Sinus node echoes and concealed concealed conduction: Additional sinus node phenomena confirmed in man by direct sinus node electrography

J. ELECTROCARDIOLOGY 18 (3), 1985, 259-266

Sinus Node Echoes and Concealed Concealed Conduction: Additional Sinus Node Phenomena Confirmed in Man by Direct Sinus Node Electrography BY JAMES A.

REIFFEL, M.D., J. TIlOMAS BIGGER, JR., M.D., KEVIN FERRICK,M.D.,

FRANK D. LIVELLI, JR., M.D., JERRY GLIKLICII, M.D., PAUL WANG, M.D. AND ROBERT BOSNER, M.D.

SUMMARY Direct sinus node electrography has been previously used to assess several aspects of sinus node physiology: sinus node pauses, overdrive suppression, sinoatrial entrance block. This report presents data in which sinus node electrograms confirm two additional physiologic phenomena in man: concealed conduction in the sinoatrial junction and sinus node reentry. These findings verify the presence of previously suspected phenomena by careful deductive analysis of electrocardiographic and electrographic tracings.

D i r e c t s i n u s n o d e e l e c t r o g r a m s (SNE) h a v e prov i d e d a m e a n s to d i r e c t l y a s s e s s in v i v o h u m a n s i n u s n o d e p h y s i o l o g y a n d p a t h o p h y s i o l o g y ~9. P r i o r to t h e i r d e v e l o p m e n t , o u r k n o w l e d g e of h u m a n s i n u s n o d e p h y s i o l o g y w a s b a s e d u p o n ext r a p o l a t i o n f r o m a n i m a l i n v e s t i g a t i o n , u p o n observ a t i o n s m a d e w i t h indirect e l e c t r o p h y s i o l o g i c a l t e c h n i q u e s or p h a r m a c o l o g i c a l m a n i p u l a t i o n , 10 or upon deductive electrocardiographic reasoning, u s u a l l y b y a n a l o g y to t h e A-V node 11. Since 1980, m a n y of t h e c o n c l u s i o n s a b o u t h u m a n s i n u s n o d a l a n d p e r i n o d a l p h y s i o l o g y d r a w n f r o m the p r e v i o u s indirect a n a l y s e s have b e e n r e - e x a m i n e d b y s t u d i e s u s i n g direct sinus n o d e recordings. T h o s e h a v e s h o w n t h a t b o t h sinus n o d e a u t o m a t i c i t y and/or s i n o a t r i a l c o n d u c t i o n m a y b e d e p r e s s e d b y overd r i v e p a c i n g or b y carotid s i n u s m a s s a g e ~. 12, t h a t sinus n o d e e n t r a n c e block m a y e x i s t in the a b s e n c e of s i n u s n o d e exit block 6, a n d t h a t s i n o a t r i a l cond u c t i o n t i m e a n d sinus cycle l e n g t h are d i r e c t l y

r e l a t e d 7. I n this report, we u s e d direct sinus n o d e recordings to elucidate two m o r e p h e n o m e n a : sinus n o d e echoes 13-2~ a n d c o n c e a l e d c o n d u c t i o n 22-2~ in the sinoatrial junction.

MATERIALS A N D M E T H O D S The observations reported herein are based upon sinus node electrograms recorded in two patients. The first patient, a 75-year-old man with syncope, aortic stenosis, and left ventricular hypertrophy, had sinus rhythm, incomplete A-V block (PR inteval 220 msec), a QRS of 120 msec, a normal QT interval, and QRST abnormalities suggesting left ventricular hypertrophy with left anterior fascicular block on electrocardiography. Electrolytes were normal, as was neurological examination. A 24-hour ambulatory electrocardiogram recording revealed no bradycardia, no second or third degree A-V block, and no tachyarrhythmias. Electrophysiological study revealed normal sinus cycle length {mean 880 msec), corrected sinus node recovery time (260 msec), atrial and A-V nodal refractory periods, P-A (25 msec) and H-V (50 msec) intervals. Mild A-V nodal conduction delay was evident: the resting A-H interval was 130 msec and A-V nodal Wenckebach occurred at an atrial paced cycle length of 500 msec. Similarly, mild sinoatrial conduction delay was evident: the resting sinoatrial conduction time was 120 msec and the PCLp was 700 msec. The second patient, a 31-year-old man with recurrent episodes of near syncope, had several 24-hour ambulatory electrocardiograms which revealed only variable sinus bradycardia (without associated symptoms), frequent atrial premature depolarizations (some blocked), and episodes of non-sustained atrial flutter with relatively slow ventricular response. Exercise testing, echocardiography, neurological evaluation, and electrolytes were normal. His electrocardiogram showed a sinus rate of 44,

From the Division of Cardiology, Department of Medicine, Columbia University, New York, New York 10032 and The Arrhythmia Control Unit, The Columba-Presbyterian Medical Center, New York, New York 10032. Supported in part by United States Public Health Service grants ttL12738 and RR00645, and the Dana Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "'advertisement" in accordance with 18 U.S.C. w solely to indicate this fact. Reprint requests to: James A. Reiffel, M.D., Department of Medicine, Columbia University, 630 West 168th Street, New York, N.Y. 10032.

259

260

REIFFEL ET AL

I

I

AVF _

|

!

_ _

!11!

Vl

"

v'---"

I

SNE/---"J I

9oo

i

87o

I I . I

atrial premature depolarizations, a PR interval of 0.23 msec, and left anterior fascicular block. On electrophysiologic study, the sinus cycle length (1250-1450 msec}, P-A interval (45 msec), corrected sinus recovery time (630 msec), PCLp (800 msec), paced atrial cycle length yielding A-V nodal Wenckebach (800 msec), and sinoatrial conduction time (see below) were all prolonged. The A-H and H-V intervals were normal. No ventricular tachyarrhythmias were induced by programmed ventricular stimulation, but non-sustained atrial flutter and sinus node echoes (see below) were induced by atrial stimulation. It is interesting to note that following parasympathetic blockade with intravenous incremental doses of atropine to a total of 4 mg, sinus cycle length, sinoatrial conduction time, sinus recovery time, and Ao V nodal response to atrial pacing all became normal. In both patients, stable, bipolar sinus node electrograras were obtained via the right femoral venous approach using our previously reported technique z. In the first patient, a second electrode catheter to be used for atrial premature stimulation was positioned in the right atrial appendage. In this patient, after direct sinus node recordings were obtained during sinus rhythm, atrial premature stimuli were placed after every eighth sinus beat using a programmable stimulator {Bloom Assoc.). The stimuli, twice diastolic threshold and two msec in duration, were moved in 20 msec intervals until all of atrial diastole was scanned. The sinus node electrogram was recorded simultaneously with body surface electrocardiograra leads I, AVF, and V1 and all were displayed on.an Electronics for Medicine VR 16 recorder and printed on photographic paper at 100 mm/msec for data processing. Premature atrial stimulation was not performed in the second patient due to the presence of frequent, spontaneous atrial premature depolarizations. His recordings were displayed and processed in the same manner as for patient number one. All measurements were made on the original tracings. However, to enhance black and white contrast for photographic presentation,

860

I

Fig. 1. Sinus node electrogram in sinus rhythm from patient number 1. ECG leads I, AVF, and V1 are recorded simultaneously with the sinus node electrogram {SNE} during sinus rhythm. A representative sinus node depolarization is denoted by the arrow. The sinus cycle lengths, in msec, are noted in the time brackets. The time pips at the bottom of the figure are at 40 {small pipsl and 200 (large pips) msec apart respectively. The unlabelled channel between V1 and the SNE is a stimulus marker channel which displays stimulation artifacts during programmed stimulation. No stimuli are present in this figure but they are displayed on this channel in Fig. 2.

the tracings were xerographically copied and then reassembled prior to photographing the figures in this manuscript.

RESULTS Figure 1 shows the SNE recorded during normal sinus r h y t h m (NSR) in the first patient. He had very little sinus arrhythmia. Note the presence and configuration of the sinus node {SN) deflection preceeding atrial activation {arrow} as well as the presence and nature of the low frequency deflections inscribed on the sinus node electrogram during the PR segments on the body surface electrocardiogram. These latter deflections occur in each cycle, and have a constant configuration. I t is unikely t h a t they represent atrial depolarization extending as they do all the way to the QRS and they cannot be A-V nodal in origin in this bipolar recording over the sinoatrial junction. They almost certainly represent atrial repolarization, a phenomenon which is known to be visualzed on the sinus node electrogram s at this location in the cardiac cycle. The constancy of configuration in both sinus node depolarization and atrial repolarization should be compared to the findings in Fig. 2. Note also the prolonged sinoatrial conduction time of 140 msec. Fig. 2 shows responses to p r e m a t u r e atrial stimuli in the first patient. From panel 1 to panel 3 the induced atrial premature depolarization is placed progressively more prematurely. In panel 1 the atrial premature depolarization (A2} has a coupling interval of 730 msec. It is 540 msec in panel 2 and 400 msec in panel 3. As expected, sinus node depolarizations {second arrow in each panel) follow the a t r i a l p r e m a t u r e d e p o l a r i z a t i o n s . However, several pieces of evidence suggest t h a t

J. ELECTROCARDIOLOGY 18 (3), 1985

DIRECT

i

'L_fd_.J

,

" I

1

~

, i

~

!

SINUS

NODE

~ I. i~t~_ I

ELECTROGRAPHY

~ ! A._J

I

261

~.!~

i

AvF ~ v - -

I

' ?30

I

v

~

v

',

SNE~

i |

I

'

v

~zo

I

I

:

,ooo

I.:l"

I i

I

I

I

130

,*

~o

I

~o,~

I

.o

I h.lhm],,:l."l":l::"l:l

I

-

v v'---"

I

I

]

[

I

2

AVFv v,y

1 v~- - - - - - - ' - - v ~

~

%

ezo

I

6oo

'

~

w ~

V"--'-'--

~

I

o

I

900

I

9Z0

i d., ~b~:,l I- '1" I. 'l,zllil.~L~lfl~:,l,,,hl~l[.

i l i - i

v,

~

[

[

II 11

9

i

AVF

V--

AIAt i AIAII/IO

,,o,o,,

I

v'----

"

v

v--

~,f

t

, v

v

~

; ,'1',:~

V"

V

~,

/'

SNE

I~

A~xz400

Ax%mO

'1

*

[

'

/,oo

9I i,~.l,.I

I

C,o

I !

!

I

I

"

,

I I

I

.I-i,:,1

I

I tl,.,I,l..l.,I

these post atrial premature depolarization sinus node deflections are sinus node echoes rather than spontaneous sinus node recovery. First, the atrial T wave of A2 (first arrow) is altered compared to sinus rhythm. Although this might be considered to represent a repolarization sequence alteration associated with premature depolarization, detailed evaluation of this phenomena across the panels (as is discussed below) strongly suggests that this r e p r e s e n t s s u p e r i m p o s i t i o n of r e t r o g r a d e depolarization of the sinus node 9 upon the atrial T wave and that there is cycle length dependent c o n d u c t i o n d e l a y of r e t r o g r a d e s i n u s n o d e depolarization. Second, the p o s t atrial premature depolarization sinus depolarization (second arrow) is premature and is associated with a sinoatrial conduction defect. Third, the sinoatrial cycle following A3 is prolonged. Fourth, the post atrial premature depolarization sinus node depolarization (second arrow) is fixed coupled to the atrial T wave/sinus node depolarization complex. In panel 1 the post atrial premature depolarization sinus node (second arrow) deflection occurs 590 msec following the in-

J. ELECTROCARDIOLOGY

-

1;

18 (3), 1985

l

I

I

I

',

Fig. 2. SNE from patient number 1 during atrial premature stimulation. Each of the 3 panels is laid out in identical fashion to Fig. 1. P waves, the QRS, sinus node depolarization (SN), atrial depolarization (A), and ventricular depolarization (V) are marked for clarity at the onset of panel 3. The interval from A1, the last atrial depolarization preceeding the induced APD, to the induced APD, A2, and from A2 to the next atrial depolarization, A3, are stated. See text for discussion of the figure, including the horizontal time bars and the arrows. The time pips are the same as in Fig. 1.

scription of the atrial T wave]retrograde sinus node depolarization complex indicated by the first arrow. In panel 2 it again occurs about 600 msec after the atrial T wave]retrograde sinus node depolarization complex. In panel 3 where A2 is more premature and fails to conduct to the ventricles, the sinus node depolarization indicated by the first arrow is again followed by a sinus node depolarization (second arrow) with a coupling interval of 600 msec. Hence, these post atrial premature depolarization sinus node deflections (second arrows) are fixed coupled and premature, are associated with prior atrio-sinus conduction delay, reset the sinus node, and have prolonged sinoatrial conduction. Fig. 3 shows the sinus node electrogram recorded in the second patient during sinus rhythm. He, too, had no significant sinus arrhythmia. This figure, like Fig. 1, is provided as a basis against which to compare the findings in the presence of atrial premature depolarizations (Fig. 4). Note, in Fig. 3 the marked sinus bradycardia and the extremely long sinoatrial conduction time. Fig. 4 shows the response of the sinus node to spontaneous atrial

262

R E I F F E L ET A L

I '--.-~,' LL-P " r ~

AVF __..-.. VI

~C " v 13gO

!

| 1410

1410,

i

%

-

i! i:

!

I SNE

i

A

JliJIJll.i ~[II 1! II I I I II I I ~II

i

'

1111111111

I~41,~, I, Hi

I/ 111, ,i

Fig. 3. Sinus node electrogram in sinus rhythm from patient number 2. ECG leads I, AVF, and V1 are recorded simultaneously with an SNE during sinus rhythm. The sinus node depolarizations are indicated by the heavy arrows. Dashed vertical markers intersecting the SNE recording indicate the termination of the ventricular T wave on the surface ECG. Horizontal time bars above the SNE indicate the sinus cycle length in msec (measured from onset of sinus node depolarization to onset of sinus node depolarization) and horizontal time brackets below the SNE indicate the antegrade sinoatrial conduction time (SACT) in msee. The time pips at the bottom of the figure are at 100 (small pips) and 500 (large pips) intervals apart respectively.

premature depolarizations in the second patient. In panels i and 2 the atrial premature depolarizations are single; in panel 3 two atrial premature depolarizations occur in sequence. Note t h a t in each panel, as in Fig. 2, the T wave of the atrial premature depolarization (thin arrows) is altered as compared to sinus rhythm, probably as the result of r e t r o g r a d e sinus node depolarization. 9 Also note in panels 1, 2, and 3 t h a t as in Fig. 2 the last of the atrial T wave/retrograde sinus node depolarization complexes (indicated by the thin arrows) is followed by a sinus node depolarization which is premature (second arrow) and hence cannot represent normal sinus node depolarization following interpolated atrial ectopy. These too are fixed coupled (700-740 msec) to the preceeding atrial T wave/retrograde sinus node depolarization complex. In panels 1 and 2, the premature sinus node depolarization which conducts to A3 is associated with prolongation of the sinoatrial conduction time. The findings in Fig. 4, therefore, strongly resemble the observations in Fig. 2, and thus also suggest the presence of sinus node echoes. We should note additional observations in Fig. 2, panel 3 and Fig. 4, panel 4. In contrast to panels 1 and 2 of Fig. 2, in panel 3 the post atrial premature depolarization sinus node deflection (first arrow) occurs 870 msec after the previous

sinus node depolarization, i.e., an interval within the range of the spontaneous sinus cycle lengths, and hence is "on time". Thus, in this case, A2 may be interpolated, though retrograde depolarization of the sinus node from it could coincidentally occur at this particular time. The post A2 sinus node depolarization either does not conduct to A3 or does so with a marked delay. If interpolation has occurred, the conduction delay or exit block of this post A2 sinus node depolarization which is 330 msec after A2 m u s t result from concealed conduction in the perinodal tissue due to the atrial premature depolarization. ~. ~3-~5.26-27 Similar events occur in Fig. 4, panel 4. As in Fig. 2, panel 3, the sinus node depolarization following the atrial ectopy (second arrow) is 1490 msec after the sinus node depolarization (heavy arrow) which preceeds the atrial ectopy, an interval very similar to the baseline sinus cycle length. This, too, probably r e p r e s e n t s interpolation. A less likely possibility is retrograde sinus node depolarization due to the atrial premature depolarization coincidentally occurring at this time. As in Fig. 2, panel 3, the sinus node depolarization following A2 conducts to the atria with a prolonged sinoatrial conduction time--now 1180 msec--probably the result of concealed conduction in the sinoatrial junction from the last atrial premature depolarization.

J. E L E C T R O C A R D I O L O G Y 18 (3), 1985

DIRECT SINUS NODE ELECTROGRAPHY

263

1

I j s~-~ \

i

,

.

AVF%------Yi~/

-

20OO

I

920 I

74Q

l

!!

I

IL L~

AIA 2 590

,NE\ L

I

,;

a A oo

llliJ.rlll

Fig. 4a

2

,~-~--~.~, / ' ~ " . .

I AVF

t

,

Vl 2070

~1-% ~ I

i'

910

i ;: AIA 2 570

t----J~

I

700

I SNE ..,/-,~

j

I 550 I ~ l:,i.,lI I I Fig. 4b

~ j

IJl

3

2100

1320

I AIA 2 480

';11

I

I

1070

700

I

)~ iIi i ~t IV~ i 1II,II~ l l l I I l

Fig. 4c

J. ELECTROCARDIOLOGY 18 (3), 1985

Fig. 4. SNE from patient 2 during periods of atrial ectopy. The figure consists of 4 panels recorded during the presence of spontaneous atrial premature depolarization (APD), each of which is laid out in identical fashion to figure 3. The first (heavy) arrow in each panel indicates the last sinus node depolarization prior to any APD. Panels 1 and 2 (Figs. 4a and 4b)were recorded when sinus rhythm was perturbed by isolated APDs; panels 3 and 4 (Figs. 4c and 4d) were recorded when sinus rhythm was perturbed by pairs of APDs. All intervals are in msec. See text for further discussion. The time pips are the same as in figure 3.

264

REIFFEL ET AL

4 q' 'L-z-4"~

,_'/

~

--

, , "

D

!

~_._J~...--

----%,

1490

!

AIA 2 520

11 !

500

I

I I I I I I Jl

..I

.IV41.4.

4.I.I I!

I:

I ]

Fig. 4d

DISCUSSION

As suggested above, the observations made in Figs. 2 and 4 are best accounted for by retrograde sinoatrial conduction and sinus node reentry. 13-2~ Some also indicate the likelihood of concealed conduction 22-25in the sinoatrial junction ~. 13-~5.26-27 Two reasonable explanations are possible for the deflection occurring between the atrial premature depolarization and its associated QRS: (1) altered atrial repolarization, and (2) retrograde sinus node depolarization. Although an altered sequence of atrial repolarization due to premature depolarization might explain the difference when the atrial premature depolarization is compared to sinus rhythm, it alone probably does not explain the change from panel 1 to panel 2 to panel 3 in Fig. 2. One might argue that the longer PR interval of A2 in panel 2 (320 msec) as compared to panel 1 (280 msec) could allow more atrial repolarization to be visible prior to inscription of the QRS, and thus allow the waveform to appear different. However, careful examination of the three panels in Fig. 2 will reveal that the configurational changes are not simply the result of moving the QRS away from the atrial depolarization {panel 2) or loss of the QRS (panel 3). A second and more like~ ly explanation for this waveform is depolarization of the sinus node following the atrial premature depolarization ~ superimposed on the atrial T wave. The difference between panel 1 and panel 2 would again have to be accounted for, at least in part, by facilitated visibility due to the prolonged PR interval. However, the progressive delay from atrial depolarization to the onset of this waveform's inscription from panel 1 (140 msec) to panel 2 (180

msec) to panel 3 (330 msec) is the cycle length behavior that is expected to occur in the sinoatrial junction as the coupling interval of the atrial premature depolarizations are shortened, 9, ~7-zs and would be u n e x p e c t e d for atrial T wave. Although one cannot decide with absolute certainty between the two explanations, the cycle length related changes in both configuration and coupling interval strongly suggest to us that sinus node depolarization simultaneous with atrial repolarization is the more likely explanation for this complex waveform. As above, we shall therefore continue to refer to it below as atrial T wave/retrograde sinus node depolarization complex.

Sinus Node Echoes

Due to the minimal variation in spontaneous sinus cycle lengths present in each patient (see the basic sinus cycles in Figs. 1-4), it is clear that the sinus node depolarizations which initiates A3 is displaced prematurely in time in panels 1 and 2 of Fig. 2, and in panels 1 through 3 of Fig. 4. The sinus node depolarization are much earlier than anticipated following either non-interpolated or interpolated atrial premature depolarizations, whether or not the atrial premature depolarization reset the sinus node pacemaker, l0 The prematurity is evident whether or not one believes retrograde sinus node depolarization associated with the atrial premature depolarization is present and thus whether one determines the timing of the sinus node depolarization initiating A3 from the onset of A2 or from the atrial T wave/retrograde sinus node depolarization complex. This suggests that the sinus node depolarizations which initiate A3

J. ELECTROCARDIOLOGY 18 (3), 1985

DIRECT SINUS NODE ELECTROGRAPHY

must result from the preceeding atrial premature depolarization. Other evidence suggesting that these are sinus node echoes '3'' includes: the fixed coupling interval between the sinus node deflections and the preceeding retrograde sinus node depolarization (approximately 600 msec in Fig. 2 and 700 msec in Fig. 4), the retrograde conduction delay from the atrial premature depolarization into the sinus node preceeding the echo '3'6. "~ (140 and 180 msec in Fig. 2 for example), and the prolongation of the sinus cycle length following A3 {shown in Fig. 2). Additional evidence for sinus node echos are the specific coupling intervals of 600 and 700 msec in Fig. 2 and 4. These coupling intervals are typical of those seen in sinus node echoes studied by indirect techniques and of the cycle lengths of the sinus nodal reentrant paroxysmal supraventricular tachycardia. ~32' The presence of one or two premature complexes rather than sustained paroxysmal supraventricular tachycardia is also typical of sinus node reentry as determined by indirect methodsY ~ Although retrograde conduction is prolonged in the second patient, note that it is faster than antegrade sinoatrial conduction. Although this may be unusual, it is in keeping with behavior seen in the A-V node in some patients who conduct with different conduction velocities and/or over different AV nodal pathways in the antegrade and retrograde directionY9 Specifically, it resembles patients with high grade antegrade AV nodal block but normal retrograde conduction or those patients with dual AV nodal pathways which are functionally important in the genesis of paroxysmal supraventricular tachycardia?~ Concealed Conduction The observations made in Fig. 2, panel 3 and Fig. 4, panel 4 strongly suggest concealed conduction. That is, there is antegrade conduction delay in the cycle following an i n t e r p o l a t e d p r e m a t u r e depolarization. This resembles behavior at the AV node following v e n t r i c u l a r p r e m a t u r e depolarizations22. 23. In Fig. 2, panel 3 the sinus node depolarization (second arrow), which follows the development of impaired conduction in the sinoatrial junction, is premature and, as the other panel previously discussed, appears to represent a sinus node echo in which the conduction alteration is important in its genesis. '3'6' 2~ In Fig. 4 panel 4 the post interpolation conduction delay is marked. There is evidence suggesting that the sinus node potential following the last atrial premature depolarization in this panel is in

J. ELECTROCARDIOLOGY 18 (3), 1985

265

fact conducting to the atria and that the atrial depolarization is not an escape complex. The evidence is that the configuration of both the atrial e l e c t r o g r a m and the P wave in the three orthogonal leads is identical to that present in sinus rhythm before the atrial premature depolarizations. Although dramatic, by analogy to that which has been reported at the A-V node,3', this long conduction time (1180 msec) is not impossible. The sinoatrial conduction delay must be an effect of the atrial premature depolarizations and, therefore, appears to indicate concealed conduction. In light of this long sinoatrial conduction time, we might briefly reexamine panel 3 of Fig. 4. Although in panel 3 the apparent sinoatrial conduction time of the sinus node echo is 495 msec, the baseline sinoatrial conduction time of greater than 500 msec and the sinoatrial conduction time following sinus node echo of 600 msec or more in panels 1 and 2 as well as the data from panel 4 suggest that it is possible that the preceeding sinus node depolarization {second thin arrow} rather than the echo (terminal heavy arrow) is actually the one which conducts to A3 with prolonged sinoatrial conduction time due to concealed conduction from the preceeding atrial ectopy. In any case, since neither the r e t r o g r a d e c o n d u c t i o n from the atrial premature depolarizations to the sinus node nor the prolonged sinoatrial conduction time demonstrated above can be seen on the body surface electrocardiogram in any of these panels of Figs. 2 or 4, the type of concealed conduction they represent might be t e r m e d concealed concealed sinoatrial conduction. Conclusions The sinus node electrograms recorded in these patients provide direct evidence for sinus node reentry and concealed conduction in the sinoatrial junction in man. These two phenomena have been previously assumed to occur in man and have been demonstrated directly in previous studies in animal models. Their confirmation in man not only further solidifies the apparent similarities between the human sinus and A-V nodes but also provides additional documentation of the utility of the sinus node electrogram in advancing our understanding of human sinus node physiology. 1-7.,or, REFERENCES 1. REIFFEL,J A, GANG,E S, GLIKLICII,J I, "~VEIsS,M B, DAvis JC, PATTONJN ASD BIGGER,J T, JR: The human sinus node electrogram: A transvenous catheter technique and a comparison of directly measured and indirectly estimated sinoatrial con-

266

2.

3.

4.

5.

6.

T.

8.

9

10. II.

12.

13.

14.

15.

16.

REIFFEL ET AL duction time in adults. Circulation 62:1324, 1980 GOMES,J A, KANG,P S ANDEL'SUERIF, N: The sinus node electrogram in patients with and without sick sinus syndrome: Techniques and correlation between directly measured and indirectly estimated sinoatrial conduction time- Circulation 66:864, 1982 CASTILI.O-FENOY,A, THEBOUT,J F, ACnARD, F AND DELANGENI1AGEN, B: Identifcation du potential sinusal par electrocardiographic endocavitaire chez l'homme: Criteres d'identifications, r e s u l t a t s preliminaires. Arch Mal Coeur, 72:948, 1979 HARIMAN,R J, KRONGRAD,E, BOXER, R A, WEISS, M B, STEEG, C N, ANn HOFFMAN, B D: Method for recording electrical activity of the sinoatrial node and automatic atrial foci during cardiac catheterization in human subjects. Am J Cardio145:775, 1980 ASSEMAN, P, BERZiN, B, DESREY, D, DURAND, P, DELMOTTE, C AND LEKIEFFRE, J: Persistant sinus nodal electrograms during abnormally prolonged post pacing atrial pauses in human sick sinus syndrome: Sinoatrial block versus overdrive suppression. (Abstr) Circulation 64:IV-298, 1981 REIFFEL, J A, GANG, B S, LIVELLI, F D, JR, GLIKLICH,J I ANDBIGGER, J T, Jm Clinical and electrophysiologic characteristics of sinoatrial entrance block evaluated by direct sinus node electrography. A m Heart J 102:1011, 1981 REIFFEL,J A, GANG,E, LIVEI.L1,F D, JR, GLIKLICIi, J, AND BIGGER, J T, Jm Relationships between sinoatrial conduction time and sinus cycle length revisited. (Abstr) Am J Cardiol 49:909, 1982 REIFFEL, J A ANn BIGGER, J T, JR." Current status of direct recordings of the sinus node electrogram. PACE, 6:1143, 1983 CRAMER,M, SIEGAL, M, BIGGER, J T, JR AND HOFFMAN, B F: Characteristics of extracellular potentials recorded from the sinoatrial pacemaker of the rabbit. Circ Res 41:292, 1977 BIGGER, J T, JR AND REIFFEL, J A: The sick sinus syndrome. Ann Rev Med 30:91, 1979 LANGENDORF,R, LESSER,M, PLOTKIN,P ANDLEVIN, B: Atrial parasystole with interpolation. Observation on prolongedsinoatrial conduction. Am Heart J 63:649, 1962 GOMES, J A, CIlOWDIlRY, I, HARIMAN, R AND ELSnERIF, N: New application of direct sinus node recording in man: assessment of sinus node recovery time. J Am Coll Cardiol 1:635, 1983 DUINGRA, R C, WYNDIIAM, C, AMAT-Y-LEoN, F, DENES, P, Wu, D AN[) ROSEN, K: Sinus nodal responses to atrial extra stimuli in patients without apparent sinus node disease. Am J Cardiol 36:445, 1975 CIIII.DERS,R ~V,ARNSDORF,M F ANDFUENTE, D J D: Sinus nodalechoes:clinical case report and canine studies. Am J Cardiol 31:220, 1973 BONKE, F I M, BOUMAN, L N ANDSCIIOPMAN,F T G: Effect of an early atrial premature beat on activity of the sinoatrial node and atrial rhythm in the rabbit. Circ Res 29:704, 1971 PAULAY,K L, VARGIIESE,P J AND DAMATO,A N:

17.

18.

19.

20.

21.

22.

23.

24.

25.

26.

27.

28. 29.

Sinus node reentry. An in vivo demonstration in the dog. Circ Res 32:455, 1973 PAULEY, K L, VARGIIESE, P J AND DAMATO, A N: Atrial r h y t h m s in response to an early atrial premature depolarization in man. A m H e a r t J 85:323, 1973 AMAT-Y-LEoN,F, I,Vu, D, DmNGRA, R, DENES, P, ~VYNDHAM, C, SIMPSON, R AND ROSEN K: Electrophysiological mechanism of supraventricular tachyarrhythmia in patients with sinus node disease (Abstr) Circulation 56:III-106, 1973 ~VEISFOGEI.,G M, BATSFORD,W P, JOSEPIISON, M E, PAULEY,K L AND DAMATO,A N: Sinus node reentrant tachycardia in man. (Abstr) Circulation 53:IV-122, 1973 Wu, D, DIIINGRA, R, DENES, P, '~VYNDIIAM,C AND ROSEN, K: Sustained sinus or atrial reentrance in patients with paroxysmal tachycardia. (Abstr) Circulation 50:III-251, 1974 NARULA,O S: Sinus node reentry: A mechanism for supraventricular tachycardia. Circulation 50:1114, 1974 LANGENDORFR: Concealed AV conduction: the effect of blocked impulses on the formation and conduction of subsequent impulses. Am Heart J 35:542, 1948 MOE, G K, ABILDSKOV,J A AND MENDEZ, C: An experimental s t u d y of concealed conduction. Am Heart J 67:338, 1964 SUNG, R J, h{YERIIURG, R J A N n CAS'FEI.LANOS, A: Electrophysiological demonstration of concealed conduction in the h u m a n atrium. Circulation58:940, 1978 LANGENDORF, R: Newer aspects of concealed conduction of the cardiac impulse. In The Conduction System of the Heart. H J J Wellens, Ed. Lea and Febiger, Philadelphia, 1976, pp. 410-423 FLEISIIMAN, P: Interpolation of atrial premature beats of infra-atrial origin due to concealed A-S conduction. Am H e a r t J 66:309, 1963 EL-SllERIF, N: Observations on atrio-sinus conduction. Single repetitive, and complete atriosinus block. Atrio-sinus concealed and Wenckebach conduction. J. Electrocardiol 6:113, 1973 GOLDREYER,B N ANDDAMATO,A N: Sinoatrial node entrance block. Circulation 44:781, 1971 GOLDREYER, B N AND BIGGER, J T, JR: Ventriculoatrial conduction in man. Circulation 41:935, 1970

30. DENES, P, Wu, D, AMAT-Y-LEoN,F, DIIINGItA, R, I~VYNDUAM, C AND ROSEN, K M: The determinants of atrioventricular reentrance with premature atrial s t i m u l a t i o n in p a t i e n t s with dual A-V nodal pathways. Circulation 56:253, 1977 31. HURST, J W, MARRIOTT, H J L AND hIYERBERG, R J: Cardiac arrhythmias and conduction disturbances. In J W H u r s t and R B Logue, Eds. The Heart. McGraw Hill Book Co. New Yorker, 1970, p 524

J. ELECTROCARDIOLOGY 18 (3), 1985