electrocardiogram leads are shown below. 4/20/71 http://heart.bmj.com/ -.. ..- lI l.. ..-. l ' ...lj;lll ll;l B||l;4 ~ ~ ~ _~ ~ ~ ~. .. ... .. ....._-... ... b 4/22/71 on September 23, 2021 by guest. Protected 1-1'0 1 t 1 - ' 1 1 1 1 1 - 1'1 1 1-~~~~~~~~....01'~~~~~1.11:-'1:'1'1':'1'.'1'11'1'1 1'1: .1''1'''1-1'1.'11''.1.'1.'-1.'..1.'1'1 1 I LlblA;~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~. .. .. s l l l l ! - W : 1 L-3L-3L--Llil~~~~~~~~~~~..~~~~~~~~~~~. 4;Xlt lll111 111IWL L-1~~~~~~~~~~~~~~~~~~~~~~L-2L-3:aVR aVL:aV , ~~~v ~~~~~~~~~~~~~~~~~~~~~~~~~ Second-degree Wenckebach type AV block due to block within the atrium 1129 Br Heart J: first published as 10.1136/hrt.34.11.1127 on 1 November 1972. Downloaded from L-1 Al ! ~ A2? A3 A-A 1435 msec :.. 1230 p1 .l.l 1490 . -e- i1 IJ B Al-Pt 1130 msec Pt-A2 100 misc I A IV A 1410 S;H; 840 tpi 1460 mAi: t ;1 1Al.Pt740 msec C Pl 0C2I1.ms*c A3 A.A 1350 msec Al ) 625 t1. I.1 -*'ri 01Ai.r;Ii465 mselc D Pt-A2 160 ms.c 1 copyright. ;' Al1 AlI Al5 1270 Pi 1260 J /i1505 fW.t r f n;-r %! I I l.1 E Al-Pi 425mse http://heart.bmj.com/ FI G. 2 Case i. Effect ofprematuirity ofpremature atrial beats on the pacing impulse (PI) to atrial (A) activation (PI-A) time. (A-D) Simultaneous bipolar (BE) recordingsfrom the area of the A Vjunction (BH) with standard electrocardiogram lead I. During induced premature atrial beats, as the coupling interval (Ai-PI) was shortened froM 1220 to 465 msec, the PI to premature atrial activation (A2) in the area of the A Vjunction (PI-A2) time progressively on September 23, 2021 by guest. Protected lengthened from 90 msec (Panel A) to i6o msec (Panel D). (E) A more premature stimulus (PI) at a coupling interval (AI-PI) of 425 msec showed absolute refractoriness of the atrium. A = Atrial electrogram during normal sinus rhythm. A2 = Atrial electrogram during induced premature atrial beats. BH= Bipolar His bundle electrogram. V= Ventricular activation recorded from the area of the AVjunction. Time lines in this and subsequent Figures = sec. During atrial pacing, the PR interval progres- plex was blocked and the pacing impulse (PI) was sively lengthened with increase in rate (cycle not followed by an A wave (Fig. 4). The lengthen- length from 1000 to 530 msec) (Fig. 3). The latter ing of the pacing impulse-atrial time was not pro- PR interval prolongation was caused by a gressive though it increased from I05 to 330 lengthening of the pacing impulse-atrial (PI-A) msec preceding the dropped beat.
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