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Progression of partial to advanced interatrial block
Journal of Electrocardiology 39 (2006) 177 – 179 www.elsevier.com/locate/jelectrocard
Progression of partial to advanced interatrial block Vignendra Ariyarajah, MDa,b, David H. Spodick, MDc,T a
Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC), Veterans Affairs Boston Healthcare System, Boston, MA, USA b Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA c Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA Received 20 July 2005
Abstract
Interatrial block (IAB), prolonged conduction between the atria, is denoted by P waves of 110 milliseconds or more and may manifest as partial or advanced. Theoretically, partial IAB may progress to its advanced counterpart if conduction delay increases to complete block. However, there have been no reports of such progression, and electrophysiologic studies have not shown this phenomenon. We briefly review the interatrial conducting pathways of IAB and present the first documentation of possible progression of partial to advanced IAB. D 2006 Elsevier Inc. All rights reserved.
Keywords:
Partial interatrial block; Advanced interatrial block; Bachmann’s bundle; Progression
1. Background Interatrial block (IAB) is caused by delay in electrical impulse transmission between the right (RA) and left atria (LA), and implies subsequent delayed LA activation [1]. Although normal P-wave duration is defined by the World Health Organizational/International Society and Federation of Cardiology Task Force as less than 110 milliseconds [2], what is depicted on the electrocardiogram (ECG), P waves 110 milliseconds or more, is block (on the ECG, time = duration of conduction; excessive time or delay = block). Interatrial block was shown to be highly prevalent in 2 separate but comparable general hospital populations of 1000 patients each (41.1% in one [3] and 47% in the other [4]), with both series demonstrating a higher prevalence among those older than 59 years. Interatrial block is a predictor of atrial tachyarrhythmias, especially atrial fibrillation, with a reported prevalence of 52% in such patients when compared with 18% of the investigated control group [5,6]. Interatrial block is also strongly associated with LA enlargement (88% prevalence) [7], LA electromechanical dysfunction (mean LA kinetic
T Corresponding author. University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655. Fax: +1 508 856 4571. E-mail address: [email protected] (D.H. Spodick). 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2005.08.016
energy of 19.8 vs 64.7 kdyne/cm per second in controls, P b .0001) [7], and risk for embolism (80% prevalence in embolic strokes) [8]. Because discrete lesions produced experimentally in the Bachmann bundle (BB) delay activation of the LA and result in the typical prolonged, often notched, P waves seen in IAB, abnormality of this classically preferred route for interatrial impulse transmission is thought to be the principal mechanism of IAB [1,9]. Two forms of interatrial conduction delay have been classified: partial and advanced IAB [1,9,10]. 2. Partial and advanced IAB In partial IAB, an incomplete block occurs in the BB, delaying sinus impulses generated in the RA from reaching the LA. This produces wide, usually bifid, P waves [1]. However, when conduction via the BB is completely blocked, sinus impulses can no longer cross the BB but are believed to instead first depolarize the RA with an inferior course toward the atrioventricular (AV) junction and then spread superiorly to produce a caudocephalic depolarization of the LA. This is described as advanced IAB and is captured on the ECG as biphasic (F) P waves in the inferior leads [10]. James [11] and, later, Treux [12] described 3 different internodal pathways that traverse the RA from the sinus to the AV node: anterior, middle, and posterior. Any one of
178
V. Ariyarajah, D.H. Spodick / Journal of Electrocardiology 39 (2006) 177–179
Fig. 1. Patient’s ECG depicting partial IAB (see text).
these routes is thought to facilitate depolarization of the RA. Although the exact mechanism of activation within the LA is much less known, let alone such caudocephalic spread of depolarization from the AV node in advanced IAB, other potential interatrial connections have been studied. Through RA electroanatomic mapping, Roithinger
et al [13] demonstrated several functional pathways by pacing the coronary sinus or the LA. Markides et al [14] used a noncontact mapping system to show that posterior interatrial connections could also conduct to the LA. Absence of discrete tracts, however, has left their existence open to dispute.
Fig. 2. Patient’s ECG now showing advanced IAB (see text).
V. Ariyarajah, D.H. Spodick / Journal of Electrocardiology 39 (2006) 177–179
Nevertheless, in theory, partial IAB [9] could at some point progress to advanced IAB [10] if the severity of its BB conduction block appears complete. However, there have been no electrophysiologic atrial pathway mapping studies to date that have documented such progression or even hinted at a possibility of such occurrence, and no case reports of this phenomenon have been presented. We present 2 ECGs of the same patient showing progression from partial to advanced IAB over the course of 5 years. The patient was a 71-year-old male with a history of hypertension, chronic obstructive pulmonary disease, and left ventricular hypertrophy. Fig. 1 shows one of the patient’s ECGs from 1999, depicting partial IAB with classic bifid P waves of 120 milliseconds or more. Fig. 2 shows the patient’s ECG from 2004 with distinct biphasic (F) P waves of 120 milliseconds or more in the inferior leads, denoting advanced IAB. Over the course of 5 years, his blood pressure had increased and a second antihypertensive medication was added. He had also developed a right bundle branch block (Fig. 2). Clinically, however, the patient’s condition remained unchanged and he had declined further investigation.
3. Discussion and conclusion This patient’s ECGs (Figs. 1 and 2) suggest that partial IAB [9] progressed to its advanced counterpart [10] possibly because of increasing block in BB. Absence of an electrophysiologic evaluation, however, severely limits our ability to confirm this interesting hypothesis. The absence of reports and documentation of such progression is surprising. However, the lack of observations may be explained in part because interatrial conduction disorder has been largely omitted in general medical, and cardiology text books [15]. Therefore, many clinicians fail to recognize IAB merely because of the lack of knowledge of this medical entity, with consequent underreporting of its prevalence. Also, advanced IAB is uncommon compared with its partial counterpart, further resulting in a decrease of clinical recognition [15]. However, the clinical significance of one IAB-type versus the other is unknown, and it cannot be ascertained if our patient’s worsening hypertension was a precursor or, in fact, a presentation of such IAB progression. Furthermore, the significance of the right bundle-branch block (Fig. 2) or any other concurrent ECG finding in relation to this BB abnormality remains poorly studied. Clearly, our
179
knowledge on IAB is still very much at its infancy. However, neither this nor the limited emphasis toward its diagnosis by the American College of Cardiology/American Heart Association Task Force on Practice Guidelines at present should be an excuse to undermine the importance of this entity given the magnitude of risks IAB harbors such as atrial tachyarrhythmias, LA enlargement, LA dysfunction, and potential embolism [5-8]. It is therefore important that clinicians be aware of the distinct forms of IAB (Figs. 1 and 2) and that there can be progression from one type of IAB to another. References [1] Bayes de Luna A. Electrocardiographic alterations due to atrial pathology. Clinical electrocardiography: a textbook. New York7 Futura Company Inc; 1998. p. 169. [2] Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for intraventricular conduction disturbances and pre-excitation. World Health Organizational/International Society and Federation for Cardiology Task Force Ad Hoc. J Am Coll Cardiol 1985;5(6):1261. [3] Jairath UC, Spodick DH. Exceptional prevalence of interatrial block in a general hospital population. Clin Cardiol 2001;24:548. [4] Asad N, Spodick DH. Prevalence of interatrial block in a general hospital population. Am J Cardiol 2003;91:609. [5] Agarwal YK, Aronow WS, Levy JA, et al. Association of interatrial block with the development of atrial fibrillation. Am J Cardiol 2003;91:882. [6] Leier CV, Meacham JA, Schaal SF. Prolonged atrial conduction. A major predisposing factor for the development of atrial flutter. Circulation 1978;57:213. [7] Goyal SB, Spodick DH. Electromechanical dysfunction of the left atrium associated with interatrial block. Am Heart J 2001;142:823. [8] Lorbar M, Levrault R, Phadke JG, et al. Interatrial block as a predictor of embolic stroke. Am J Cardiol 2005;95(5):667. [9] Cohen J, Scherf D. Complete interatrial and intra-atrial block (atrial dissociation). Am Heart J 1965;70:23. [10] Ariyarajah V, Spodick DH. Advanced interatrial block: a classic electrocardiogram. Cardiology 2005;104(1):33. [11] James TN. The specialized conducting tissue of the atria. In: Dreifus LS, Likoff W, editors. Mechanisms and therapy of the cardiac arrhythmias. New York7 Grune and Stratton; 1966. p. 97. [12] Treux RC. Anatomical considerations of the human atrioventricular junction. In: Dreifus LS, Likoff W, editors. Mechanisms and therapy of cardiac arrhythmias. New York7 Grune and Stratton; 1966. p. 333. [13] Roithinger FX, Cheng J, Sippens Groenewegen A, et al. Use of electroanatomic mapping to delineate transseptal atrial conduction in humans. Circulation 1999;100:1791. [14] Markides V, Schilling RJ, Ho SY, et al. Characterization of left atrial activation in the intact human heart. Circulation 2003;107:733. [15] Spodick DH. Unappreciated prevalence of interatrial block and associated consequences: a poorly perceived pandemic. Mayo Clin Proc 2004;79(5):668.
Progression of partial to advanced interatrial block Vignendra Ariyarajah, MDa,b, David H. Spodick, MDc,T a
Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC), Veterans Affairs Boston Healthcare System, Boston, MA, USA b Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA c Division of Cardiovascular Medicine, Department of Medicine, University of Massachusetts Medical School, Worcester, MA, USA Received 20 July 2005
Abstract
Interatrial block (IAB), prolonged conduction between the atria, is denoted by P waves of 110 milliseconds or more and may manifest as partial or advanced. Theoretically, partial IAB may progress to its advanced counterpart if conduction delay increases to complete block. However, there have been no reports of such progression, and electrophysiologic studies have not shown this phenomenon. We briefly review the interatrial conducting pathways of IAB and present the first documentation of possible progression of partial to advanced IAB. D 2006 Elsevier Inc. All rights reserved.
Keywords:
Partial interatrial block; Advanced interatrial block; Bachmann’s bundle; Progression
1. Background Interatrial block (IAB) is caused by delay in electrical impulse transmission between the right (RA) and left atria (LA), and implies subsequent delayed LA activation [1]. Although normal P-wave duration is defined by the World Health Organizational/International Society and Federation of Cardiology Task Force as less than 110 milliseconds [2], what is depicted on the electrocardiogram (ECG), P waves 110 milliseconds or more, is block (on the ECG, time = duration of conduction; excessive time or delay = block). Interatrial block was shown to be highly prevalent in 2 separate but comparable general hospital populations of 1000 patients each (41.1% in one [3] and 47% in the other [4]), with both series demonstrating a higher prevalence among those older than 59 years. Interatrial block is a predictor of atrial tachyarrhythmias, especially atrial fibrillation, with a reported prevalence of 52% in such patients when compared with 18% of the investigated control group [5,6]. Interatrial block is also strongly associated with LA enlargement (88% prevalence) [7], LA electromechanical dysfunction (mean LA kinetic
T Corresponding author. University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655. Fax: +1 508 856 4571. E-mail address: [email protected] (D.H. Spodick). 0022-0736/$ – see front matter D 2006 Elsevier Inc. All rights reserved. doi:10.1016/j.jelectrocard.2005.08.016
energy of 19.8 vs 64.7 kdyne/cm per second in controls, P b .0001) [7], and risk for embolism (80% prevalence in embolic strokes) [8]. Because discrete lesions produced experimentally in the Bachmann bundle (BB) delay activation of the LA and result in the typical prolonged, often notched, P waves seen in IAB, abnormality of this classically preferred route for interatrial impulse transmission is thought to be the principal mechanism of IAB [1,9]. Two forms of interatrial conduction delay have been classified: partial and advanced IAB [1,9,10]. 2. Partial and advanced IAB In partial IAB, an incomplete block occurs in the BB, delaying sinus impulses generated in the RA from reaching the LA. This produces wide, usually bifid, P waves [1]. However, when conduction via the BB is completely blocked, sinus impulses can no longer cross the BB but are believed to instead first depolarize the RA with an inferior course toward the atrioventricular (AV) junction and then spread superiorly to produce a caudocephalic depolarization of the LA. This is described as advanced IAB and is captured on the ECG as biphasic (F) P waves in the inferior leads [10]. James [11] and, later, Treux [12] described 3 different internodal pathways that traverse the RA from the sinus to the AV node: anterior, middle, and posterior. Any one of
178
V. Ariyarajah, D.H. Spodick / Journal of Electrocardiology 39 (2006) 177–179
Fig. 1. Patient’s ECG depicting partial IAB (see text).
these routes is thought to facilitate depolarization of the RA. Although the exact mechanism of activation within the LA is much less known, let alone such caudocephalic spread of depolarization from the AV node in advanced IAB, other potential interatrial connections have been studied. Through RA electroanatomic mapping, Roithinger
et al [13] demonstrated several functional pathways by pacing the coronary sinus or the LA. Markides et al [14] used a noncontact mapping system to show that posterior interatrial connections could also conduct to the LA. Absence of discrete tracts, however, has left their existence open to dispute.
Fig. 2. Patient’s ECG now showing advanced IAB (see text).
V. Ariyarajah, D.H. Spodick / Journal of Electrocardiology 39 (2006) 177–179
Nevertheless, in theory, partial IAB [9] could at some point progress to advanced IAB [10] if the severity of its BB conduction block appears complete. However, there have been no electrophysiologic atrial pathway mapping studies to date that have documented such progression or even hinted at a possibility of such occurrence, and no case reports of this phenomenon have been presented. We present 2 ECGs of the same patient showing progression from partial to advanced IAB over the course of 5 years. The patient was a 71-year-old male with a history of hypertension, chronic obstructive pulmonary disease, and left ventricular hypertrophy. Fig. 1 shows one of the patient’s ECGs from 1999, depicting partial IAB with classic bifid P waves of 120 milliseconds or more. Fig. 2 shows the patient’s ECG from 2004 with distinct biphasic (F) P waves of 120 milliseconds or more in the inferior leads, denoting advanced IAB. Over the course of 5 years, his blood pressure had increased and a second antihypertensive medication was added. He had also developed a right bundle branch block (Fig. 2). Clinically, however, the patient’s condition remained unchanged and he had declined further investigation.
3. Discussion and conclusion This patient’s ECGs (Figs. 1 and 2) suggest that partial IAB [9] progressed to its advanced counterpart [10] possibly because of increasing block in BB. Absence of an electrophysiologic evaluation, however, severely limits our ability to confirm this interesting hypothesis. The absence of reports and documentation of such progression is surprising. However, the lack of observations may be explained in part because interatrial conduction disorder has been largely omitted in general medical, and cardiology text books [15]. Therefore, many clinicians fail to recognize IAB merely because of the lack of knowledge of this medical entity, with consequent underreporting of its prevalence. Also, advanced IAB is uncommon compared with its partial counterpart, further resulting in a decrease of clinical recognition [15]. However, the clinical significance of one IAB-type versus the other is unknown, and it cannot be ascertained if our patient’s worsening hypertension was a precursor or, in fact, a presentation of such IAB progression. Furthermore, the significance of the right bundle-branch block (Fig. 2) or any other concurrent ECG finding in relation to this BB abnormality remains poorly studied. Clearly, our
179
knowledge on IAB is still very much at its infancy. However, neither this nor the limited emphasis toward its diagnosis by the American College of Cardiology/American Heart Association Task Force on Practice Guidelines at present should be an excuse to undermine the importance of this entity given the magnitude of risks IAB harbors such as atrial tachyarrhythmias, LA enlargement, LA dysfunction, and potential embolism [5-8]. It is therefore important that clinicians be aware of the distinct forms of IAB (Figs. 1 and 2) and that there can be progression from one type of IAB to another. References [1] Bayes de Luna A. Electrocardiographic alterations due to atrial pathology. Clinical electrocardiography: a textbook. New York7 Futura Company Inc; 1998. p. 169. [2] Willems JL, Robles de Medina EO, Bernard R, et al. Criteria for intraventricular conduction disturbances and pre-excitation. World Health Organizational/International Society and Federation for Cardiology Task Force Ad Hoc. J Am Coll Cardiol 1985;5(6):1261. [3] Jairath UC, Spodick DH. Exceptional prevalence of interatrial block in a general hospital population. Clin Cardiol 2001;24:548. [4] Asad N, Spodick DH. Prevalence of interatrial block in a general hospital population. Am J Cardiol 2003;91:609. [5] Agarwal YK, Aronow WS, Levy JA, et al. Association of interatrial block with the development of atrial fibrillation. Am J Cardiol 2003;91:882. [6] Leier CV, Meacham JA, Schaal SF. Prolonged atrial conduction. A major predisposing factor for the development of atrial flutter. Circulation 1978;57:213. [7] Goyal SB, Spodick DH. Electromechanical dysfunction of the left atrium associated with interatrial block. Am Heart J 2001;142:823. [8] Lorbar M, Levrault R, Phadke JG, et al. Interatrial block as a predictor of embolic stroke. Am J Cardiol 2005;95(5):667. [9] Cohen J, Scherf D. Complete interatrial and intra-atrial block (atrial dissociation). Am Heart J 1965;70:23. [10] Ariyarajah V, Spodick DH. Advanced interatrial block: a classic electrocardiogram. Cardiology 2005;104(1):33. [11] James TN. The specialized conducting tissue of the atria. In: Dreifus LS, Likoff W, editors. Mechanisms and therapy of the cardiac arrhythmias. New York7 Grune and Stratton; 1966. p. 97. [12] Treux RC. Anatomical considerations of the human atrioventricular junction. In: Dreifus LS, Likoff W, editors. Mechanisms and therapy of cardiac arrhythmias. New York7 Grune and Stratton; 1966. p. 333. [13] Roithinger FX, Cheng J, Sippens Groenewegen A, et al. Use of electroanatomic mapping to delineate transseptal atrial conduction in humans. Circulation 1999;100:1791. [14] Markides V, Schilling RJ, Ho SY, et al. Characterization of left atrial activation in the intact human heart. Circulation 2003;107:733. [15] Spodick DH. Unappreciated prevalence of interatrial block and associated consequences: a poorly perceived pandemic. Mayo Clin Proc 2004;79(5):668.