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49. 50.

51. 52.

Pearson G: Environmental factors in hypertension. In, The Epidemiology of Hypertension. Proceedings of an International Symposium, edited by Stamler J, Stamler R, Pullman TN. New York, Grune & Stratton, 1967, pp 269-271 Miall WE: Follow-up study of arterial pressure in the population of a Welsh mining valley. Br Mod J 2: 1205, 1959 Dole VP, Dahl LD, Cotzias GC, Dziewiatkowski DD, Harris C: Dietary treatment of hypertension. II. Sodium depletion as related to therapeutic effect. J Clin Invest 30: 584, 1951 Corcoran AC, Taylor RD, Page IH: Controlled observations on the effect of low sodium dietotherapy in essential hypertension. Circulation 3: 1, 1951 Sasaki N: The relationship of salt intake to hypertension in the Japanese. Geriatrics 19: 735, 1964

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53. Laragh JD, Baer L, Brunner HR, Buhler FR, Sealey JE, Vaughan ED Jr: The renin-angiotensin-aldosterone system in pathogenesis and management of hypertensive vascular disease. In, Hypertension Manual, edited by Laragh JH. New York, Yorke Medical Books, 1973, pp 313-351 54. Padfield PL, Broun JJ, Lever AF, Scalekamp MAD, Beevers DG, Davies DL, Robertson JIS, Tree M: Is low-renin hypertension a stage in the development of essential hypertension or a diagnostic entity? Lancet 1: 548, 1975 55. Bourgorgnie JJ, Catanzaro FJ, Perry HM Jr: Renin-angiotensinaldosterone system during chronic thiazide therapy of benign hypertension. Circulation 37: 27, 1968 56. Ueda H, Kaneko Y, Takeda T, Ikeda T, Yagi S: Observations on the mechanism of renin release by hydralazine in hypertensive patients. Circ Res 27 (suppl II): 11-201, 1970

Second Degree Block During Reciprocal Atrioventricular Nodal Tachycardia HEIN J. J. WELLENS,

M.D.,

JAN C. WESDORP, M.D., DONALD R. DOREN, AND K. I. LIE, M.D.

M.D.,

SUMMARY Of 67 patients with reciprocal atrioventricular (A-V) nodal tachyeardia consecutively studied by programmed electrical stimulation of the heart, nine patients showed second degree block toward the ventricle and one patient toward the atrium during tachycardia. In four patients the occurrence of block was critically related to the prematurity of the test stimulus initiating the tachycardia. In three patients block developed following increase in rate of tachycar-

dia. In two patients block could be elicited by introducing premature ventricular stimuli during tachycardia. Our observations indicate that different mechanisms may be responsible for second degree block during reciprocal supraventricuiar tachycardia. The finding of second degree block during reciprocal supraventricular tachycardia excludes a tachycardia with A-V conduction over the A-V node - His pathway and V-A conduction over an accessory A-V pathway.

ONLY A FEW EXAMPLES of second degree block during reciprocal atrioventricular (A-V) nodal tachycardia have been reported in the literature.`8 To determine the incidence and to study the mechanism of block, data were reviewed from 76 patients, in whom during programmed electrical stimulation of the heart a reproducible tachycardia could be initiated and terminated by appropriately timed premature beats. Signs of pre-excitation were not present in these patients during sinus rhythm and/or atrial pacing. All showed initiation of tachycardia following a critical delay in A-V nodal transmission time and a low-high sequence of atrial activation during tachycardia. Application of the criteria given elsewhere9 for differentiation between a tachycardia circuit confined to the A-V node and a tachycardia circuit using an accessory A-V pathway suggested that in nine patients an accessory A-V pathway only conducting in the retrograde direction participated in the tachycardia circuit. During electrically-induced tachycardia episodes of second-degree block either toward the ventricle (7 patients) or toward the atrium (1 patient) were demonstrated in eight of the remaining 67 patients in whom the tachycardia circuit was thought to be confined to the A-V

node. In two more patients persistence of tachycardia could be demonstrated in spite of block distal to the bundle of His, provoked by giving two closely spaced ventricular premature beats during tachycardia.

From the University Department of Cardiology, Wilhelmina Gasthuis, Amsterdam, The Netherlands. Address for reprints: Hein J. J. Wellens, M.D., University Department of Cardiology, Wilhelmina Gasthuis, Eerste Helmersstraat 104, Amsterdam, The Netherlands. Received September 29, 1975; revision accepted for publication November 13, 1975.

Material and Methods Characteristics of the ten patients reported are given in table 1. None of the patients were receiving medication at the time of study. Following informed consent all were studied in the nonabsorptive state. Initiation of tachycardia was studied by means of the single test stimulus method during atrial and ventricular pacing and by regular pacing of atrium and ventricle at increasing frequencies. With the help of the synchronizing circuit of our stimulator, the effect of timed atrial and ventricular stimuli on the time relations during tachycardia and termination of tachycardia was subsequently studied. A description of the stimulator employed has been given previously.9 Simultaneous recordings were made of leads I, II, III, V,, and V6, an intracavitary high right atrial lead and a His bundle electrogram.'0 All data were stored on magnetic tape using an Ampex FR 1300 recorder. The figures presented here show only those leads considered to be relevant. Results The reproducible initiation and termination of tachycardia by critically timed premature beats strongly suggested re-entry as the underlying mechanism"' for tachycardia in

596

VOL. 53, No. 4, APRIL 1976

CI RCU LATION TALEiV 1. Clinical Data and Findlings Obtainedlduring Programmecd Elcr ieatl Stimu lation It- R interval

Pt/Age/Sex Init of T. 1 APB A8/75/M 1 APB B,37/23/F 1 APIH C7/42/M 1 APB 1)6 /28 / I APBI EF/27/F 1 APB F/20/M 1 APB GT/34/M 11 48/ M 1 APB 1 APB I/41 /F J/86 1\1I APB, I VPlB

(msec)

Site oi dluek A-V-node-Hlls Ilis or dist-:al A-V-node-Illis lis or1 dist.al A-V-niodle-Ilis IIs or distal Ills or distal. A- V-node-Atriulm Ilis or distal Ills ol distial

83(0(1( 260 820 295 8(00 235-260 280

270 38.-5 29(

i'atientt A. ti, C andi I) fiave been reported previously. Ablres atins: Pt initiation; I patient; iit tachy eardia; R-It intersal termnination; APB atrial prematuLre beat; VPS ventricular premature beat. =

=

=

=

=

Tferm of T. 2 APB, 2 VPB 2 VPB 2 APB, 2 VPB 2 VPB 2 VPB 8 APB, 2 VPB 2 APIS, 2 VP13 8 AIPB, 2 VPB 2 VPMI 2 VPB

atluring T at time of ilock; Terrn interal

=

our patients. Application of criteria given elsewhere8 pointed to the A-V node as the site of the re-entry circuit.

the atrium) resulted in tachycardia with always a 2 to 1 relation between atrial and ventricular activation. This patient, who has been described previously,7 showed a gap in A-V conduction in the premature beat interval range 390 to 300 msec. In four patients (patients A, D, F, and G) the development of block during tachycardia depended upon the timing of the tachycardia initiating atrial premature beat. A typical example is given in figures 1 and 2. During atrial pacing with a basic cycle length of 600 msec, atrial premature beats at a range of coupling intervals of 290 to 240 msec resulted in tachycardia with a I to 1 relation between atrial and ventricular activation (fig. 1, top). Atrial premature beats given

Initiation of Tachyeardia and Development of Block During Tachyeardia

In nine of the ten patients tachycardia could be initiated only by a single atrial premature beat during atrial pacing, not by ventricular stimuli during ventricular pacing (table I); in the remaining patient both an atrial and a ventricular premature beat produced the rhythm. In one patient (patient C) atrial premature beats given in the interval range 290 to 260 msec (the refractory period of

Ill

,--,!A

RA

His~

H

A

A

A

k

H

H

H

~~H

H

H

H

FIGURE 1. Patient F. Top panel) Initialion of tachycardia by a single atrial premature beat given after 290 msec during atrial pacing with a basic cycle length of 600 msec. During tachycardia a I to I relation between atrial and ventricular activation is present. Lower panel) An atrial premature beat given after 200 msec is followed by tachycardia showing a 2 to I relation between atrial and ventricular activation. The His bundle recording shows that the site of 2 to I block was either in the bundle of His distal to the recording site, or more distally in the bundle branch system. Note that during tachycardia alternation in cycle duration between subsequent His bundle activation is present, and that the atrial rate during tachycardia in the lower panel is higher than in the top panel.

V6 atrium 1 AVnode His

290

600

360

2701

275 1 275

a

l

600

370

600

ventricle

275 275

270

370

270

370

1255

275

275

III RA

His

HF

H

VI V6 atrium AVnode

600

12001

235

260

240

255

1245

0c

His

600

ventricle

600

400

|

400

255

235

490

260

240

500

255

245

490

BLOCK DURING RECIPROCAL TACHYCARDIA/ Wellens et al.

RA

----A

_

Ir

I,-

A

A

R~~~~~~~~~I

A

FIGURE 2. Same patient as figure 1. An atrial premature beat given after 230 msec initiates a tachycardia showing a Wenckebach type of second degree block between the bundle of His and the ventricle. This is followed by a 2 to I block between bundle of His and ventricle. The configuration of the QRS complexes during the Wenckebach sequence supports a localization of the conduction delay in the fascicles of the left bundle branch. The His spike of the complex which blocks proximal to the ventricle is probably lost within the preceding ventricular electrogram.

H i S S; %, ^ ^1

HT

H

1230

300

H

HHE

HH

Vi V6 600 atrium AVnode 43ix 600 His

ventricle

230 240 250

270

230 25

/3X 370

370

600

23

270

270

250

240 20

290

230 250

480

in the interval range 220 to 200 msec however initiated a tachycardia showing a 2 to I relation between atrial and ventricular activation (lower part of fig. 1). Atrial premature beats given in the interval range 240 to 220 initiated a tachycardia showing a Wenckebach second degree block in the His-Purkinje system distal to the site of His bundle recording (fig. 2). In all four patients premature beats given up to a certain interval initiated a tachycardia with a 1 to 1 relation between atrial and ventricular activation, while premature beats given at shorter intervals resulted in tachycardia with block. As shown in figure 1 when second degree block occurred during tachycardia, the atrial rate during tachycardia was always higher than in the absence of block.

A

A

His

HH

H.H

'A

In three patients (B, E, and H) the tachycardia, which was initiated by a single atrial premature beat always showed at first a 1 to 1 relation between atrial and ventricular activation, to be followed, 15 to 60 beats later, by the sudden development of 2 to I block. An example is given in figure 3. Site of Block

The table lists the most likely site of block in our patients. As shown, in four patients block was located distal to the site of the catheter recording from the His bundle, suggesting either block within the bundle of His or block distal to the bundle of His. In three patients block was located in the A-V node. In one patient (patient H) the location of 2 to I V-A block during tachycardia was either between the

A

A

HH

H

H

FIGcURE 3. Patient H. Top panel) Initiation of tachycardia by an atrial premature beat given after 260 msec during atrial pacing with a basic cycle length of 600 msec. There is a I to I relation between atrial and ventricular activation during tachycardia. Lower panel) Following increase in rate of tachycardia, 2 to 1 block developed between the site of re-entry circuit and the atrium. The most likely site of block is either the A-V node, above the re-entry circuit or between the

atrium

AVnode His

ventricle 11

< His

_t

Z

540

i

2''

Second degree block during reciprocal atrioventricular nodal tachycardia.

Of 67 patients with reciprocal atrioventricular (A-V) nodal tachycardia consecutively studied by programmed electrical stimulation of the heart, nine ...
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