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Letter to the Editor

Pseudobradycardia-dependent BundleBranch Block Alternans

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o the Editor:

I read with interest the recent report by Carbone andedesco (1) describing a case of bradycardia-dependentundle branch block (BBB) on alternate beats. I wouldike to report an unusual case of pseudobradycardia-ependent BBB alternans.A 72-year-old man with hypertensive dilated cardio-yopathy and chronic left BBB was admitted to theospital with the diagnosis of unstable angina. A coro-ary arteriography revealed nonsignificant stenosis in 3essels and severe myocardial dysfunction with an eyec-ion fraction of 20%. He was discharged 5 days later onreatment with aspirin, furosemide, amlodipine, and ni-roglycerin.

Figure 1 shows a 12-lead electrocardiogram (ECG)n admission during the anginal attack. The patient isn regular sinus rhythm at 92 beats/min, and theR-interval measured at 0.16 s. There are 2 differentypes of QRS complexes on alternate beats: 1) a wideRS complex (0.18 s) revealing typical left BBB pat-

ern; and 2) a narrow QRS complex (0.10 s) showingeft ventricular hypertrophy with systolic overloadT-wave inversion, and convex upward ST-segmentloping depression in leads I and V6), and symetric-wave inversion (mostly terminal T-wave inversion)n leads V2 to V5 characteristic of the anamnestic-wave alterations routinely observed in cases of inter-ittent left BBB (2– 4). Figure 2A reveals details of

elected leads (aVL and aVF) of the same ECG. Subse-uently, once the pain was relieved with the adminis-ration of sublingual nitroglycerin, the ECG returned tois baseline persistent left BBB configuration. Alter-ans left BBB could not be induced either spontane-usly or after induced changes in cardiac rate withyperventilation or carotid sinus massage. Figure 2Becorded 2 days later shows rhythm strips from moni-or. There are a slight sinus arrhythmia with heart ratearying between 48 and 55 beats/min and a wide QRSomplexes with left BBB pattern. The persistence of leftBB at rate at which the QRS would be expected toormalize suggests that the persistent left BBB ispparently bradycardia-dependent and that the left

© 2003 Elsevier Inc. All rights reserved.0022-0736/03/3603-0014$30.00/0

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BB on alternate beats is a lesser manifestation of thisame bradycardia-dependency. Figure 2C recordedeveral seconds later shows other rhythm strips fromonitor. The first 3 beats show sinus rhythm at 50/min

nd a wide QRS complexes with left BBB configura-ion; the next 3 beats are premature ventricular con-ractions whereas the last 3 beats, occurring after a longostextrasystolic pause of 1.6 s, reveals severe sinusradycardia at 37/min and narrow QRS complexes. Thebrupt intraventricular conduction normalization co-nciding with severe bradycardia shows a tachycardia-ependent BBB mechanism.Although the left BBB on alternate beats appearedithout any cycle length change between wide andarrow QRS complexes, which would lead to an erro-eous diagnosis of nonrate dependent BBB, we believe

hat the conduction defect was rate-dependent becausehe conventional surface ECG is unable to recognizemall changes in cycle length (5). Left BBB cannot beonsidered a bradycardia-dependent block because theonduction disturbance disappeared after a long dia-tolic interval. Therefore, 2 tachycardia-dependentphase-3) mechanisms may be postulated to explainlternating BBB during a regular rhythm. First, aachycardia-dependent 2:1 anterograde block in theeft bundle branch without retrograde transeptal acti-ation during the aberrantly conducted beats (bidirec-ional block) (1,6,7). This occurs when the effectiveefractory period of the involved bundle branch isonger than the sum of 1 RR-interval and the retro-rade transeptal conduction time, and shorter than 2R-intervals. Second, a tachycardia-dependent antero-rade block in the left bundle branch associated with asupernormal” conduction due repetitive transeptaletrograde concealed penetration by impulses propa-ating along the contralateral bundle (1,8 –10). In suchircumstances, when exists an early phase of improvedesponsiveness in the blocked bundle, the impulsesalling alternately within this period of “supernormal”onduction will produce narrow QRS complexeshereas those falling outside will result in a BBB

onfiguration.A change from alternans to persistent BBB with a

urther slowing of the cardiac rate may simulate bra-ycardia-dependent block, as in the present case. Co-en et al. (6,7) proposed the name “pseudobradycar-

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Fig. 1. Twelve-lead ECG on admission showing in alternate beats a left BBB at constant RR interval (92 beats/min).

Fig. 2. (A) Detail of selected ECG leads reveals a heart rate at 92 beats/min and a left BBB on alternate beats. (B) Serialelectrocardiographic rhythm strips from monitor showing heart rate varying between 48 and 55 beats/min andcontinuous left BBB suggesting a bradycardia-dependent mechanism; and (C) shift from left BBB (at 50 beats/min) tonarrow QRS complex (at 37 beats/min) after a postextrasystolic pause showing a tachycardia-dependent type.

the subsequent disappearance of BBB with additionalincrease of the cycle length showed a tachycardia-dependent mechanism. The presence of persistent BBBat slower rate may be explained by an anterogradeblock along with retrograde transeptal activation of theblocked bundle branch (unidirectional block). Whenthe effective refractory period of the affected bundlebranch is longer than one RR interval, but is shorterthan the sum of its cycle and the transeptal conductiontime, the bundle branch will remain refractory foranterograde propagation. At the same time, the leftBBB is perpetuated by concealed transeptal retrogradeactivation in each beat (5).

A transition from persistent to normal intraventricularconduction after a long postextrasystolic pause occurswhen the interval from retrograde transeptal conductionto attempt anterograde conduction is longer than theeffective refractory period of the affected bundle branch.

In summary, persistent BBB may be caused by afunctional phenomenon without underlying structuralcardiac conduction disease.

Julian Ortega-Carnicer, MDJavier Blanco, MD

Filomena Ceres, MDFrom the Intensive Care Unit

Hospital Alarcos, Spain

References

1. Carbone V, Tedesco MA: Bundle branch block on alternatebeats: By what mechanism? J Electrocardiol 35:147, 2002

2. Denes P, Pick A, Miller RH, et al: A characteristic precordialrepolarization abnormality with intermittent left bundlebranch block. Ann Intern Med 89:55, 1978

3. Surawicz B: Transient T wave abnormalities in intermittentbundle branch block. Am J Cardiol 50:363, 1982

4. Michelotti MM, Swiryn S: Intermittent left bundle branchblock and associated T wave abnormalities. Arch Intern Med145:1667, 1985

5. Fish C, Zipes DP, McHenry PL: Rate dependent aberrancy.Circulation 48:714, 1973

6. Cohen HC, D’Cruz I, Arbel ER, et al: Tachycardia andbradycardia-dependent bundle branch block alternans.Clini-cal observations. Circulation 55:242, 1977

7. Cohen HC, D’Cruz IA, Pick A: Effects of stable andchanging rates and premature ventricular beats on tran-sient tachycardia-, pseudobradycardia-, and bradycardia-dependent bundle branch block alternans. J Electrocardiol12:151, 1979

8. Klein HO, Segni E, Kaplinsky E, et al: The supernormalphase of intraventricular conduction: Normalization of in-traventricular conduction of premature atrial beats. J Elec-trocardiol 15:89, 1982

9. Luzza F, Consolo A, Oreto G: Bundle branch block inalternate beats: The role of supernormal and concealedbundle branch conduction. Heart Lung 24:312, 1995

10. Erdogan O, Altun A: Electrocardiographic demonstration ofintermittrnt left bundle branch block because of the “link-ing” phenomenon. J Electrocardiol 35:143, 2002

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