ABERRANT CONDUCTION IN SUPRAVENTRICULAR EXTRASYSTOLES ELIMINATED BY EXERCISE WILLIAM
S.
BOIKAN,
M.D.,
F.A.C.P., CHICAGO,
AND ROLF M. GUNNAK,
M.S., M.D.
11.~.
T HAS been shown that aberrant conduction in premature auricular systoles may be a physiologic phenomenon.1-4 Sir Thomas Lewis5 demonstrated that the recovery curve of the conducting tissue normally begins earlier as the heart rate increases, and that the recovery curve depends on the length of the preceding cycle. This means that the refractory period is roughly proportional to the length of the cardiac cycle. Sherf4 and Gouaux and Ashman’ used this phenomenon to explain the aberration which may occur clinically when a beat with a short R-R interval occurs after beats of a longer cycle. In this case the long cycle determines a long refractory period and the impulse arriving from the succeeding short cycle meets a refractory conduction system. The refractoriness frequently manifests itself only in one bundle and usually in the right, giving aberration with the picture of right bundle branch block. Apart from this physiologic phenomenon, aberration may be produced in premature beats of supraventricular origin because of disease of the conducting tissue. It has been shown in the experimental animal that aberration of premature beats may be the only electrocardiographic sign of disease of the specialized tissue6. Vesel17emphasized that aberration may be due to exceeding the “critical rate” for the normal propagation of the impulse-that the diseased bundle branch required a longer refractory period than the normal branch. Therefore, after a certain rate is passed, the diseased branch remains refractory and is no longer able to transmit the impulse. It is then transmitted down the still functioning bundle and later across the septum as in bundle branch block. It is then possible that in an otherwise normal electrocardiogram, auricular premature systoles with aberrancy may represent either a normal phenomenon (Ashman phenomenon), or may represent the early evidence of disease, carrying the same significance as intermittent bundle branch block. However, it seems possible to separate the two phenomena by increasing the heart rate. The preceding cycle would thus be shortened and in the normal heart the recovery of the conducting tissue would begin earlier5 and conduct the premature beat normally. In the diseasedheart where the aberration is due to exceeding the “critical rate,“’ the block should persist, increase, or even occur in the sinus beats, but not disapp2ar.
I
ment
From the University of Illinois. Department of Medicine, Chicago, Ill. Received for publicatiou Oct. 21, 1953.
of l\ledicine,
and The Cook
Count,y
Hospital,
Depart-
BOIKAN
AND
GIINNXR:
XHERR.INT
CASE
E. Ii., a 44-year-old tation. In 1946, he had in his chest. He was told told his heart was worse, On reported as normal. edema, and no symptoms
Fig.
l.-Electrocardiogram
CONDUCTION
IN
627
EXTRASYSTOLES
REPORT
male was referred to one of us (W.S.B.) in March 195.3, because of palpidetected an irregularity in his heart associated with a feeling of fullness at that time that he had heart disease. .4t yearly examinations he was but he continued working. Electrocardiograms, in 1948 and 1950, were questioning, there was no dyspnea, no effort pain, orthopnea, cough or referable to the heart other than consciousness of the premature beats.
taken at rest showing duction of the right
supraventricular bundle branch
extrasystoles type.
with
aberrant
con-
628
AMERICAN
HEART
JOURNAL
Physical examination revealed a thin, somewhat nervous white man appearing generally in good physical health. His thyroid was palpable but not enlarged. The heart was of normal size. Heart tones were normal and there were uo murmurs. Laboratory data were all normal. The electrocardiogram (Fig. 1) showed frequent supraventricular premature beats with right bundle branch block. After 13.5 two-steps, another electrocardiogram (Fig. 2) showed that the rate was increased
Fig. Z.-Electrocardiogram supraventricular
taken immediately after 135 two-step test showing persistence extrasystoles but disappearance of the aberrant conduction.
of the
from 83 per minute to 111 per minute, and the premature beats, although still present, were normally conducted. The R-R interval had decreased from 0.72 sec. to 0.54 sec. and the R extrasystole R interval had decreased from 0.46 sec. to 0.36 sec. The loss of aberrant conduction, indicated that this patient had a normal conduction system.
BOIKAN
AND
GUNNAR:
ABERRANT
CONDUCTION
IN
EXTRASYSTOLES
629
SUMMARY
A patient with premature supraventricular systoles associated conduction of the right bundle branch type was exercised. The heart rate caused the aberrancy to disappear showing that the normal conduction system. This indicated that the aberration festation of a normal physiologic phenomenon and not an early
with aberrant increase in the patient had a was the manisign of disease.
REFERENCES
1. 2. 3. 4. 5. 6.
7.
Gouaux,
J. L., and Ashman, R.: Auricular Fibrillation With Aberration Simulating Ventricular Paroxysmal Tachycardia, AM. HEART J. 34:366, 1947. Berliner, K., and Lewithin, L. P.: Auricular Premature Systole: I. Aberration of the Ventricular Complex in the Electrocardiogram, AM. HEART J. 29:449, 1945. Langendorf, R.: Aberrant Ventricular Conduction, AM. HEART J. 41:700, 19.51. Sherf, D.: Ueber intraventrikulare Stijrungen der Erregungsausbreitung bei den Wenkebachschen Perioden, Wien. Arch. f. inn. Med. 18:403, 1929. Lewis, T., and Master, A. M.: Observations Upon Conduction in the Mammalian Heart: A-V Conduction, Heart 12:209, 1925. StenstrBm, Nils.: An Experimental and Clinical Study of Incomplete Bundle Branch Block, Acta med. Scandinav. 60552, 1924. Vesell, H.: Critical Rates in Ventricular Conduction, Am. J. M. SC. 202:198, 1941.