First-degree sinoatrial heart block: Sinoatrial block in the sick,sinus syndrome Toby R. Engel, M.D.* Roger C. Bond, M.D.* Stephen F. Schaal, M.D. Philadelphia, Pa., and Columbus, Ohio
Sinoatrial (SA) heart block is one of the r h y t h m disturbances included in the spectrum of the "sick-sinus syndrome" (SSS). 1-3 T he incidence of SA block is uncertain because of inability to recognize latent degrees of block or distinguish high-grade block from sinus arrest. Recent observations in the rabbit atrium 4 have demonstrated the existence of perinodal tissues as a possible site of sinoatrial conduction delay. Corollary clinical observations and studies by several groupsS: 8 have suggested th at the application of atrial premature depolarizations (APD's) can be used to estimate the conduction interval from sinus node to atrium. T h e methodology is based on the concepts delineated by Langendorf and associates 9 in determination of sinoatrial conduction delay from the surface electrocardiogram (ECG) in a patient with atrial parasystole. The purpose of this investigation is to define the abnormalities of sinoatrial conduction in patients with the SSS. Methods
Thirty-nine patients were studied without premedication in the postabsorptive state. Nineteen were considered to have SSS and 20 were normal control subjects. No cardioactive drugs From the Departments of Medicine, Medical College of Pennsylvania, Philadelphia, Pa., and Ohio State University College of Medicine, Columbus, Ohio. This study was supported in part by grants from the National Heart and Lung Institute (No. HE-5786, HL-5035, HE-5546, HL-5968 and a Program Project Award No. 1 PO 1 HE-11504) and the Central Ohio Chapter of the American Heart Association. Received for publication Feb. 4, 1975. Reprint requests: Toby R. Engel, M.D., 3300 Henry Ave. Philadelphia, Pa. 19129. *This investigation was performed while a Postdoctoral Trainee for the National Heart and Lung Institute.
March, 1976, Vol. 91, No. 3, pp. 303-310
were received the week prior to study. Informed written consent was obtained from all patients. Atrial electrograms at 40 to 500 Hz and standard ECG Leads I, II, and III a t 0.1 to 20 Hz were recorded generally at a paper speed of 100 mm. per second from a bipolar catheter, with ring electrodes 1 mm. wide and 1 cm. apart, positioned at the high right atrium in the region of the sinus node. Another such catheter was positioned at the lateral wall of the high right atrium for purposes of rapid atrial pacing and application of programmed APD's after every six to eight basic beats during sinus rhythm. Rectangular stimuli 2 msec. in duration at 189 diastolic threshold were delivered from a Grass Stimulator Model $88 and isolation unit as digitally determined with a Quartec APS-2 programmer. In most instances, His bundle electrograms were recorded f r o m a catheter passed via the right femoral vein and positioned across the tricuspid valve. TM Sinoatrial recovery times (SART) were measured as the maximal interval to ret urn of spontaneous atrial activity after termination of atrial overdrive suppression. 11 Pacing for 30 to 60 seconds was performed at a variety of heart rates from 80 to 160 per minute. Recovery times corrected for heart rate (CRT) were calculated by subtraction of the basic prepaced cycle length (normal < 390 msec?~). Abnormal A-V node conduction was defined as the presence of an atrium-His (A-H) interval 140 msec. or greater, 12 or incomplete A-V block with dropped beats, type I (Wenckebach phenomenon) during atrial pacing at 130 b.p.m. 13 Calculation of SACT. Sinoatrial conduction times (SACT) were estimated from the delay in atrial recovery time after APD's applied in the midportion of atrial diastole where the recovery
American Heart Journal
303
Engel, Bond,
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bundle electrogram(HBE) and three standard leads have been recorded. In this instance the basic cycle length (A to A) is 880 msec., a test depolarization (AT)is applied at 340 msec., and the recovery interval (AT to AR) is 1,100 msec.
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Fig. 2. The length of the recovery cycle after an APD (AT to AR) plotted as a function of the degree of prematurity of the test APD (A to AT). The same normal patient as in Fig. 1 is illustrated. Each interval has been "normalized" by dividing the interval by the basic cycle length (A to A). The dotted line projected on the Y axis is a reference line for one basic cycle length. The responses to the APDs plateau with increasing prematurity of test APDs as midcycle is approached and terminate at the atrial refractory period (ARP). Abbreviations are as in Fig. 1. interval was r a t h e r c o n s t a n t 2 S A C T were estim a t e d only from beats in which t h e recovery A wave and P wave m o r p h o l o g y were very similar to the sinus morphology, and in which the sequence of atrial depolarization was u n c h a n g e d . S A C T was measured as the recovery time m i n u s the basic cycle length. Fig. 1 illustrates the response to an A P D in a n o r m a l patient. T h e atrial potentials are labeled as A. T h e atrial p o t e n t i a l of the A P D is labeled A T (T for test). T h e s u b s e q u e n t 304
spontaneous atrial potential is labeled A R (R for recovery). T h e next atrial potential is labeled A'. In the instance illustrated the basic cycle length was 880 msec., with a test A P D applied at 340 msec. and a recovery interval (AT-A~) of 1,100 msec. S A C T is the interval (AT-AR) m i n u s (A-A), and in this instance was 220 msec. Fig. 2 illustrates a plot of the atrial r e c o v e r y time (AT-AR) as a function of the p r e m a t u r i t y of the test stimulus (A-AT) in the same n o r m a l patient. E a c h interval has been " n o r m a l i z e d " by dividing the interval by the preceding basic cycle length (A-A). With progressive increasing prematurity of test A P D ' s , an interval is reached where further p r e m a t u r i t y does n o t lengthen the recovery interval. This has been referred to as a plateau of responses to A P D ' s 2 T h e calculation of S A C T was based on those intervals in the plateau phase of recovery. In all b u t three instances sufficient d a t a were obtained to allow exclusion of values obtained from the first half of atrial diastole in order to minimize possible effects u p o n a u t o m a t i c i t y or changes in refractoriness or action potential d u r a t i o n of sinus or perinodal tissues. 14,15 E n t r a n c e block, sinus echoes, or abbreviation of sinus cycles seen with very early A P D ' s 1~ were excluded from calculalions. W h e n a plateau of m a x i m a l recovery intervals was n o t achieved before the atrial r e f r a c t o r y period, t h e longest recovery interval obtained from the most p r e m a t u r e A P D ' s was used in numerically describing the SACT. This underestim a t e d S A C T but occurred only in SSS patients, in w h o m S A C T was clearly prolonged. N o r m a l values for S A C T were obtained from March, 1976, Vol. 91, No. 3
First-degree sinoatrial heart block
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Fig. 3. The relationship between cycle length, as an index of automaticity, and sinoatrial conduction time (SACT). The empty circles represent normal subjects and the filled circles sick-sinus syndrome (SSS) patients. No correlation is evident between cycle length and SACT in normal subjects (r = 0.05) or SSS patients (r = 0.16).
patients with normal heart rates, SART's, and C R T ' s , a n d n o e v i d e n c e o f A - V n o d e or d i s t a l conduction abnormalities. T h e distribution of S A C T f o r n o r m a l s u b j e c t s w a s d e s c r i b e d as t h e m e a n S A C T in t h e s e p a t i e n t s _~ s t a n d a r d d e v i a t i o n s (S.D.). R e s u l t s w e r e o t h e r w i s e e x p r e s s e d as m e a n • the s t a n d a r d error of the m e a n (S.E.M.). Statistical comparisons were made with either linear regression analysis or S t u d e n t ' s t test, w i t h a H e w l e t t - P a c k a r d , M o d e l 9100 A c o m p u t e r . Results
I n 20 n o r m a l p a t i e n t s t h e m e a n S A C T w a s 169 msec. -~ 45.5 (S.D.) w i t h a r a n g e o f 57 t o 231 msec. T h u s 2 S.D. a b o v e m e a n S A C T f o r n o r m a l s u b j e c t s was 260 msec. T h e cycle i m m e d i a t e l y following r e c o v e r y (AR-A') was c o m p a r e d t o t h e c y c l e p r e c e d i n g t h e A P D (A-A) in o r d e r t o e s t i m a t e t h e d e g r e e t o which depression of a u t o m a t i c i t y with prolongat i o n o f s i n u s c y c l e l e n g t h p a r t i c i p a t e d in t h e recovery intervals. P r o l o n g a t i o n was 3 per c e n t -=_ 0.6 ( S . E . M . ) in t h e n o r m a l p a t i e n t s a n d w a s 1 p e r c e n t + 0.9 ( S . E . M . ) in 19 p a t i e n t s w i t h S S S (see below). N o r m a l p a t i e n t s s h o w e d n o c o r r e l a t i o n b e t w e e n b as i c c y c l e l e n g t h a n d S A C T (r =
A m e r i c a n Heart Journal
Table I. Sinoatrial conduction time in normal patients* I
Sex M M M F F F M F F M F M F M F M M F F F
Heart rate ] SART (b.p.mJ ] (msec.) 72 63 74 70 83 78 85 8O 82 87 94 102 72 7O 71 73 65 83 94 76
940 1020 1140 1160 1240 760 880 1000 950 1,250 msec. a n d 15 h a d C R T > 390 msec. Nine of the 19 SSS p a t i e n t s h a d S A C T longer t h a n 2 S.D. a b o v e t h e m e a n S A C T seen in n o r m a l subjects (260 msec.) ( T a b l e II). Only t w o of the 19 SSS p a t i e n t s d e m o n s t r a t e d i n t e r m i t t e n t second-degree SA block On E C G ' s or m o n i t o r e d periods prior to study. T h e s e t w o patients showed the m o s t prolonged S A C T (401 and 426 msec.). T h e presence of prolonged SA c o n d u c t i o n was a s s o c i a t e d with the presence of a b n o r m a l A-V nodal conduction (Fig. 5). E i g h t of t h e 10 SSS p a t i e n t s with a b n o r m a l A-V n o d a l c o n d u c t i o n as defined in this s t u d y h a d prolonged S A C T . I n contradistinction, only two of t h e nine SSS p a t i e n t s with n o r m a l A-V c o n d u c t i o n h a d a prolonged SACT. 306
Discussion
L a n g e n d o r f and associates 9 a n d l a t e r Fleischm a n n 16 d e m o n s t r a t e d t h a t t h e interval following a p r e m a t u r e atrial b e a t is d e t e r m i n e d b y properties of SA conduction as well as a u t o m a t i c i t y . N u m e r o u s investigators ~'8 h a v e f o u n d t h a t increasing the p r e m a t u r i t y of a single A P D does not result in f u r t h e r p r o l o n g a t i o n of the atrial recovery t i m e in m a n as m i g h t be expected if t h e d o m i n a n t effect of the A P D were depression of sinus a u t o m a t i c i t y . Instead, a p l a t e a u of response to progressively m o r e p r e m a t u r e A P D ' s is found. as is illustrated in Fig. 1. T h e prolongation of recovery t i m e b e y o n d a reset sinus cycle p r o b a b l y for the m o s t p a r t represents SA conduction delay2. 17 SA junctional tissue with distinctive action p o t e n t i a l characteristics has been d e m o n s t r a t e d in the rabbit right atrial p r e p a r a t i o n a n d h a s been shown to be a p o t e n t i a l site of c o n d u c t i o n delay. 4 Increasing refractoriness of this j u n c t i o n a l tissue or the sinus node or p o r t i o n s of the sinus node with increasingly p r e m a t u r e s t i m u l a t i o n TM is consistent w i t h the p h e n o m e n o n of SA e n t r a n c e block n o t e d in p a t i e n t s 2 Fig. 6 offers a d i a g r a m matic e x p l a n a t i o n for the c o n s t a n t r e c o v e r y t i m e March, 1976, Vol. 91, No. 3
First-degree sinoatrial heart block
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Fig. 6: A ladder diagram in explanation of the responses to atrial premature depolarizations in the plateau phase that has been illustrated in Fig. 2. The Premature depolarization recorded in Fig. 1 has been used as an example: The impulses are generated hi the sinus node as illustrated in the upper panel, with a basic cycle length of 880 msec. The impulses are conducted through the sinoatrial junction (middle panel) Over an interval to the atrium (lower panel) where they may be recorded (A). A test atrial depolarization is applied at 340 msec. (AT). This impulse ascefids the sinoatriat junction over an interval to discharge the sinus node. After a basic cycle length of 880 msec. the reset sinus node generates an impulse which descends to be recorded in the atrium (AR): The atrial recovery time (ATto AR)is comprised of (a) the basic cycle length and (b) the interval required for retrograde and antegrade sinoatrial junction conduction.
in the p l a t e a u p h a s e based on t h e c o n c e p t of SA conduction delay. T h e r e is a n i n t e r v a l required for a t e s t A P D to t r a v e r s e SA j u n c t i o n tissue in ascent of the i m p u l s e to discharg e t h e Sinus node. After a basic cycle length t h e reset sinus i m p u l s e requires a n o t h e r i n t e r v a l in d e s c e n t to t h e a t r i u m . T h e ~itrial recovery t i m e a f t e r a n A P D in midcycle therefore consists of t h r e e c o m p o n e n t s : (1) the t i m e of c o n d u c t i o n of t h e t e s t atrial i m p u l s e to the sinus node, (2) t h e t i m e of t h e basic cycle of sinus impulse generation, a n d (3) t h e t i m e of American Heart Journal
conduction Of t h e sinus i m p u l s e to t h e a t r i u m where it m a y be recorded. A reflection o f t h e t o t a l t i m e of sinoatrial conduction (SACT) is o b t a i n e d b y s u b t r a c t i n g the basic cycle length f r o m 'the r e c o v e r y i n t e r v a l in the p l a t e a u phase. T h i s e s t i m a t e is t h e s u m of antegrade a n d r e t r o g r a d e c o n d u c t i o n ; these m a y b e of t h e s a m e order Of m a g n i t u d e as h a s been shown b y s i m u l t a n e o u s r e c o r d i n g s f r o m r a b b i t a t r i u m a n d sinus node during A P D ' s . 15 T h e y m a y not a l w a y s be e q u i v a l e n t a n d for this r e a s o n 307
Engel, Bond, and,Schaal
Sinoatrial conduction in patients with sick-sinus syndrome
Table II.
(b.p,m.) (msec.) (msec.) 42 59 55 60 53 52 49 60 58 49 57 63 62 39 53 61 56 64 59
1,925 5,000 1,380 1,490 1,370 1,640 1,800 1,370 1,300 1,780 1,500 1,370 1,660 6,600 1,670 1,800 1,800 1,500 2,270
496 3,983 290 490 238 486 576 370 266 556 447 418 692 5,062 538 816 729 562 1,253
bach* 95 104 106 116 135 145 156 167 167 198 265 266 268 270 310 333 355 401 426
150 110 85 70 65 170 -100 90 80 120 -150 110 130 80 90 140 190
130 > 160 150 > 160 160 90 !60 > 160 > 160 160 > 160 110 100 110 150 150~: 80 125 110
I 1.00 1.01 1.01 1.03 0.98 1.02 1.01 1.04 0.95 1.01 .99 1.00 1.09 1.00 1.01 1.02 1.01 1.03 1.03
*The lowest atrial pacing rate at which intermittent A-V block with dropped beats, Type I (Wenckebach phenomenon) was observed. ~Ratio as explained in legend of Table I. :~This patient was very apprehensive in the laboratory and demonstrated normal A-V node conduction. Previous ECG's showed PR interval prolongation. She has been classified as a patient with abnormal A-V node conduction in the text and Fig. 5.
SACT is reported as the total conduction time without arbitrary division into antegrade and retrograde conduction times. The validity of SACT as measured in man. It is impossible to precisely measure SACT in the individual patient because many factors undoubtedly influence the duration of the return cycle after an APD in addition to the conduction time itself. These include electrotonic influences with alteration of sinus cycle length as well as possible changes in pacemaker distance from the margin of the node. Depression of automaticity by the APD may prolong the cycle length of the reset sinus impulse and contribute to the recovery time, b u t evidence suggests t h a t such depression of automaticity is minimal in the plateau phase. (1) Measurement of the cycle length immediately following the recovery time in normal subjects reveals only minimal prolongationS; in our normal patients the average prolongation was only 3 per cent. This prolongation of the postrecovery cycle may be a result of a persistent but small delay in sinoatrial conduction as well as a
308
reflection of depressed automaticity. (2) In our patients with SSS and possible depressed automaticity a similar i per cent prolongation was observed. Those patients with the most prolonged SART or SACT show equivalent minimal prolongation of basic cycle length. The possibility t h a t an unchanged basic cycle length following the recovery interval may be explained by repetitive discharge of an escape pacemaker should be considered. TM (3) In our normal and SSS patients there was no correlation between cycle length or SART and SACT. Similar data have been obtained by other investigators. 6, 7 However, the contribution of depressed automaticity to the post-APD recovery interval and the measurement of SACT remains undefined in man. Klein and associates 1~compared sinus node and atrial cycles following APDs by means of transmembrane recordings from the rabbit sinus node. In the phase of prematurity t h a t appears to be equivalent to the plateau in man there was minimal prolongation of the sinus cycle after an APD. The change in the deviation of the atrial recovery cycle usually closely paralleled the underlying SA nodal recovery cycle. The prolongation of the recovery cycle was predominantly caused by conduction to and from the sinus node. Bonke and associates 14 and Klein and associates ~5 have demonstrated no significant increase in conduction time of rabbit sinoatrial junctional tissue with increasing prematurity of an APD until early in the cycle. Therefore, SACT remains of clinical utilityS-despite the complexity of this interval as presently determined in the catheter laboratory in m a n - i n the detection of major deviations from the normal response to APD's t h a t appear to represent latent SA block. This concept was tested in our series in two patients who appeared to have intermittent second-degree SA block observed on the standard ECG. Neither demonstrated spontaneous SA block at the time of study but both presumably had latent degrees of SA block, i.e., first-degree SA block. They had the longest SACT t h a t we have measured. There is an additional difficulty in defining a normal range for SACT in man. SACT appears to vary as a function of the pulse rate of stimuli presented to the SA conduction tissue. ~9 This resembles the response of the A-V node as measured by the A-H interval. If the generator of stimuli presented to the A-V node does not alter
March, 1976, Vol. 91, No. 3
First-degree sinoatrial heart block
properties of A-V node c o n d u c t i o n when pulse rate c h a n g e s - a s in the case of right atrial pacing with an external pulse g e n e r a t o r - t h e n the A-H interval varies as a f u n c t i o n of pulse rate. Analogously, the pulse generator presenting stimuli to SA conduction tissue resides in the sinus node. A range of normal S A C T can be determined only for normal h e a r t rates. This range c a n n o t be applied to evaluate S A C T in patients with a different set of h e a r t rates, as seen with SSS. However, since slower h e a r t rates should abbreviate SACT, patients with b r a d y c a r d i a a n d prolonged S A C T would be expected to have even longer S A C T if their h e a r t rates were normal. Therefore the range of S A C T we report in n o r m a l subjects c a n n o t be strictly applied in the exclusion of latent SA c o n d u c t i o n abnormalities in patients with bradycardia. C o m p a r i n g S A C T in our SSS patients to t h a t of n o r m a l subjects tends to underestimate the incidence of a b n o r m a l S A C T in the SSS group. S A C T in SSS. T h e incidence a n d i m p o r t a n c e of S A block in S S S are uncertain because of inherent difficulties in the recognition of intermittent block with routine E C G observations. Conduction disease in the form of sinoatrial block as a cause of E C G abnormalities has been infrequent in our experience with S S S and in the' experience of others. 2~ 21 However, some authors have found S A block to be the most c o m m o n presentation of SSS. 2, 3 T h e latter experience is in keeping with the high incidence of A - V node and distal conduction disease in SSS. 22-~' Latent S A block was usually associated with latent A - V nodal block in our S S S patients. F e w of our S S S patients with normal A - V nodal conduction had a prolonged S A C T . This association between S A block and A - V conduction disease has been suggested in the past ~5, 26 a n d has been related to the long pauses sometimes seen without an escape mechanism in SA block. T h e association suggests two classes of SSS: (1) patients with abnormalities primarily of a u t o maticity and (2) patients having c o n c o m i t a n t a n d diffuse conduction abnormalities. Some of the latter m a y present with evidence of A-V block. 24 The results of this s t u d y suggest t h a t SA conduction disturbances can be detected a n d appear to be c o m m o n within the heterogeneous grouping of SSS. T h e presence of SA block in this group of patients m a y be suspected by the finding of A-V node c o n d u c t i o n delay.
American Heart Journal
Summary Sinoatrial conduction time ( S A C T ) was estim a t e d from the delay in the atrial recovery period after p r e m a t u r e depolarization applied in t h a t portion of atrial diastole where increasing prematurity resulted in a c o n s t a n t recovery interval. I n 20 n o r m a l patients S A C T was 169 msec. _+ 91 (2 S.D.). A t least nine of 19 patients with "sick-sinus s y n d r o m e " (SSS) d e m o n s t r a t e d S A C T t h a t were longer t h a n seen in these n o r m a l subjects. S A C T was prolonged in seven of nine SSS patients with a b n o r m a l A-V nodal conduction. A m o n g 10 SSS patients with normal A-V conduction, only two had prolonged SACT. This s t u d y identifies firstdegree sinoatrial block as a f r e q u e n t manifestation of SSS associated with the presence of A-V node conduction abnormalities. The preparation of this manuscript was made possible by the expert secretarial assistance of Mrs. Rachel Chatburn, Miss Beverly Burak, and Mrs. Shirley Rothstein.
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15. Klein, H. 0., Singer, D. H., and Hoffman, B. F.: Effects of atrial premature systoles on sinus rhythm in the rabbit, Circ. Res. 32:480, 1973. 16. Fleischmann, P.: Interpolation of atrial premature beats of infra-a~rial origin due to concealed A-S conduction, AM. HEART J. 66:309, 1963. 17. Fleischmann, P.: Sinoatrial node entrance block (letter to the editor), Circulation 47:210, 1973. 18. Pick, A., Langendorf, R.; and Katz, L. N.: Depression of cardiac pacemakers by premature impulses, AM. HEART J. 41:49, 1951. 19. Bigger, J. T., Jr., Reiffel, J. A., and Konstam, M, A.: The relationship between sinoatrial conduction time and sinus cycle length during spontaneous Sinus arrhythmia in adults, Circulation 50:924, 1974. 20. Eraut, D., and Shaw, D. B.: Sinus bradycardia, Br. Heart J. 33:742, 1971. 21. Rubenstein, J. J., Schulman, C. L., Yurchak, P. M., and
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22.
23. 24. 25. 26.
DeSanctis, R. W.: Clinical spectrum of the sick sinus syndrome, Circulation 46:5, 1972. Rosen, M. K., Loeb, H. S., Sinno, M. Z., Rahimtoola, S. H., and Gunnar, R. M.: Cardiac conduction in patients with symptomatic sinus node disease, Circulation 43:836, 1971. Naruia, O. S.: Atrioventricular conduction defects in patients with sinus bradycardia, Circulation 44:1096, 1971. Engel, T. R., Boudoulas, H., and Schaal, S. F.: The relationship of sinoatrial dysfunction to atrioventricular conduction, Clin~ Res. 21:417, 1973. Greenwood, R. J,, and Finkelstein, D.: Sinoatrial heart block, Springfield, Ill., 1964, Charles C Thomas, Publisher. Miiller, O. F., and Finkelstein, D.: Adams-Stokes syndrome due to sinoatrial block, Am. J. Cardiol. 17:433, 1966.
March, 1976, Vol. 91, No. 3
Sinoatrial (SA) heart block is one of the r h y t h m disturbances included in the spectrum of the "sick-sinus syndrome" (SSS). 1-3 T he incidence of SA block is uncertain because of inability to recognize latent degrees of block or distinguish high-grade block from sinus arrest. Recent observations in the rabbit atrium 4 have demonstrated the existence of perinodal tissues as a possible site of sinoatrial conduction delay. Corollary clinical observations and studies by several groupsS: 8 have suggested th at the application of atrial premature depolarizations (APD's) can be used to estimate the conduction interval from sinus node to atrium. T h e methodology is based on the concepts delineated by Langendorf and associates 9 in determination of sinoatrial conduction delay from the surface electrocardiogram (ECG) in a patient with atrial parasystole. The purpose of this investigation is to define the abnormalities of sinoatrial conduction in patients with the SSS. Methods
Thirty-nine patients were studied without premedication in the postabsorptive state. Nineteen were considered to have SSS and 20 were normal control subjects. No cardioactive drugs From the Departments of Medicine, Medical College of Pennsylvania, Philadelphia, Pa., and Ohio State University College of Medicine, Columbus, Ohio. This study was supported in part by grants from the National Heart and Lung Institute (No. HE-5786, HL-5035, HE-5546, HL-5968 and a Program Project Award No. 1 PO 1 HE-11504) and the Central Ohio Chapter of the American Heart Association. Received for publication Feb. 4, 1975. Reprint requests: Toby R. Engel, M.D., 3300 Henry Ave. Philadelphia, Pa. 19129. *This investigation was performed while a Postdoctoral Trainee for the National Heart and Lung Institute.
March, 1976, Vol. 91, No. 3, pp. 303-310
were received the week prior to study. Informed written consent was obtained from all patients. Atrial electrograms at 40 to 500 Hz and standard ECG Leads I, II, and III a t 0.1 to 20 Hz were recorded generally at a paper speed of 100 mm. per second from a bipolar catheter, with ring electrodes 1 mm. wide and 1 cm. apart, positioned at the high right atrium in the region of the sinus node. Another such catheter was positioned at the lateral wall of the high right atrium for purposes of rapid atrial pacing and application of programmed APD's after every six to eight basic beats during sinus rhythm. Rectangular stimuli 2 msec. in duration at 189 diastolic threshold were delivered from a Grass Stimulator Model $88 and isolation unit as digitally determined with a Quartec APS-2 programmer. In most instances, His bundle electrograms were recorded f r o m a catheter passed via the right femoral vein and positioned across the tricuspid valve. TM Sinoatrial recovery times (SART) were measured as the maximal interval to ret urn of spontaneous atrial activity after termination of atrial overdrive suppression. 11 Pacing for 30 to 60 seconds was performed at a variety of heart rates from 80 to 160 per minute. Recovery times corrected for heart rate (CRT) were calculated by subtraction of the basic prepaced cycle length (normal < 390 msec?~). Abnormal A-V node conduction was defined as the presence of an atrium-His (A-H) interval 140 msec. or greater, 12 or incomplete A-V block with dropped beats, type I (Wenckebach phenomenon) during atrial pacing at 130 b.p.m. 13 Calculation of SACT. Sinoatrial conduction times (SACT) were estimated from the delay in atrial recovery time after APD's applied in the midportion of atrial diastole where the recovery
American Heart Journal
303
Engel, Bond,
and Schaal
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bundle electrogram(HBE) and three standard leads have been recorded. In this instance the basic cycle length (A to A) is 880 msec., a test depolarization (AT)is applied at 340 msec., and the recovery interval (AT to AR) is 1,100 msec.
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Fig. 2. The length of the recovery cycle after an APD (AT to AR) plotted as a function of the degree of prematurity of the test APD (A to AT). The same normal patient as in Fig. 1 is illustrated. Each interval has been "normalized" by dividing the interval by the basic cycle length (A to A). The dotted line projected on the Y axis is a reference line for one basic cycle length. The responses to the APDs plateau with increasing prematurity of test APDs as midcycle is approached and terminate at the atrial refractory period (ARP). Abbreviations are as in Fig. 1. interval was r a t h e r c o n s t a n t 2 S A C T were estim a t e d only from beats in which t h e recovery A wave and P wave m o r p h o l o g y were very similar to the sinus morphology, and in which the sequence of atrial depolarization was u n c h a n g e d . S A C T was measured as the recovery time m i n u s the basic cycle length. Fig. 1 illustrates the response to an A P D in a n o r m a l patient. T h e atrial potentials are labeled as A. T h e atrial p o t e n t i a l of the A P D is labeled A T (T for test). T h e s u b s e q u e n t 304
spontaneous atrial potential is labeled A R (R for recovery). T h e next atrial potential is labeled A'. In the instance illustrated the basic cycle length was 880 msec., with a test A P D applied at 340 msec. and a recovery interval (AT-A~) of 1,100 msec. S A C T is the interval (AT-AR) m i n u s (A-A), and in this instance was 220 msec. Fig. 2 illustrates a plot of the atrial r e c o v e r y time (AT-AR) as a function of the p r e m a t u r i t y of the test stimulus (A-AT) in the same n o r m a l patient. E a c h interval has been " n o r m a l i z e d " by dividing the interval by the preceding basic cycle length (A-A). With progressive increasing prematurity of test A P D ' s , an interval is reached where further p r e m a t u r i t y does n o t lengthen the recovery interval. This has been referred to as a plateau of responses to A P D ' s 2 T h e calculation of S A C T was based on those intervals in the plateau phase of recovery. In all b u t three instances sufficient d a t a were obtained to allow exclusion of values obtained from the first half of atrial diastole in order to minimize possible effects u p o n a u t o m a t i c i t y or changes in refractoriness or action potential d u r a t i o n of sinus or perinodal tissues. 14,15 E n t r a n c e block, sinus echoes, or abbreviation of sinus cycles seen with very early A P D ' s 1~ were excluded from calculalions. W h e n a plateau of m a x i m a l recovery intervals was n o t achieved before the atrial r e f r a c t o r y period, t h e longest recovery interval obtained from the most p r e m a t u r e A P D ' s was used in numerically describing the SACT. This underestim a t e d S A C T but occurred only in SSS patients, in w h o m S A C T was clearly prolonged. N o r m a l values for S A C T were obtained from March, 1976, Vol. 91, No. 3
First-degree sinoatrial heart block
6 (D (I)
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Fig. 3. The relationship between cycle length, as an index of automaticity, and sinoatrial conduction time (SACT). The empty circles represent normal subjects and the filled circles sick-sinus syndrome (SSS) patients. No correlation is evident between cycle length and SACT in normal subjects (r = 0.05) or SSS patients (r = 0.16).
patients with normal heart rates, SART's, and C R T ' s , a n d n o e v i d e n c e o f A - V n o d e or d i s t a l conduction abnormalities. T h e distribution of S A C T f o r n o r m a l s u b j e c t s w a s d e s c r i b e d as t h e m e a n S A C T in t h e s e p a t i e n t s _~ s t a n d a r d d e v i a t i o n s (S.D.). R e s u l t s w e r e o t h e r w i s e e x p r e s s e d as m e a n • the s t a n d a r d error of the m e a n (S.E.M.). Statistical comparisons were made with either linear regression analysis or S t u d e n t ' s t test, w i t h a H e w l e t t - P a c k a r d , M o d e l 9100 A c o m p u t e r . Results
I n 20 n o r m a l p a t i e n t s t h e m e a n S A C T w a s 169 msec. -~ 45.5 (S.D.) w i t h a r a n g e o f 57 t o 231 msec. T h u s 2 S.D. a b o v e m e a n S A C T f o r n o r m a l s u b j e c t s was 260 msec. T h e cycle i m m e d i a t e l y following r e c o v e r y (AR-A') was c o m p a r e d t o t h e c y c l e p r e c e d i n g t h e A P D (A-A) in o r d e r t o e s t i m a t e t h e d e g r e e t o which depression of a u t o m a t i c i t y with prolongat i o n o f s i n u s c y c l e l e n g t h p a r t i c i p a t e d in t h e recovery intervals. P r o l o n g a t i o n was 3 per c e n t -=_ 0.6 ( S . E . M . ) in t h e n o r m a l p a t i e n t s a n d w a s 1 p e r c e n t + 0.9 ( S . E . M . ) in 19 p a t i e n t s w i t h S S S (see below). N o r m a l p a t i e n t s s h o w e d n o c o r r e l a t i o n b e t w e e n b as i c c y c l e l e n g t h a n d S A C T (r =
A m e r i c a n Heart Journal
Table I. Sinoatrial conduction time in normal patients* I
Sex M M M F F F M F F M F M F M F M M F F F
Heart rate ] SART (b.p.mJ ] (msec.) 72 63 74 70 83 78 85 8O 82 87 94 102 72 7O 71 73 65 83 94 76
940 1020 1140 1160 1240 760 880 1000 950 1,250 msec. a n d 15 h a d C R T > 390 msec. Nine of the 19 SSS p a t i e n t s h a d S A C T longer t h a n 2 S.D. a b o v e t h e m e a n S A C T seen in n o r m a l subjects (260 msec.) ( T a b l e II). Only t w o of the 19 SSS p a t i e n t s d e m o n s t r a t e d i n t e r m i t t e n t second-degree SA block On E C G ' s or m o n i t o r e d periods prior to study. T h e s e t w o patients showed the m o s t prolonged S A C T (401 and 426 msec.). T h e presence of prolonged SA c o n d u c t i o n was a s s o c i a t e d with the presence of a b n o r m a l A-V nodal conduction (Fig. 5). E i g h t of t h e 10 SSS p a t i e n t s with a b n o r m a l A-V n o d a l c o n d u c t i o n as defined in this s t u d y h a d prolonged S A C T . I n contradistinction, only two of t h e nine SSS p a t i e n t s with n o r m a l A-V c o n d u c t i o n h a d a prolonged SACT. 306
Discussion
L a n g e n d o r f and associates 9 a n d l a t e r Fleischm a n n 16 d e m o n s t r a t e d t h a t t h e interval following a p r e m a t u r e atrial b e a t is d e t e r m i n e d b y properties of SA conduction as well as a u t o m a t i c i t y . N u m e r o u s investigators ~'8 h a v e f o u n d t h a t increasing the p r e m a t u r i t y of a single A P D does not result in f u r t h e r p r o l o n g a t i o n of the atrial recovery t i m e in m a n as m i g h t be expected if t h e d o m i n a n t effect of the A P D were depression of sinus a u t o m a t i c i t y . Instead, a p l a t e a u of response to progressively m o r e p r e m a t u r e A P D ' s is found. as is illustrated in Fig. 1. T h e prolongation of recovery t i m e b e y o n d a reset sinus cycle p r o b a b l y for the m o s t p a r t represents SA conduction delay2. 17 SA junctional tissue with distinctive action p o t e n t i a l characteristics has been d e m o n s t r a t e d in the rabbit right atrial p r e p a r a t i o n a n d h a s been shown to be a p o t e n t i a l site of c o n d u c t i o n delay. 4 Increasing refractoriness of this j u n c t i o n a l tissue or the sinus node or p o r t i o n s of the sinus node with increasingly p r e m a t u r e s t i m u l a t i o n TM is consistent w i t h the p h e n o m e n o n of SA e n t r a n c e block n o t e d in p a t i e n t s 2 Fig. 6 offers a d i a g r a m matic e x p l a n a t i o n for the c o n s t a n t r e c o v e r y t i m e March, 1976, Vol. 91, No. 3
First-degree sinoatrial heart block
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Fig. 6: A ladder diagram in explanation of the responses to atrial premature depolarizations in the plateau phase that has been illustrated in Fig. 2. The Premature depolarization recorded in Fig. 1 has been used as an example: The impulses are generated hi the sinus node as illustrated in the upper panel, with a basic cycle length of 880 msec. The impulses are conducted through the sinoatrial junction (middle panel) Over an interval to the atrium (lower panel) where they may be recorded (A). A test atrial depolarization is applied at 340 msec. (AT). This impulse ascefids the sinoatriat junction over an interval to discharge the sinus node. After a basic cycle length of 880 msec. the reset sinus node generates an impulse which descends to be recorded in the atrium (AR): The atrial recovery time (ATto AR)is comprised of (a) the basic cycle length and (b) the interval required for retrograde and antegrade sinoatrial junction conduction.
in the p l a t e a u p h a s e based on t h e c o n c e p t of SA conduction delay. T h e r e is a n i n t e r v a l required for a t e s t A P D to t r a v e r s e SA j u n c t i o n tissue in ascent of the i m p u l s e to discharg e t h e Sinus node. After a basic cycle length t h e reset sinus i m p u l s e requires a n o t h e r i n t e r v a l in d e s c e n t to t h e a t r i u m . T h e ~itrial recovery t i m e a f t e r a n A P D in midcycle therefore consists of t h r e e c o m p o n e n t s : (1) the t i m e of c o n d u c t i o n of t h e t e s t atrial i m p u l s e to the sinus node, (2) t h e t i m e of t h e basic cycle of sinus impulse generation, a n d (3) t h e t i m e of American Heart Journal
conduction Of t h e sinus i m p u l s e to t h e a t r i u m where it m a y be recorded. A reflection o f t h e t o t a l t i m e of sinoatrial conduction (SACT) is o b t a i n e d b y s u b t r a c t i n g the basic cycle length f r o m 'the r e c o v e r y i n t e r v a l in the p l a t e a u phase. T h i s e s t i m a t e is t h e s u m of antegrade a n d r e t r o g r a d e c o n d u c t i o n ; these m a y b e of t h e s a m e order Of m a g n i t u d e as h a s been shown b y s i m u l t a n e o u s r e c o r d i n g s f r o m r a b b i t a t r i u m a n d sinus node during A P D ' s . 15 T h e y m a y not a l w a y s be e q u i v a l e n t a n d for this r e a s o n 307
Engel, Bond, and,Schaal
Sinoatrial conduction in patients with sick-sinus syndrome
Table II.
(b.p,m.) (msec.) (msec.) 42 59 55 60 53 52 49 60 58 49 57 63 62 39 53 61 56 64 59
1,925 5,000 1,380 1,490 1,370 1,640 1,800 1,370 1,300 1,780 1,500 1,370 1,660 6,600 1,670 1,800 1,800 1,500 2,270
496 3,983 290 490 238 486 576 370 266 556 447 418 692 5,062 538 816 729 562 1,253
bach* 95 104 106 116 135 145 156 167 167 198 265 266 268 270 310 333 355 401 426
150 110 85 70 65 170 -100 90 80 120 -150 110 130 80 90 140 190
130 > 160 150 > 160 160 90 !60 > 160 > 160 160 > 160 110 100 110 150 150~: 80 125 110
I 1.00 1.01 1.01 1.03 0.98 1.02 1.01 1.04 0.95 1.01 .99 1.00 1.09 1.00 1.01 1.02 1.01 1.03 1.03
*The lowest atrial pacing rate at which intermittent A-V block with dropped beats, Type I (Wenckebach phenomenon) was observed. ~Ratio as explained in legend of Table I. :~This patient was very apprehensive in the laboratory and demonstrated normal A-V node conduction. Previous ECG's showed PR interval prolongation. She has been classified as a patient with abnormal A-V node conduction in the text and Fig. 5.
SACT is reported as the total conduction time without arbitrary division into antegrade and retrograde conduction times. The validity of SACT as measured in man. It is impossible to precisely measure SACT in the individual patient because many factors undoubtedly influence the duration of the return cycle after an APD in addition to the conduction time itself. These include electrotonic influences with alteration of sinus cycle length as well as possible changes in pacemaker distance from the margin of the node. Depression of automaticity by the APD may prolong the cycle length of the reset sinus impulse and contribute to the recovery time, b u t evidence suggests t h a t such depression of automaticity is minimal in the plateau phase. (1) Measurement of the cycle length immediately following the recovery time in normal subjects reveals only minimal prolongationS; in our normal patients the average prolongation was only 3 per cent. This prolongation of the postrecovery cycle may be a result of a persistent but small delay in sinoatrial conduction as well as a
308
reflection of depressed automaticity. (2) In our patients with SSS and possible depressed automaticity a similar i per cent prolongation was observed. Those patients with the most prolonged SART or SACT show equivalent minimal prolongation of basic cycle length. The possibility t h a t an unchanged basic cycle length following the recovery interval may be explained by repetitive discharge of an escape pacemaker should be considered. TM (3) In our normal and SSS patients there was no correlation between cycle length or SART and SACT. Similar data have been obtained by other investigators. 6, 7 However, the contribution of depressed automaticity to the post-APD recovery interval and the measurement of SACT remains undefined in man. Klein and associates 1~compared sinus node and atrial cycles following APDs by means of transmembrane recordings from the rabbit sinus node. In the phase of prematurity t h a t appears to be equivalent to the plateau in man there was minimal prolongation of the sinus cycle after an APD. The change in the deviation of the atrial recovery cycle usually closely paralleled the underlying SA nodal recovery cycle. The prolongation of the recovery cycle was predominantly caused by conduction to and from the sinus node. Bonke and associates 14 and Klein and associates ~5 have demonstrated no significant increase in conduction time of rabbit sinoatrial junctional tissue with increasing prematurity of an APD until early in the cycle. Therefore, SACT remains of clinical utilityS-despite the complexity of this interval as presently determined in the catheter laboratory in m a n - i n the detection of major deviations from the normal response to APD's t h a t appear to represent latent SA block. This concept was tested in our series in two patients who appeared to have intermittent second-degree SA block observed on the standard ECG. Neither demonstrated spontaneous SA block at the time of study but both presumably had latent degrees of SA block, i.e., first-degree SA block. They had the longest SACT t h a t we have measured. There is an additional difficulty in defining a normal range for SACT in man. SACT appears to vary as a function of the pulse rate of stimuli presented to the SA conduction tissue. ~9 This resembles the response of the A-V node as measured by the A-H interval. If the generator of stimuli presented to the A-V node does not alter
March, 1976, Vol. 91, No. 3
First-degree sinoatrial heart block
properties of A-V node c o n d u c t i o n when pulse rate c h a n g e s - a s in the case of right atrial pacing with an external pulse g e n e r a t o r - t h e n the A-H interval varies as a f u n c t i o n of pulse rate. Analogously, the pulse generator presenting stimuli to SA conduction tissue resides in the sinus node. A range of normal S A C T can be determined only for normal h e a r t rates. This range c a n n o t be applied to evaluate S A C T in patients with a different set of h e a r t rates, as seen with SSS. However, since slower h e a r t rates should abbreviate SACT, patients with b r a d y c a r d i a a n d prolonged S A C T would be expected to have even longer S A C T if their h e a r t rates were normal. Therefore the range of S A C T we report in n o r m a l subjects c a n n o t be strictly applied in the exclusion of latent SA c o n d u c t i o n abnormalities in patients with bradycardia. C o m p a r i n g S A C T in our SSS patients to t h a t of n o r m a l subjects tends to underestimate the incidence of a b n o r m a l S A C T in the SSS group. S A C T in SSS. T h e incidence a n d i m p o r t a n c e of S A block in S S S are uncertain because of inherent difficulties in the recognition of intermittent block with routine E C G observations. Conduction disease in the form of sinoatrial block as a cause of E C G abnormalities has been infrequent in our experience with S S S and in the' experience of others. 2~ 21 However, some authors have found S A block to be the most c o m m o n presentation of SSS. 2, 3 T h e latter experience is in keeping with the high incidence of A - V node and distal conduction disease in SSS. 22-~' Latent S A block was usually associated with latent A - V nodal block in our S S S patients. F e w of our S S S patients with normal A - V nodal conduction had a prolonged S A C T . This association between S A block and A - V conduction disease has been suggested in the past ~5, 26 a n d has been related to the long pauses sometimes seen without an escape mechanism in SA block. T h e association suggests two classes of SSS: (1) patients with abnormalities primarily of a u t o maticity and (2) patients having c o n c o m i t a n t a n d diffuse conduction abnormalities. Some of the latter m a y present with evidence of A-V block. 24 The results of this s t u d y suggest t h a t SA conduction disturbances can be detected a n d appear to be c o m m o n within the heterogeneous grouping of SSS. T h e presence of SA block in this group of patients m a y be suspected by the finding of A-V node c o n d u c t i o n delay.
American Heart Journal
Summary Sinoatrial conduction time ( S A C T ) was estim a t e d from the delay in the atrial recovery period after p r e m a t u r e depolarization applied in t h a t portion of atrial diastole where increasing prematurity resulted in a c o n s t a n t recovery interval. I n 20 n o r m a l patients S A C T was 169 msec. _+ 91 (2 S.D.). A t least nine of 19 patients with "sick-sinus s y n d r o m e " (SSS) d e m o n s t r a t e d S A C T t h a t were longer t h a n seen in these n o r m a l subjects. S A C T was prolonged in seven of nine SSS patients with a b n o r m a l A-V nodal conduction. A m o n g 10 SSS patients with normal A-V conduction, only two had prolonged SACT. This s t u d y identifies firstdegree sinoatrial block as a f r e q u e n t manifestation of SSS associated with the presence of A-V node conduction abnormalities. The preparation of this manuscript was made possible by the expert secretarial assistance of Mrs. Rachel Chatburn, Miss Beverly Burak, and Mrs. Shirley Rothstein.
REFERENCES 1. Ferrer, M. I.: The sick sinus syndrome in atrial disease, J. A. M. A. 206:645. 1968. 2. Easley,R. M., Jr., and Goldstein, S.: Sinoatrial syncope, Am. J. Med. 50"166, 1971. 3. Rasmussen, K.: Chronic sinoatrial heart block, AM. HEART J. 81:38, 1971. 4. Strauss,H. C., and Bigger, J. T., Jr.: Electrophysiological properties of the rabbit sinoatrial perinodal fibers, Circ. Res. 31:490, 1972. 5. Strauss, H. C., Saroff, A. L., BiggeD J. T., Jr., and Giardina, E. G. V.: Premature atrial stimulation as a key to the understanding of sinoatrial conduction in man, Circulation 47:86, 1973. 6. Goldreyer, B. N., and Damato, A. N.: Sinoatrial node entrance block, Circulation 44:789, 1971. 7. Narula,O. S., Samet, P., and Javier, R. P.: Significanceof the sinus-node recovery time, Circulation 45:140, 1972. 8. Bigger,J. T., Jr.: A simple, rapid method for the diagnosis of first-degreesinoatrialblock in man. AM. HEART J. 87:731, 1974. 9. Langendorf,R., Lesser,M. E., Plotkin,P., and Levin. B. D.: Atrial parasystole with interpolation.Observations on prolonged sinoatrial conduction, AM. HEART J. 63:649, 1962. 10. Scherlag, B. J., Lau, S. H., Helfant, R. H., Berkowitz, W. D., Stein, E., and Damato, A. N.: Catheter technique for recording His bundle activity in man, Circulation 39:13, 1969. 11. Engel,T: R., and Schaal, S. F.: Digitalis in the sick sinus syndrome, Circulation 48:1201, 1973. 12. Rosen, K. M.: Evaluation of cardiac conduction in the cardiac catheterization laboratory, Am. J. Cardiol. 30:701, 1972. 13. Schuilenburg, R. M., and Durrer, D.: Observations of atrioventricular conduction in patients with bilateral bundle branch block, Circulation 41:967, 1970. 14. Bonke, F. I. M., Bouman, L. N., and Van Rijn, H. E.: Change of cardiac rhythm in the rabbit after an atrial premature beat, Circ. Res. 24:533, 1969.
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March, 1976, Vol. 91, No. 3
