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New Irregular Rhythm in a Patient with Baseline Left Bundle Branch Block
N e w I r re g u l a r R h y t h m i n a Patient with Baseline Left B undle Branch B loc k Marwan M. Refaat, MDa, Byron K. Lee, MD, MASb,* KEYWORDS Bundle branch block Implantable cardioverter-defibrillator Ventricular tachycardia
KEY POINTS Transition from wide to narrow QRS complex has several mechanisms such as heart rate change, “peel-back” refractoriness, rate-dependent progressive shortening of bundle branch refractoriness, gap phenomena, supernormal conduction, loss of preexcitation, premature ventricular complex, or ventricular tachycardia (VT) ipsilateral to the bundle branch block and equal conduction delay in both of the bundle branches. The QRS complexes can be normal or near normal in width when the VT originates from the ventricular conduction system or near the ventricular conduction system.
A 63-year-old man with a history of Reiter syndrome, nonischemic idiopathic cardiomyopathy, and baseline left bundle branch block (LBBB) had a syncopal episode and episodes of nonsustained ventricular tachycardia (VT). He underwent biventricular implantable cardioverterdefibrillator (ICD) placement. Four months later, the patient presented with fatigue and episodes of palpitations. He was admitted for further management. Twelve-lead electrocardiograms (ECGs) recorded during his initial presentation are shown in Fig. 1.
CLINICAL QUESTION What is the rhythm in this patient with baseline LBBB pattern?
ELECTROPHYSIOLOGY STUDY AND CLINICAL COURSE The patient had an irregular tachycardia at 138 beats/min with QRS complexes much narrower than his baseline LBBB QRS. The QRS duration was generally 105 milliseconds, but there were some occasional wide complex beats. P waves could not be clearly identified on the baseline ECG. The rhythm on the initial 12-lead ECG was diagnosed as atrial fibrillation with occasional aberrant beats or premature ventricular complexes (PVCs). This diagnosis was later proved to be wrong. The true diagnosis was VT, which was determined from the ICD interrogation that clearly showed atrioventricular dissociation (Fig. 2). The atrial beats march out at about 65 beats/min, whereas the ventricular beats are occurring at
Disclosures: None of the authors have any conflicts to disclose relevant to this article. a Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, University of California, San Francisco, 500 Parnassus Avenue, San Francisco, CA 94143, USA; b Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, University of California, San Francisco, 500 Parnassus Avenue, Box 1354, MU 429, San Francisco, CA 94143, USA * Corresponding author. E-mail address: [email protected] Card Electrophysiol Clin 4 (2012) 655–657 http://dx.doi.org/10.1016/j.ccep.2012.08.027 1877-9182/12/$ – see front matter Ó 2012 Elsevier Inc. All rights reserved.
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Refaat & Lee
Fig. 1. Twelve-lead electrocardiograms of the patient’s presenting rhythm show an irregular tachycardia at a rate of 138 beats/min with QRS complexes narrower than his baseline left bundle branch block. There are occasional wider complex beats.
about 140 beats/min but somewhat irregularly. There are more ventricular beats than atrial beats and there is no relationship between the atrial and ventricular rhythms, confirming that the ventricular rhythm must be VT. The patient underwent an electrophysiology study, which revealed an easily inducible stable VT with earliest activation mapping to the septal superior anterior left ventricle, which terminated the VT.
DISCUSSION This patient’s baseline 12-lead ECG showed LBBB. By contrast, his presenting ECG showed
a tachycardia with QRS complexes much narrower than his baseline LBBB. Transition from wide to narrow QRS complex has several mechanisms such as heart-rate change, “peel-back” refractoriness, rate-dependent progressive shortening of bundle branch refractoriness, gap phenomena, supernormal conduction, loss of preexcitation, PVC, or VT ipsilateral to the bundle branch block and equal conduction delay in both of the bundle branches.1–3 The patient had a baseline LBBB, no evidence of premature atrial complex, no delay in the right bundle, or change in conduction intervals. He had a left ventricular VT originating ipsilateral to
Fig. 2. ICD interrogation confirming ventricular tachycardia. Atrial channel markers and the P waves on the Canto-superior vena cava electrogram (arrows) show that the atrial beats are marching out slower and are independent of the ventricular beats.
Irregular Rhythm in Patient with LBBB bundle branch block, which can cause normal or near normal QRS duration mimicking a supraventricular arrhythmia. In this instance, the rhythm was misdiagnosed as atrial fibrillation. The QRS complexes can be normal or near normal in width when the VT originates from the ventricular conduction system or near the ventricular conduction system. In summary, this case illustrates the physiology described previously in a patient with an LBBB who is detected to have a near normal QRS complex rhythm.
REFERENCES 1. Prystowsky EN, Klein GJ. Cardiac arrhythmias: an integrated approach for the clinician. New York: McGraw-Hill; 1994. p. 64–9. 2. Akhtar M, Damato AN, Batsford WP, et al. Unmasking and conversion of gap phenomenon in the human heart. Circulation 1974;49:624–30. 3. Massumi RA, Amsterdam EA, Mason DT. Phenomenon of supernormality in the human heart. Circulation 1972;46:264–75.
657
KEY POINTS Transition from wide to narrow QRS complex has several mechanisms such as heart rate change, “peel-back” refractoriness, rate-dependent progressive shortening of bundle branch refractoriness, gap phenomena, supernormal conduction, loss of preexcitation, premature ventricular complex, or ventricular tachycardia (VT) ipsilateral to the bundle branch block and equal conduction delay in both of the bundle branches. The QRS complexes can be normal or near normal in width when the VT originates from the ventricular conduction system or near the ventricular conduction system.
A 63-year-old man with a history of Reiter syndrome, nonischemic idiopathic cardiomyopathy, and baseline left bundle branch block (LBBB) had a syncopal episode and episodes of nonsustained ventricular tachycardia (VT). He underwent biventricular implantable cardioverterdefibrillator (ICD) placement. Four months later, the patient presented with fatigue and episodes of palpitations. He was admitted for further management. Twelve-lead electrocardiograms (ECGs) recorded during his initial presentation are shown in Fig. 1.
CLINICAL QUESTION What is the rhythm in this patient with baseline LBBB pattern?
ELECTROPHYSIOLOGY STUDY AND CLINICAL COURSE The patient had an irregular tachycardia at 138 beats/min with QRS complexes much narrower than his baseline LBBB QRS. The QRS duration was generally 105 milliseconds, but there were some occasional wide complex beats. P waves could not be clearly identified on the baseline ECG. The rhythm on the initial 12-lead ECG was diagnosed as atrial fibrillation with occasional aberrant beats or premature ventricular complexes (PVCs). This diagnosis was later proved to be wrong. The true diagnosis was VT, which was determined from the ICD interrogation that clearly showed atrioventricular dissociation (Fig. 2). The atrial beats march out at about 65 beats/min, whereas the ventricular beats are occurring at
Disclosures: None of the authors have any conflicts to disclose relevant to this article. a Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, University of California, San Francisco, 500 Parnassus Avenue, San Francisco, CA 94143, USA; b Section of Cardiac Electrophysiology, Division of Cardiology, Department of Medicine, University of California, San Francisco, 500 Parnassus Avenue, Box 1354, MU 429, San Francisco, CA 94143, USA * Corresponding author. E-mail address: [email protected] Card Electrophysiol Clin 4 (2012) 655–657 http://dx.doi.org/10.1016/j.ccep.2012.08.027 1877-9182/12/$ – see front matter Ó 2012 Elsevier Inc. All rights reserved.
cardiacEP.theclinics.com
CLINICAL PRESENTATION
656
Refaat & Lee
Fig. 1. Twelve-lead electrocardiograms of the patient’s presenting rhythm show an irregular tachycardia at a rate of 138 beats/min with QRS complexes narrower than his baseline left bundle branch block. There are occasional wider complex beats.
about 140 beats/min but somewhat irregularly. There are more ventricular beats than atrial beats and there is no relationship between the atrial and ventricular rhythms, confirming that the ventricular rhythm must be VT. The patient underwent an electrophysiology study, which revealed an easily inducible stable VT with earliest activation mapping to the septal superior anterior left ventricle, which terminated the VT.
DISCUSSION This patient’s baseline 12-lead ECG showed LBBB. By contrast, his presenting ECG showed
a tachycardia with QRS complexes much narrower than his baseline LBBB. Transition from wide to narrow QRS complex has several mechanisms such as heart-rate change, “peel-back” refractoriness, rate-dependent progressive shortening of bundle branch refractoriness, gap phenomena, supernormal conduction, loss of preexcitation, PVC, or VT ipsilateral to the bundle branch block and equal conduction delay in both of the bundle branches.1–3 The patient had a baseline LBBB, no evidence of premature atrial complex, no delay in the right bundle, or change in conduction intervals. He had a left ventricular VT originating ipsilateral to
Fig. 2. ICD interrogation confirming ventricular tachycardia. Atrial channel markers and the P waves on the Canto-superior vena cava electrogram (arrows) show that the atrial beats are marching out slower and are independent of the ventricular beats.
Irregular Rhythm in Patient with LBBB bundle branch block, which can cause normal or near normal QRS duration mimicking a supraventricular arrhythmia. In this instance, the rhythm was misdiagnosed as atrial fibrillation. The QRS complexes can be normal or near normal in width when the VT originates from the ventricular conduction system or near the ventricular conduction system. In summary, this case illustrates the physiology described previously in a patient with an LBBB who is detected to have a near normal QRS complex rhythm.
REFERENCES 1. Prystowsky EN, Klein GJ. Cardiac arrhythmias: an integrated approach for the clinician. New York: McGraw-Hill; 1994. p. 64–9. 2. Akhtar M, Damato AN, Batsford WP, et al. Unmasking and conversion of gap phenomenon in the human heart. Circulation 1974;49:624–30. 3. Massumi RA, Amsterdam EA, Mason DT. Phenomenon of supernormality in the human heart. Circulation 1972;46:264–75.
657