Circulation: Arrhythmia and Electrophysiology. 2008;1:145-146
doi: 10.1161/CIRCEP.108.779199
Images and Case Reports in Arrhythmia and Electrophysiology |
Paroxysmal Atrioventricular Block Induced by a Single Ventricular Premature Beat in the Absence of Overt Atrioventricular Conduction System Disease
Manish Undavia, MD
and
Avi Fischer, MD
From the Section of Electrophysiology, Mount Sinai Medical Center, New York, NY.
Correspondence to Avi Fischer, MD, Electrophysiology Section, Cardiovascular Institute, Mount Sinai Medical Center, One Gustave L. Levy Place, Box 1054, New York, NY 10029. E-mail avi.fischer{at}mssm.edu
Paroxysmal atrioventricular (AV) block is an unusual phenomenon that has been previously described. We report the case of a 78-year-old man who presented after an episode of syncope while seated in church. On presentation to the hospital, the initial electrocardiogram showed sinus rhythm with a normal PR interval, QRS duration, and corrected QT interval. During telemetry monitoring, several episodes of high-grade AV block were observed, and all episodes occurred after a single premature ventricular complex (Figure). AV conduction resumed after several nonconducted P waves (Figure). Ultimately, the patient was implanted with a dual-chamber pacemaker.

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Figure. AV block after a premature ventricular complex. The sinus rate is unchanged before and after the AV block. Resumption of AV conduction occurs with a narrower QRS and with delayed conduction.
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Advanced AV block has been known to occur after a single ventricular
premature complex in patients with advanced His-Purkinje system
disease. Transient AV conduction abnormalities, as a result
of rapid ventricular pacing, is thought to occur as a result
of depressed amplitude and excitability of Purkinje fibers and
may require retrograde conduction to the Purkinje system.
1 Perpetuation
of the AV conduction disturbance may result from phase 4 block;
however, this phenomenon generally occurs in the presence of
preexistent intraventricular and AV conduction disturbances
such as bundle-branch block and Mobitz II block.
2 It has also
been described in the absence of overt AV conduction disease.
The precise mechanism for the occurrence of paroxysmal AV block
remains speculative but is thought to be the result of concealed
retrograde conduction into the abnormal His-Purkinje system.
Retrograde activation after a single ventricular premature complex
can either worsen or improve conduction by altering the degree
of cellular uncoupling and the site of block.
3 Under abnormal
conditions, paroxysmal AV block can be observed after acceleration
or deceleration of the sinus rate, because of prolonged refractoriness.
4 Another possible explanation in our patient is that intra-Hisian
conduction disease was present but not manifest on the surface
electrocardiogram. On several occasions, the first QRS complex
after AV block is narrower and conducted with delay, raising
the possibility of equalized conduction delay within the His-Purkinje
system.
In this patient, with no evidence of preexisting AV conduction disease on the surface electrocardiogram, paroxysmal AV block followed a single ventricular premature complex and led to syncope.
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Disclosures
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None.
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References
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1. Gilmour RF Jr, Davis JR, Zipes DP. Overdrive suppression of conduction at the canine Purkinje-muscle junction.
Circulation. 1987; 76: 1388–1396.
[Abstract/Free Full Text]2. Josephson ME. Clinical Cardiac Electrophysiology—Techniques and Interpretations. 3rd ed. Philadelphia: Lippincott Williams and Wilkins; 2002.
3. Gonzalez MD, Scherlag BJ, Mabo P, Lazzara R. Functional dissociation of cellular activation as a mechanism of Mobitz type II atrioventricular block. Circulation. 1993; 87: 1389–1398.[Abstract/Free Full Text]
4. Chiale PA, Sanchez RA, Franco DA, Elizari MV, Rosenbaum MB. Overdrive prolongation of refractoriness and fatigue in the early stages of human bundle branch disease. J Am Coll Cardiol. 1994; 23: 724–732.[Abstract]