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Laughter-Induced Left Bundle Branch BlockGRANT V. CHOW, M.D., DIPAN DESAI, D.O., DAVID D. SPRAGG, M.D.,

and SAMMY ZAKARIA, M.D.

From the Department of Medicine and Division of Cardiology, Johns Hopkins Bayview Medical Center, Johns Hopkins University Schoolof Medicine, Baltimore, Maryland, USA

Laughter-Induced LBBB. We present the case of a patient with ischemic heart disease and inter-mittent left bundle branch block, reproducibly induced by laughter. Following treatment of ischemia withsuccessful deployment of a drug-eluting stent, no further episodes of inducible LBBB were seen. Transientischemia, exacerbated by elevated intrathoracic pressure during laughter, may have contributed to onsetof this phenomenon. (J Cardiovasc Electrophysiol, Vol. pp. 1-3)

inducible arrhythmia, ischemia, left bundle branch block

Case Report

A 66-year-old man with diabetes, hypertension, dyslipi-demia, and chronic tobacco dependence presented with syn-cope immediately after a bout of laughter and coughing.There were no other prodromal symptoms, chest pain, pal-pitations, dyspnea, bowel or bladder dysfunction, or seizure-like activity prior to the event. Witnesses reported that hehad fallen forward, striking a nearby table, which led tosuperficial nasal and forehead trauma. He then remained un-

No disclosures.

Address for correspondence: Grant Chow, M.D., Johns Hopkins UniversitySchool of Medicine, 600 N. Wolfe Street, Baltimore, MD 21287, USA. Fax:410-550-1094; E-mail: gchow2@jhmi.edu

Manuscript received 15 December 2011; Revised manuscript received13 January 2012; Accepted for publication 24 January 2012.

doi: 10.1111/j.1540-8167.2012.02296.x

Figure 1. Baseline electrocardiogram showing normal sinus rhythm with first degree atrioventricular block, left atrial enlargement, and nonspecific T-wavechanges. QRS complexes are narrow.

conscious for “several minutes,” but spontaneously awokewith a normal mental status.

After he was brought to the hospital, the patient revealed ahistory of exertional, left-sided, dull chest pain that radiatedto his dorsal neck. The pain was mild to moderate in inten-sity, occurred most days of the week, and generally resolvedwith rest. His initial evaluation was largely normal, includingunremarkable vital signs, physical exam, laboratory studies,and serial cardiac enzymes. However, he did have abnor-malities on his admission electrocardiogram (ECG), with afirst-degree atrioventricular delay, left atrial abnormality, andnonspecific T-wave changes (Fig. 1).

Assessment

To evaluate symptoms of syncope and exertional chestpain, an exercise treadmill nuclear stress test was performed.During exercise, the patient experienced no ischemic symp-toms, lightheadedness, or syncope. His ECG did not revealany ST segment changes consistent with ischemia, although

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Figure 2. A: Electrocardiogram (ECG) near peak stress (126 beats per minute), showing sinus tachycardia with frequent left bundle pattern beats. B: ECGduring the post-stress (resting) period, in which intermittent left bundle branch block (LBBB) was repetitively inducible during laughter (arrows). Note thatheart rates were significantly slower (86 beats per minute), and did not change with laughter.

Chow et al. Laughter-Induced LBBB 3

he developed frequent left bundle branch block (LBBB) pat-tern beats (Fig. 2A) with higher levels of exercise.

In the post-stress rest period, the patient began tellingjokes to staff members and soon started laughing. An abruptchange was noted in the ECG tracing, which showed a newLBBB temporally associated with bouts of laughter, with-out change in the heart rate or PR interval (Fig. 2B). Whenthe patient was asked to stop laughing, QRS complex widthimmediately narrowed to the normal range. The patient thenresumed laughing, and his LBBB reappeared. His laughterevents reoccurred several times in the recovery period, withthe patient exhibiting apparent volitional control over his con-duction abnormality. During this time, the patient remainedfree of chest pain, shortness of breath, dizziness, or light-headedness. He subsequently underwent nuclear perfusionimaging, which showed a moderate-sized, moderate severity,partially reversible defect in the inferolateral wall, consistentwith prior infarct with inducible peri-infarct ischemia. Leftventricular ejection fraction was grossly normal.

The patient was referred for cardiac catheterization. Uponarrival to the catheterization laboratory, the LBBB had be-come persistent, without noted inducible changes. Coronaryangiography showed triple vessel coronary disease with se-vere stenosis of the circumflex coronary artery, and revascu-larization was successfully performed with deployment of adrug-eluting stent.

Discussion

Initially, the patient was thought to have transient LBBBsecondary to increased heart rates during episodes of laugh-ter (rate-related LBBB). However, evaluation of the ECGtracings during stress revealed a narrow QRS complex atsignificantly faster heart rates than those observed duringthe post-stress resting phase. Given that no pharmacologicagents had been administered and no other reversible factorswere apparent, the patient was diagnosed with intermittentLBBB, triggered by laughter, in the setting of ischemic heartdisease. Even hours following the recovery period, the pa-tient retained the ability to induce LBBB with laughter whilesocializing with his roommate.

Although variants of transient or intermittent LBBB arecommonly seen in cases of reversible ischemia,1 tachycar-dia,2 or electrolyte abnormalities,3 reproducible volitionalcontrol of intermittent LBBB via other routes is rare. Thelargest case series regarding volitional control of LBBB waspublished in 1964,4 in which Bauer reported a series of5 patients, 4 of whom had ischemic heart disease. In hisreport, inciting or suppressing maneuvers associated withLBBB included carotid sinus massage, rapid or deep breath-ing, the Valsalva maneuver, physical exertion with increased

heart rate, carotid sinus pressure, and direct ocular pressure.These maneuvers produced varying effects, with suppressionof LBBB likely related to increased vagal tone and resultantbradycardia. An online literature search revealed no prior re-ported cases of volitional induction of LBBB with laughter.

In our patient, we suspect that changes in intrathoracicpressure during laughter may have led to compromised car-diac perfusion and attendant LBBB. Evidence to supportthis mechanism includes the observation that LBBB wassustained only during laughter, that LBBB occurred in theabsence of heart rate changes, and that LBBB could not be in-duced with laughter after revascularization. Persistent LBBBafter a single nonconducted beat can be seen with transsep-tal conduction and retrograde penetration of the left-sidedfascicles; that linking phenomenon and persistent LBBB,though, would not be dependent on sustained laughter. Phase3 (tachycardia mediated) or phase 4 (pause dependent) LBBBare equally unlikely in this case, given the lack of heart rateperturbation with laughter.

As for the patient’s presenting symptom of syncope, thetwo most likely etiologies of his syncopal event involve ei-ther activation of the Bezold–Jarisch reflex during coughingwith laughter, or transient arrhythmia resulting in brief hy-poperfusion of the brain (Stokes–Adams syndrome). A thirdpotential mechanism involves hemodynamic compromise as-sociated with laughter-induced LBBB; however, given thatthe patient had no lightheadedness during LBBB episodeswhile admitted, this appears unlikely.

Two weeks after revascularization, our patient contin-ued to be free of further chest pain, pressure, or syncopalepisodes. Six weeks later, he underwent repeat exercise tread-mill stress testing with a “laughter challenge,” which showedconsistently narrow QRS complexes and no evidence of in-ducible LBBB. The patient remained asymptomatic through-out the stress and post-stress period, and no further invasivestudies or procedures were planned.

Acknowledgment: The authors wish to thank Mary Hannah, P.A.-C., forher assistance in the care of our patient during his inpatient admission, andfor bringing this phenomenon to our attention.

References

1. Abben R, Denes P, Rosen KM. Evaluation of criteria for diagnosisof myocardial infarction: Study of 256 patients with intermittent leftbundle branch block. Chest 1979;75:575-578.

2. Vasey C, O’Donnell J, Morris S, McHenry P. Exercise-induced leftbundle branch block and its relation to coronary artery disease. Am JCardiol 1985;56:892-895.

3. Indik JH. A pointed clue. Am J Med 2005;118:1221-1222.4. Bauer GE. Bundle-branch block under voluntary control. Br Heart J

1964;26:167-179.