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Widely split P waves in the presence of interatrial block
Journal of Electrocardiology 38 (2005) 324 – 326 www.elsevier.com/locate/jelectrocard
Widely split P waves in the presence of interatrial block Vignendra Ariyarajah, MDa, Navaid Asad, MDb, David H. Spodick, MD, DScc,T a
Department of Medicine, Saint Vincent Hospital, Worcester, MA 01608, USA Division of Cardiology, Saint Vincent Hospital, Worcester, MA 01608, USA c Cardiology Division, University of Massachusetts Medical School, USA Received 13 December 2004; revised 8 February 2005; accepted 17 March 2005 b
Abstract
Interatrial block (IAB; P wave z 110 milliseconds), conduction delay between the atria, is highly prevalent and is associated with atrial tachyarrhythmias, left atrial electromechanical dysfunction, as well as a potential risk for systemic embolism. However, much is still yet to be known of IAB’s exact pathophysiology and how it may manifest in relation to medical disease. We present an unusual case of widely split P waves in the presence of IAB in a severely ill patient. D 2005 Elsevier Inc. All rights reserved.
Keywords:
Interatrial block; Widely split P waves; Atrial conduction
1. Introduction Interatrial block (IAB; P wave z110 milliseconds) denotes prolonged conduction between the right and left atria (LA) [1,2]. However, because the mode IAB P-wave duration is 120 milliseconds, for increased diagnostic specificity, P waves z120 milliseconds are usually used. The degree of IAB, classified by Bayes de Luna [3,4] as partial or advanced, is denoted respectively by bifid (notched) or biphasic (F) P waves, the latter (much less common) in inferior leads. IAB’s importance is dictated by its high prevalence [5,6], as well as its associations with LA enlargement [7], LA electromechanical dysfunction [8], and especially atrial tachyarrhythmias [3,4,9,10]. As such, most electrophysiological (EP) studies have been tailored toward the investigation of atrial fibrillation and not directly toward IAB, forcing its definition and our understanding of this entity to heavily rely on electrocardiographic series and, perhaps, outdated observations. We present a unique case of an unusually widely split P wave in a patient with IAB. 2. Case history A 75-year-old man with history of systolic congestive heart failure, myocardial infarction, coronary angioplasty,
T Corresponding author. Tel.: +1 508 856 4891; fax: +1 508 856 4751. E-mail address: [email protected] (D.H. Spodick). 0022-0736/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2005.03.014
hypertension, and chronic obstructive pulmonary disease was referred to Saint Vincent Hospital for EP study after having ventricular fibrillation. He admitted to dyspnea and intermittent dizziness over 2 years, and his primary medications were ipratropium, albuterol, aspirin, digoxin, isosorbide dinitrate, furosemide, and lisinopril. He had bilateral basal pulmonary crackles and a grade 3/6 (old) systolic murmur; there are no other abnormalities. Complete blood count, basic metabolic panel, and cardiac enzymes were normal. His electrocardiogram (ECG) revealed sinus rhythm at 99 beats per minute with (known) first-degree atrioventricular blocks and incomplete IAB with P waves N160 milliseconds (Fig. 1). 2.1. Hospital course On EP study, he had no inducible ventricular arrhythmia, and an internal cardioverter-defibrillator was not implanted. Atrial stimulation tests revealed atrial premature contractions with paroxysmal atrial fibrillation despite normal sinoatrial node function and did not incorporate any further atrial conduction study. The patient was commenced on amiodarone 1200 mg/d and was monitored on telemetry with daily ECGs. Two days later, he developed mild dyspnea, and his ECG showed P-wave duration increase from 160 to 200 milliseconds with more pronounced notches (wider separation of right and left atria components). Dyspnea persisted, and cephalosporin was started for a right lower lobe infiltrate on chest x-ray film. The next day, however, as symptoms improved, his ECG
V. Ariyarajah et al. / Journal of Electrocardiology 38 (2005) 324 – 326
325
Fig. 1. ECG on admission showing interatrial block.
revealed an extremely widely split P wave in a single beat (Fig. 2) after a lone blocked premature P wave (caught in the S wave of that beat that preceded a dropped QRS complex during a 320-millisecond pause) in addition to PR-interval prolongation and widened QRS. Although
captured on the telemonitor, subsequent ECGs failed to show recurrence of this phenomenon, but IAB, with pronouncedly notched P waves continued. Forty-eight hours after this ECG abnormality first appeared, he expired having ventricular fibrillation.
Fig. 2. ECG now showing more widely split P waves.
326
V. Ariyarajah et al. / Journal of Electrocardiology 38 (2005) 324 – 326
3. Discussion This is a unique case of transient extreme P-wave splitting in a patient with partial IAB. We could find no reports of such phenomenal sudden P-wave change. Chung [11] described P-wave aberrancies after premature ventricular beats (Chung’s phenomenon) but clearly without the preceding pause or, notably, P-wave splitting. Soejima et al [12] described widely separated P waves, but IAB was absent. As such, because its vector (baxisQ) differs from that of the sinus beats, this striking split P wave is likely to be an ectopic escape beat. Although this aberrant P wave’s width was greater than that of its sinus counterpart, this remained an incomplete (partial) IAB, because unlike advanced (bcompleteQ) IAB, its second LA component was not inverted in inferior leads. With regard to the pause and PR-interval change, it is possible that the blocked premature P wave preceding the pause (Fig. 2) could have invaded the already slowed interatrial conducting pathway and further prolonged refractoriness without completely blocking it, hence greatly increasing P-wave duration. Although unlikely, it is difficult to ascertain whether this degree of split is in fact a manifestation of IAB or an unreported medication effect such as that of amiodarone as there have been few studies directed toward its effects on the atria, specifically in relation to P-wave splitting or IAB [13]. Careful evaluation of serial ECGs and close monitoring of IAB patients might unearth more examples or provide clearer explanation. References [1] Willems JL, Demedina EO, Bernard R, et al. World Health Organization International Society and Federation of Cardiology Task
[2] [3]
[4]
[5] [6] [7]
[8] [9]
[10]
[11] [12]
[13]
Force criteria for intraventricular conduction disturbances and preexcitation. J Am Coll Cardiol 1985;5:1261. Cohen J, Scherf D. Complete interatrial and intra-atrial block (atrial dissociation). Am Heart J 1965;70:23. Bayes de Luna A. Electrocardiographic alterations due to atrial pathology. Clinical electrocardiography: a textbook. New York7 Futura Company Inc; 1998. p. 69. Bayes de Luna A, Cladellas M, Oter R, et al. Interatrial conduction block and retrograde activation of the left atrium and paroxysmal supraventricular tachyarrhythmia. Eur Heart J 1988;9(10):1112. Jairath UC, Spodick DH. Exceptional prevalence of interatrial block in a general hospital population. Clin Cardiol 2001;24:548. Asad N, Spodick DH. Prevalence of interatrial block in a general hospital population. Am J Cardiol 2003;91:609. Velury V, Spodick DH. Axial correlates of P-VI in left atrial enlargement and relation to interatrial block. Am J Cardiol 1994; 73:998. Goyal SB, Spodick DH. Electromechanical dysfunction of the left atrium associated with interatrial block. Am Heart J 2001;142:823. Agarwal YK, Aronow WS, Levy JA, et al. Association of interatrial block with the development of atrial fibrillation. Am J Cardiol 2003; 91:882. Leier CV, Meacham JA, Schaal SF. Prolonged atrial conduction. A major predisposing factor for the development of atrial flutter. Circulation 1978;57:213. Chung EK. Principles of cardiac arrhythmias. Baltimore7 Williams & Wilkins; 1989. p. 495. Soejima K, Mitamura H, Miyazaki T, et al. A case of widely split double P waves with marked intra-atrial conduction delay. J Cardiovasc Electrophysiol 1997;8:1296. Banasiak W, Telichowski A, Anker SD, et al. Effects of amiodarone on the P-wave triggered signal-averaged ECG in patients with paroxysmal atrial fibrillation and coronary artery disease. Am J Cardiol 1999; 83(1):112, A9.
Widely split P waves in the presence of interatrial block Vignendra Ariyarajah, MDa, Navaid Asad, MDb, David H. Spodick, MD, DScc,T a
Department of Medicine, Saint Vincent Hospital, Worcester, MA 01608, USA Division of Cardiology, Saint Vincent Hospital, Worcester, MA 01608, USA c Cardiology Division, University of Massachusetts Medical School, USA Received 13 December 2004; revised 8 February 2005; accepted 17 March 2005 b
Abstract
Interatrial block (IAB; P wave z 110 milliseconds), conduction delay between the atria, is highly prevalent and is associated with atrial tachyarrhythmias, left atrial electromechanical dysfunction, as well as a potential risk for systemic embolism. However, much is still yet to be known of IAB’s exact pathophysiology and how it may manifest in relation to medical disease. We present an unusual case of widely split P waves in the presence of IAB in a severely ill patient. D 2005 Elsevier Inc. All rights reserved.
Keywords:
Interatrial block; Widely split P waves; Atrial conduction
1. Introduction Interatrial block (IAB; P wave z110 milliseconds) denotes prolonged conduction between the right and left atria (LA) [1,2]. However, because the mode IAB P-wave duration is 120 milliseconds, for increased diagnostic specificity, P waves z120 milliseconds are usually used. The degree of IAB, classified by Bayes de Luna [3,4] as partial or advanced, is denoted respectively by bifid (notched) or biphasic (F) P waves, the latter (much less common) in inferior leads. IAB’s importance is dictated by its high prevalence [5,6], as well as its associations with LA enlargement [7], LA electromechanical dysfunction [8], and especially atrial tachyarrhythmias [3,4,9,10]. As such, most electrophysiological (EP) studies have been tailored toward the investigation of atrial fibrillation and not directly toward IAB, forcing its definition and our understanding of this entity to heavily rely on electrocardiographic series and, perhaps, outdated observations. We present a unique case of an unusually widely split P wave in a patient with IAB. 2. Case history A 75-year-old man with history of systolic congestive heart failure, myocardial infarction, coronary angioplasty,
T Corresponding author. Tel.: +1 508 856 4891; fax: +1 508 856 4751. E-mail address: [email protected] (D.H. Spodick). 0022-0736/$ – see front matter D 2005 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2005.03.014
hypertension, and chronic obstructive pulmonary disease was referred to Saint Vincent Hospital for EP study after having ventricular fibrillation. He admitted to dyspnea and intermittent dizziness over 2 years, and his primary medications were ipratropium, albuterol, aspirin, digoxin, isosorbide dinitrate, furosemide, and lisinopril. He had bilateral basal pulmonary crackles and a grade 3/6 (old) systolic murmur; there are no other abnormalities. Complete blood count, basic metabolic panel, and cardiac enzymes were normal. His electrocardiogram (ECG) revealed sinus rhythm at 99 beats per minute with (known) first-degree atrioventricular blocks and incomplete IAB with P waves N160 milliseconds (Fig. 1). 2.1. Hospital course On EP study, he had no inducible ventricular arrhythmia, and an internal cardioverter-defibrillator was not implanted. Atrial stimulation tests revealed atrial premature contractions with paroxysmal atrial fibrillation despite normal sinoatrial node function and did not incorporate any further atrial conduction study. The patient was commenced on amiodarone 1200 mg/d and was monitored on telemetry with daily ECGs. Two days later, he developed mild dyspnea, and his ECG showed P-wave duration increase from 160 to 200 milliseconds with more pronounced notches (wider separation of right and left atria components). Dyspnea persisted, and cephalosporin was started for a right lower lobe infiltrate on chest x-ray film. The next day, however, as symptoms improved, his ECG
V. Ariyarajah et al. / Journal of Electrocardiology 38 (2005) 324 – 326
325
Fig. 1. ECG on admission showing interatrial block.
revealed an extremely widely split P wave in a single beat (Fig. 2) after a lone blocked premature P wave (caught in the S wave of that beat that preceded a dropped QRS complex during a 320-millisecond pause) in addition to PR-interval prolongation and widened QRS. Although
captured on the telemonitor, subsequent ECGs failed to show recurrence of this phenomenon, but IAB, with pronouncedly notched P waves continued. Forty-eight hours after this ECG abnormality first appeared, he expired having ventricular fibrillation.
Fig. 2. ECG now showing more widely split P waves.
326
V. Ariyarajah et al. / Journal of Electrocardiology 38 (2005) 324 – 326
3. Discussion This is a unique case of transient extreme P-wave splitting in a patient with partial IAB. We could find no reports of such phenomenal sudden P-wave change. Chung [11] described P-wave aberrancies after premature ventricular beats (Chung’s phenomenon) but clearly without the preceding pause or, notably, P-wave splitting. Soejima et al [12] described widely separated P waves, but IAB was absent. As such, because its vector (baxisQ) differs from that of the sinus beats, this striking split P wave is likely to be an ectopic escape beat. Although this aberrant P wave’s width was greater than that of its sinus counterpart, this remained an incomplete (partial) IAB, because unlike advanced (bcompleteQ) IAB, its second LA component was not inverted in inferior leads. With regard to the pause and PR-interval change, it is possible that the blocked premature P wave preceding the pause (Fig. 2) could have invaded the already slowed interatrial conducting pathway and further prolonged refractoriness without completely blocking it, hence greatly increasing P-wave duration. Although unlikely, it is difficult to ascertain whether this degree of split is in fact a manifestation of IAB or an unreported medication effect such as that of amiodarone as there have been few studies directed toward its effects on the atria, specifically in relation to P-wave splitting or IAB [13]. Careful evaluation of serial ECGs and close monitoring of IAB patients might unearth more examples or provide clearer explanation. References [1] Willems JL, Demedina EO, Bernard R, et al. World Health Organization International Society and Federation of Cardiology Task
[2] [3]
[4]
[5] [6] [7]
[8] [9]
[10]
[11] [12]
[13]
Force criteria for intraventricular conduction disturbances and preexcitation. J Am Coll Cardiol 1985;5:1261. Cohen J, Scherf D. Complete interatrial and intra-atrial block (atrial dissociation). Am Heart J 1965;70:23. Bayes de Luna A. Electrocardiographic alterations due to atrial pathology. Clinical electrocardiography: a textbook. New York7 Futura Company Inc; 1998. p. 69. Bayes de Luna A, Cladellas M, Oter R, et al. Interatrial conduction block and retrograde activation of the left atrium and paroxysmal supraventricular tachyarrhythmia. Eur Heart J 1988;9(10):1112. Jairath UC, Spodick DH. Exceptional prevalence of interatrial block in a general hospital population. Clin Cardiol 2001;24:548. Asad N, Spodick DH. Prevalence of interatrial block in a general hospital population. Am J Cardiol 2003;91:609. Velury V, Spodick DH. Axial correlates of P-VI in left atrial enlargement and relation to interatrial block. Am J Cardiol 1994; 73:998. Goyal SB, Spodick DH. Electromechanical dysfunction of the left atrium associated with interatrial block. Am Heart J 2001;142:823. Agarwal YK, Aronow WS, Levy JA, et al. Association of interatrial block with the development of atrial fibrillation. Am J Cardiol 2003; 91:882. Leier CV, Meacham JA, Schaal SF. Prolonged atrial conduction. A major predisposing factor for the development of atrial flutter. Circulation 1978;57:213. Chung EK. Principles of cardiac arrhythmias. Baltimore7 Williams & Wilkins; 1989. p. 495. Soejima K, Mitamura H, Miyazaki T, et al. A case of widely split double P waves with marked intra-atrial conduction delay. J Cardiovasc Electrophysiol 1997;8:1296. Banasiak W, Telichowski A, Anker SD, et al. Effects of amiodarone on the P-wave triggered signal-averaged ECG in patients with paroxysmal atrial fibrillation and coronary artery disease. Am J Cardiol 1999; 83(1):112, A9.