Concealed atrial quadrigeminy
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Volume Number
110 5
Brief
ways can be composedof tissue with properties similar to the AV node. Rare histopathologic reports of AV bypass tracts composedof cells resemblingthose of the AV node and sinus node have been published.K14In addition, it is possiblethat accessorypathway cells,normally capable of the so-called“fast response”via the sodium channel, may become partially depolarized via disease or concealed conduction and may convert to the calcium channel as a meansfor impulse conduction. This explanation has been used by El-Sherif et a1.15to explain Wenckebach type second-degreeAV block occurring in the His-Purkinje system. As an alternative explanation, GallagherI has proposedthat decremental retrograde conduction seenin the PJRT syndrome is the result of the tortuous geometric configuration of the pathway rather than of unique ionic properties. Further anatomic studies are neededto resolve this question. The potential importance of recognizing the heterogenous nature of accessoryAV pathways has both research and clinical implications. The role of AV nodal-like tissue in explaining the phenomenon of differential antegrade and retrograde conduction in accessorypathways remains to be explored. In addition, the application of therapy aimed at blocking the calcium channel might have a more prominent role in the therapy of patients discovered to have an accessorypathway possessingthese electrophysiologic properties. REFERENCES
1. Sherif L, Neufeld HN: The pre-excitation syndrome: Facts and theories. New York. 1978. Yorke Medical Books. a. 90. 2. Berker AE, ‘Anderson RH, Durrer D, Wellens HJJ: The anatomical substrates of Wolff-ParkinsonzWhite syndrome. Circulation 57:870, 1978. 3. Anderson RH, Berker AE: Gross anatomy and microscopy of the conducting system. In Mandel WJ, editor: Cardiac arrhythmias: Their mechanism, diagnosis and treatment. Philadelphia, 1980, J.B. Lippincott Co., p. 37. 4. Gallagher JJ, Pritchett ELC, Sealy WC, Kasell J, Wallace AG: The pre-excitation syndrome. Prog Cardiovasc Dis 20:285,
1978.
6. Prystowsky EN, Miles WM, Heger JJ, Zipes DP: Preexcitation syndrome. Med Clin North Am 66:831, 1984. 6. Klein GJ. Prvstowsky EN, Pritchett LC, Davis D, Gallagher JJ: Atypical patterns-of retrograde conduction over accessory atrioventricular pathways in the Wolff-Parkinson-White syndrome. Circulation 60:1477, 1979. 7. Gillette PC. Garson A. Coolev DA. McNamara DG: Prolonged and decremental antegrade conduction properties in right anterior accessory connections. AM HEART J 103:60, 1982. 8. Guarnieri ‘I’, Sealy WC, Kasell JH, German LD, Gallagher JJ: The nonpharmacologic management of the permanent form of junctional reciprocating tachycardia. Circulation 69:269, 1984. 9. Brugada P, Bar FW, Vanagt EJ, Friedman PL, Wellens HJJ: Observation in patients showing AV junctional echoes with a shorter P-R than R-P interval. Am J Cardiol 48:611, 1981. 10. Farre J, Ross D, Wiener I, Bar FW, Vanagt EJ, Wellens HJJ: Reciprocal tachycardias using accessory pathways with long conduction times. Am J Cardiol 44:1099, 1979. 11. Rosenthal ME, Oseran DS, Gang ES, Deng ZW, Mandel WJ, Peter T: Verapamil induced retrograde conduction block in a concealed atrioventricular bypass tract. Am J Cardiol55:122, 1985. 12. Tai DY, Chang MS, Svinarich JT, Chiang BN, Sung RJ:
Communications
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Mechanisms of verapamil-induced conduction block in anomalous atrioventricular bypass t,ract. ,J Am Co11 Cardiol 5:311,1985.
13. Horio Y, Matsuyama K, Morikami Y, Rokutanda M, Hirata A, Okumura K, Takaoka K, Uchida H, Kugiyama K, Araki S: Blocking effect of verapamil on conduction over a catecholamine-sensitive bypass tract in exercise-induced Wolff-Parkinson-white syndrome. J Am Co11 Cardiol 4:186, 1984. 14. James TN, Puech P: De subitanesis mortibus. IX. Type A Wolff-Parkinson-White syndrome. Circulation 50:1264, 1974. 15. El-Sherif N, Scherlag BJ, Lazzara R: Pathophysiology 01 second-degree atrioventricular block: A unified hypothesis. Am J Cardiol 35421, 1975. 16. Gallagher JJ: Variants of pre-excitation: Update 1984. In Zipes DP, Jallife J editors: Cardiac electrophysiology and arrhythmias. New York, 1985, Grune CL Stratton Inc., p. 419.
Concealed
atrial quadrigeminy
Shinji Kinoshita, M.D., Fumihiko Okada, M.D., and Michimaro Okada, M.D. Sapporo, Japan The phenomena “concealed ventricular bigeminy and trigeminy” were originally reported by Satoh et al.’ in 1960. In the classicalform of concealed bigeminy,‘v2 the number of sinus QRS complexesintervening between two successivenoninterpolated extrasystoles is always odd, i.e., 2n - 1, where n is any positive integer. In the classical form of concealedtrigeminy, it is 3n - 1. Thereafter two variants of concealed ventricular quadrigeminy were reported by Levy et a1.3More recently, Aygen et a1.4 demonstrated the presenceof the classicalform of concealed ventricular quadrigeminy, in which the number of intervening sinus QRS complexes was 4n - 1. In some patients with atria1 extrasystoles, the presence of concealed bigemine6 and trigeminy5 has also been shown. However, concealedatrial quadrigeminy has not yet been documented. The present report is the first one on concealedatrial quadrigeminy. A continuous ECG recording was obtained from a 77-year-old man with essentialhypertension. During the recording the patient was not undergoing antiarrhythmic therapy. The ECG showed sinus rhythm, with complete right bundle branch block with frequent atria1 extrasystoles and occasionalventricular extraeystoles. Fig. 1 shows parts of the long continuous recording. In the strips, P, represents the ith P wave after the preceding atria1 extrasystole labeled A. In Fig. 1, every atria1 extrasystole (A) follows a P,,- 1 wave (P,, P, or P,,), where n is a positive integer; in other words, the number of P waves intervening between two successive atria1 extrasystoles (A) is always 4n - 1. Coupling intervals of the atria1 extrasystoles to the preceding P waves are considerably variable. However, no fusion P waves are seen, and the From Reprint Hokkaido
Health
Administration
Center,
Hokkaido
requests: Shinji Kinoshita, M.D., University, Sapporo OfiO, Japan.
Health
liniversits. Administration
Center.
November,
1078
Brief Communications
American
Heart
1985 Journal
A RPA
Fig. 1. Concealedatria1 quadrigeminy. The first two strips are continuous. The last two strips are also continuous. The diagram below the secondstrip showsa probable mechanismfor concealedquadrigeminy. In the diagram, shaded bars represent prolonged absoluterefractory periods at different levels within the reentrant pathway of atrial extrasystoles. Dashed lines in the diagram represent intra-atria1 conduction of the sinus or extrasystolic impulsesleading to the entrance of the reentrant pathway. At the exit of the pathway, unidirectional block occurs. The diagram showsthat the sinusimpulsesgiving rise to the first and secondP3wavesand the P, wave passthrough the reentrant pathway and then becomemanifest atria1 extrasystoles, A. The third P3impulse alsopassesthrough the reentrant pathway, but becomesa concealed atrial extrasystole becauseof insufficient conduction delay in the pathway. The other sinus impulsesare blocked within the pathway after invading someportion of the pathway. A within the strips = manifest atrial extrasystole; A in the diagram = atria; P = sinus P wave; RPA = reentrant pathway of atria1 extrasystoles; X = ventricular extrasystole.
Table I. Distribution of the numbers of P wavesintervening between atrial extrasystoles Number
Frequency
3(=4X1-1) 7(=4x2-1) 11(=4X3-1) 15(=4X4-1) 23(=4X6-1)
42 49 9 3 1
long interectopic interval containing 7 or 11 P waves is considerably longer than two or three times the short interval containing three P waves, respectively; namely, no common denominators are found between them. This indicates the absenceof parasystole. Table I showsthe distribution of the numbers of P waves intervening between two atrial extrasystoles throughout the long continuous recording. As shown in the Table, the number of intervening P waveswas always 4n - 1. The other form of odd numbers, 4n - 3, such as 1, 5, 9, or 13, was never seen. These findings indicate the presence of concealed atrial quadrigeminy. In a recent report on concealedatria1 bigeminy, Kinoshita et a1.6suggestedthat alternate sinusimpulsespassed through the reentrant pathway of atrial extrasystoles, but that they frequently becameconcealedatria1 extrasystoles becauseof insufficient conduction delay in the reentrant
pathway. In a similar way, the mechanismof concealed atrial quadrigeminy in the present report will be explained. A probable explanation is made by the diagram below the secondstrip in Fig. 1. The diagram showsthat every sinus impulse giving rise to P4,-1 (P3 or P,) passes through the reentrant pathway of the atrial extrasystoles. After passing through the pathway, the impulse sometimes becomesa manifest atria1 extrasystole, A, but, at other times it becomes a concealed atrial extrasystole becauseof insufbcient conduction delay in the pathway. In the diagram, the impulse giving rise to the third P, becomessuch a concealed reentrant extrasystole. All of the other sinusimpulsesare blocked at two or more levels within the pathway. REFERENCES
1. Satoh T, Kinoshita S, Tanabe Y, Kawasaki T, Katou K, Oda M, Yamamoto K, Kamada H, Yoshida T: Impulse conductivity in the region surrounding the extrasystolic focus: Wenckebach phenomenon of the coupling intervals and the “rule of multiples” (in Japanese). Saishin Igaku 15:1865, 1960. 2. Kinoshita S: Concealed ventricular extrasystoles due to interference and due to exit block. Circulation 52:230, 1975. 3. Levy MN, Goldman P, Goldberg L: Concealed quadrigeminy and quintageminy. J Electrocardiol 12:431, 1979. 4. Aygen MM, Dean H, Almog H: Concealed quadrigeminy. Cardiology 66:42, 1981. 5. Levy MN, Kerin N, Rubenfire M: Concealed atrial bigeminy and trigeminy. J Electrocardiol 11:185, 1978. 6. Kinoshita S, Kato Y, Nakagawa K, Yasukouchi T: Concealed atria1 bigeminy: Mechanisms of disappearance and reappearance of manifest extrasystoles. AM HEART J 107:919, 1984.
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