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Not Necessarily a Myocardial Infarction: New Left Bundle Branch Block
ECG IMAGE OF THE MONTH Julia H. Indik, MD, PhD, Section Editor
Not Necessarily a Myocardial Infarction: New Left Bundle Branch Block Ivan B. Anderson, MD, Ezra A. Amsterdam, MD, Uma Srivatsa, MD Division of Cardiovascular Medicine, Department of Medicine, University of California Davis Medical Center, Sacramento, CA.
PRESENTATION When a new wide complex rhythm with a left bundle branch block pattern appears on the electrocardiogram (ECG), the findings should direct further investigation. We highlight a case in which a 56-year-old woman had this presentation. Careful examination of her ECG rhythm strip suggested an unusual etiology in this setting. The patient presented to the emergency department after 2 days of poorly controlled epigastric pain. One month earlier, she had been diagnosed with pancreatic adenocarcinoma. Upon arrival to the emergency department, she had stable vital signs, including a heart rate of 77 beats per minute. An ECG indicated new left bundle branch block (Figure 1). One week before, she had an ECG that revealed normal sinus rhythm with a narrow QRS complex (Figure 2). The composite of epigastric pain and new left bundle branch block in a postmenopausal female called for further cardiac evaluation. Two blood samples were drawn 3 hours apart for cardiac troponin I values. Both tests produced normal results (0.03 ng/mL; reference, <0.04 ng/mL).
ASSESSMENT Thorough examination of the rhythm strip (Figure 1) disclosed that the QRS complex morphology was changing. Funding: None. Conflict of Interest: None. Authorship: All authors independently reviewed and contributed to this manuscript. Dr. IBA is Clinical Fellow, Division of Cardiovascular Medicine, Department of Medicine, University of California(Davis) Medical Center, Sacramento, CA. Dr. EAA is Distinguished Professor, Division of Cardiovascular Medicine, and Master Clinician Educator, Department of Medicine, University of California(Davis) Medical Center, Sacramento, CA. Dr. US is Associate Professor of Medicine, Cardiac electrophysiologist, Division of Cardiovascular Medicine, Department of Medicine, University of California(Davis) Medical Center, Sacramento, CA. The Corresponding author is Ezra A. Amsterdam, MD, Cardiovascular Medicine, Suite 2820, ACC Bldg, Sacramento, CA 95817. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjmed.2015.05.004
Complexes 1-8 were wide with a left bundle branch block pattern at a rate of 75 beats per minute; P waves were visible within the wide QRS complexes (Figure 1, complexes 1-8), and the PR intervals were prolonged and variable between each. Positive P waves in leads I and II signified sinus rhythm, indicating that the atria and the ventricles were depolarized independently. There was isorhythmic atrioventricular dissociation with an atrial rate of 73 beats per minute (P-P coupling interval, 820 msec), and a ventricular rate of 75 beats per minute (V-V coupling interval, 800 msec). In the later half of the strip (Figure 1, complexes 10-13), the QRS complexes narrowed as the atrial rate increased from 73 beats per minute to 83 beats per minute, and normal atrioventricular conduction resumed.
DIAGNOSIS The patient’s diagnosis was accelerated idioventricular rhythm. In Figure 1, QRS complexes 10-13 depict normal atrioventricular conduction, while the wide QRS rhythms seen in complexes 1-8 represent a ventricular rhythm. Atrioventricular dissociation was confirmed by QRS complex 9 of Figure 1 (arrow), which represented a fusion of an impulse of ventricular origin and a concurrent impulse from the atrioventricular node. Atrioventricular dissociation often is associated with complete heart block. However, it can also be seen in a variety of rhythms in which 2 separate pacemaker sites are firing simultaneously. Examples of such rhythms include junctional tachycardia, ventricular tachycardia, isorhythmic atrioventricular dissociation, or accelerated idioventricular rhythm. Isorhythmic atrioventricular dissociation and accelerated idioventricular rhythm differ from complete heart block in that when the sinus rate increases, normal conduction resumes.1 In complete heart block, increases in the sinus rate do not lead to normal atrioventricular conduction.1 Our patient’s ventricular rhythm had a faster rate than the 20-40 beats per minute that mark a typical ventricular escape rhythm, but at the same time, the rate was too slow to be classified as ventricular tachycardia. As can be seen in
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The American Journal of Medicine, Vol -, No -,
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Figure 1 The electrocardiogram (ECG) initially read as left bundle branch block. The QRS complexes are labeled 1-13 between the V5 rhythm strip (bottom) and the standard lead II rhythm strip (second from the bottom). Arrowheads indicate P waves in complexes 1-10, and an arrow indicates that complex 9 is a fusion complex.
Figure 1, complexes 9-13, as the atrial rate increases, the atria capture the ventricles, resulting in sinus rhythm—an indication that the atrioventricular node is functioning normally. In fact, this conversion to sinus rhythm with an increase in atrial rate is the hallmark of accelerated idioventricular rhythm. The left bundle branch block morphology of the QRS complex points to a right ventricular focus, while the initiation of the QRS complex with a narrow R wave in lead V1 and the duration of 120 msec imply a septal origin. Additionally, the late transition and negative complex seen in lead III indicate right ventricular free wall exit. Further evaluation
Figure 2
for coronary artery disease was conducted with myocardial perfusion imaging, which was negative for ischemia. Computed tomography of the chest and transthoracic echocardiography also were performed. These studies revealed a large right ventricular thrombus and pulmonary emboli, both unsuspected findings (Figures 3 and 4).
MANAGEMENT Accelerated idioventricular rhythm is defined as a ventricular rhythm consisting of at least 3 QRS complexes originating from a single ventricular focus.2 The site of the
The baseline ECG demonstrated normal sinus rhythm.
Anderson et al
New Left Bundle Branch Block: Not Always Acute Myocardial Infarction
Figure 3 A transthoracic echocardiogram in the parasternal long axis view showed a large thrombus in the right ventricle (arrowhead). Ao ¼ aorta; LA ¼ left atrium; LV ¼ left ventricle; RV ¼ right ventricle.
ectopic focus can be the bundle of His, the Purkinje system, or the ventricular myocyte; rarely, accelerated idioventricular rhythm is polymorphic. Generally, the rate of accelerated idioventricular rhythm is 50-100 or 120 beats per minute. As with ventricular tachycardia, faster rates of accelerated idioventricular rhythm portend a poorer prognosis.3 Accelerated idioventricular rhythm is seen commonly with reperfusion in ST-elevation myocardial infarction.4 Other potential etiologies include drug toxicities, structural heart disease, and an idiopathic cause.2,5,6 Our patient did not have evidence of any of these.
Figure 4 Computed tomography of the chest in this patient confirmed the presence of a right ventricular thrombus (measured here at 1.8 cm 4.2 cm) and revealed multiple small pulmonary emboli (not pictured). RV ¼ right ventricle.
3
Since we suspected that the accelerated idioventricular rhythm originated in the right ventricle, the proximity of the thrombus to this location, as seen on the imaging studies, signaled a possible causal mechanism. Yet, an association between accelerated idioventricular rhythm and either pulmonary emboli or right ventricular thrombus is not well established. One case series described a single patient with accelerated idioventricular rhythm attributed to suspected pulmonary emboli.7 Focal myocardial inflammation can cause automaticity and has been associated with a variety of arrhythmic mechanisms.8,9 Perhaps a similar mechanism was at work in this patient. Accelerated idioventricular rhythm is generally transient and infrequently symptomatic. Management is typically expectant. When necessary, treatment can be pharmacologic or can include overdrive pacing. Pharmacologic termination of accelerated idioventricular rhythm with either atropine or lidocaine has been described.10 Our patient had pancreatic adenocarcinoma, a right ventricular thrombus, and multiple small pulmonary emboli. She elected to return home with hospice care. In conclusion, this case illustrates that interpretation of an ECG requires meticulous scrutiny of the rhythm strip to account for P waves and QRS complexes and the relationship between them.
References 1. Singh GD, Wong GB, Southard JA, Amsterdam EA. Food for thought: atrioventricular dissociation. Am J Med. 2013;126:1050-1053. 2. Riera AR, Barros RB, de Sousa FD, Baranchuk A. Accelerated idioventricular rhythm: History and chronology of the main discoveries. Indian Pacing Electrophysiol J. 2010;10:40-48. 3. Denes P, Gillis AM, Pawitan Y, Kammerling JM, Wilhelmsen L, Salerno DM. Prevalence, characteristics and significance of ventricular premature complexes and ventricular tachycardia detected by 24-hour continuous electrocardiographic recording in the Cardiac Arrhythmia Suppression Trial. Cast Investigators. Am J Cardiol. 1991;68:887-896. 4. Goldberg S, Greenspon AJ, Urban PL, et al. Reperfusion arrhythmia: A marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction. Am Heart J. 1983;105:26-32. 5. Castellanos A, Azan L, Bierfield J, Myerburg RJ. Digitalis-induced accelerated idioventricular rhythms: revisited. Heart Lung. 1975;4: 105-110. 6. Martini B, Nava A, Thiene G, et al. Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia. Br Heart J. 1988;59:564-571. 7. Massumi RA, Ali N. Accelerated isorhythmic ventricular rhythms. Am J Cardiol. 1970;26:170-185. 8. Vignola PA, Aonuma K, Swaye PS, et al. Lymphocytic myocarditis presenting as unexplained ventricular arrhythmias: Diagnosis with endomyocardial biopsy and response to immunosuppression. J Am Coll Cardiol. 1984;4:812-819. 9. Ross BA, Crawford FA Jr, Whitman V, Gillette PC. Atrial automatic ectopic tachycardia due to an atrial tumor. Am Heart J. 1988;115: 606-610. 10. Castellanos A Jr, Lemberg L, Arcebal AG. Mechanisms of slow ventricular tachycardias in acute myocardial infarction. Dis Chest. 1969;56:470-476.
Not Necessarily a Myocardial Infarction: New Left Bundle Branch Block Ivan B. Anderson, MD, Ezra A. Amsterdam, MD, Uma Srivatsa, MD Division of Cardiovascular Medicine, Department of Medicine, University of California Davis Medical Center, Sacramento, CA.
PRESENTATION When a new wide complex rhythm with a left bundle branch block pattern appears on the electrocardiogram (ECG), the findings should direct further investigation. We highlight a case in which a 56-year-old woman had this presentation. Careful examination of her ECG rhythm strip suggested an unusual etiology in this setting. The patient presented to the emergency department after 2 days of poorly controlled epigastric pain. One month earlier, she had been diagnosed with pancreatic adenocarcinoma. Upon arrival to the emergency department, she had stable vital signs, including a heart rate of 77 beats per minute. An ECG indicated new left bundle branch block (Figure 1). One week before, she had an ECG that revealed normal sinus rhythm with a narrow QRS complex (Figure 2). The composite of epigastric pain and new left bundle branch block in a postmenopausal female called for further cardiac evaluation. Two blood samples were drawn 3 hours apart for cardiac troponin I values. Both tests produced normal results (0.03 ng/mL; reference, <0.04 ng/mL).
ASSESSMENT Thorough examination of the rhythm strip (Figure 1) disclosed that the QRS complex morphology was changing. Funding: None. Conflict of Interest: None. Authorship: All authors independently reviewed and contributed to this manuscript. Dr. IBA is Clinical Fellow, Division of Cardiovascular Medicine, Department of Medicine, University of California(Davis) Medical Center, Sacramento, CA. Dr. EAA is Distinguished Professor, Division of Cardiovascular Medicine, and Master Clinician Educator, Department of Medicine, University of California(Davis) Medical Center, Sacramento, CA. Dr. US is Associate Professor of Medicine, Cardiac electrophysiologist, Division of Cardiovascular Medicine, Department of Medicine, University of California(Davis) Medical Center, Sacramento, CA. The Corresponding author is Ezra A. Amsterdam, MD, Cardiovascular Medicine, Suite 2820, ACC Bldg, Sacramento, CA 95817. E-mail address: [email protected] 0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved. http://dx.doi.org/10.1016/j.amjmed.2015.05.004
Complexes 1-8 were wide with a left bundle branch block pattern at a rate of 75 beats per minute; P waves were visible within the wide QRS complexes (Figure 1, complexes 1-8), and the PR intervals were prolonged and variable between each. Positive P waves in leads I and II signified sinus rhythm, indicating that the atria and the ventricles were depolarized independently. There was isorhythmic atrioventricular dissociation with an atrial rate of 73 beats per minute (P-P coupling interval, 820 msec), and a ventricular rate of 75 beats per minute (V-V coupling interval, 800 msec). In the later half of the strip (Figure 1, complexes 10-13), the QRS complexes narrowed as the atrial rate increased from 73 beats per minute to 83 beats per minute, and normal atrioventricular conduction resumed.
DIAGNOSIS The patient’s diagnosis was accelerated idioventricular rhythm. In Figure 1, QRS complexes 10-13 depict normal atrioventricular conduction, while the wide QRS rhythms seen in complexes 1-8 represent a ventricular rhythm. Atrioventricular dissociation was confirmed by QRS complex 9 of Figure 1 (arrow), which represented a fusion of an impulse of ventricular origin and a concurrent impulse from the atrioventricular node. Atrioventricular dissociation often is associated with complete heart block. However, it can also be seen in a variety of rhythms in which 2 separate pacemaker sites are firing simultaneously. Examples of such rhythms include junctional tachycardia, ventricular tachycardia, isorhythmic atrioventricular dissociation, or accelerated idioventricular rhythm. Isorhythmic atrioventricular dissociation and accelerated idioventricular rhythm differ from complete heart block in that when the sinus rate increases, normal conduction resumes.1 In complete heart block, increases in the sinus rate do not lead to normal atrioventricular conduction.1 Our patient’s ventricular rhythm had a faster rate than the 20-40 beats per minute that mark a typical ventricular escape rhythm, but at the same time, the rate was too slow to be classified as ventricular tachycardia. As can be seen in
2
The American Journal of Medicine, Vol -, No -,
-
2015
Figure 1 The electrocardiogram (ECG) initially read as left bundle branch block. The QRS complexes are labeled 1-13 between the V5 rhythm strip (bottom) and the standard lead II rhythm strip (second from the bottom). Arrowheads indicate P waves in complexes 1-10, and an arrow indicates that complex 9 is a fusion complex.
Figure 1, complexes 9-13, as the atrial rate increases, the atria capture the ventricles, resulting in sinus rhythm—an indication that the atrioventricular node is functioning normally. In fact, this conversion to sinus rhythm with an increase in atrial rate is the hallmark of accelerated idioventricular rhythm. The left bundle branch block morphology of the QRS complex points to a right ventricular focus, while the initiation of the QRS complex with a narrow R wave in lead V1 and the duration of 120 msec imply a septal origin. Additionally, the late transition and negative complex seen in lead III indicate right ventricular free wall exit. Further evaluation
Figure 2
for coronary artery disease was conducted with myocardial perfusion imaging, which was negative for ischemia. Computed tomography of the chest and transthoracic echocardiography also were performed. These studies revealed a large right ventricular thrombus and pulmonary emboli, both unsuspected findings (Figures 3 and 4).
MANAGEMENT Accelerated idioventricular rhythm is defined as a ventricular rhythm consisting of at least 3 QRS complexes originating from a single ventricular focus.2 The site of the
The baseline ECG demonstrated normal sinus rhythm.
Anderson et al
New Left Bundle Branch Block: Not Always Acute Myocardial Infarction
Figure 3 A transthoracic echocardiogram in the parasternal long axis view showed a large thrombus in the right ventricle (arrowhead). Ao ¼ aorta; LA ¼ left atrium; LV ¼ left ventricle; RV ¼ right ventricle.
ectopic focus can be the bundle of His, the Purkinje system, or the ventricular myocyte; rarely, accelerated idioventricular rhythm is polymorphic. Generally, the rate of accelerated idioventricular rhythm is 50-100 or 120 beats per minute. As with ventricular tachycardia, faster rates of accelerated idioventricular rhythm portend a poorer prognosis.3 Accelerated idioventricular rhythm is seen commonly with reperfusion in ST-elevation myocardial infarction.4 Other potential etiologies include drug toxicities, structural heart disease, and an idiopathic cause.2,5,6 Our patient did not have evidence of any of these.
Figure 4 Computed tomography of the chest in this patient confirmed the presence of a right ventricular thrombus (measured here at 1.8 cm 4.2 cm) and revealed multiple small pulmonary emboli (not pictured). RV ¼ right ventricle.
3
Since we suspected that the accelerated idioventricular rhythm originated in the right ventricle, the proximity of the thrombus to this location, as seen on the imaging studies, signaled a possible causal mechanism. Yet, an association between accelerated idioventricular rhythm and either pulmonary emboli or right ventricular thrombus is not well established. One case series described a single patient with accelerated idioventricular rhythm attributed to suspected pulmonary emboli.7 Focal myocardial inflammation can cause automaticity and has been associated with a variety of arrhythmic mechanisms.8,9 Perhaps a similar mechanism was at work in this patient. Accelerated idioventricular rhythm is generally transient and infrequently symptomatic. Management is typically expectant. When necessary, treatment can be pharmacologic or can include overdrive pacing. Pharmacologic termination of accelerated idioventricular rhythm with either atropine or lidocaine has been described.10 Our patient had pancreatic adenocarcinoma, a right ventricular thrombus, and multiple small pulmonary emboli. She elected to return home with hospice care. In conclusion, this case illustrates that interpretation of an ECG requires meticulous scrutiny of the rhythm strip to account for P waves and QRS complexes and the relationship between them.
References 1. Singh GD, Wong GB, Southard JA, Amsterdam EA. Food for thought: atrioventricular dissociation. Am J Med. 2013;126:1050-1053. 2. Riera AR, Barros RB, de Sousa FD, Baranchuk A. Accelerated idioventricular rhythm: History and chronology of the main discoveries. Indian Pacing Electrophysiol J. 2010;10:40-48. 3. Denes P, Gillis AM, Pawitan Y, Kammerling JM, Wilhelmsen L, Salerno DM. Prevalence, characteristics and significance of ventricular premature complexes and ventricular tachycardia detected by 24-hour continuous electrocardiographic recording in the Cardiac Arrhythmia Suppression Trial. Cast Investigators. Am J Cardiol. 1991;68:887-896. 4. Goldberg S, Greenspon AJ, Urban PL, et al. Reperfusion arrhythmia: A marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction. Am Heart J. 1983;105:26-32. 5. Castellanos A, Azan L, Bierfield J, Myerburg RJ. Digitalis-induced accelerated idioventricular rhythms: revisited. Heart Lung. 1975;4: 105-110. 6. Martini B, Nava A, Thiene G, et al. Accelerated idioventricular rhythm of infundibular origin in patients with a concealed form of arrhythmogenic right ventricular dysplasia. Br Heart J. 1988;59:564-571. 7. Massumi RA, Ali N. Accelerated isorhythmic ventricular rhythms. Am J Cardiol. 1970;26:170-185. 8. Vignola PA, Aonuma K, Swaye PS, et al. Lymphocytic myocarditis presenting as unexplained ventricular arrhythmias: Diagnosis with endomyocardial biopsy and response to immunosuppression. J Am Coll Cardiol. 1984;4:812-819. 9. Ross BA, Crawford FA Jr, Whitman V, Gillette PC. Atrial automatic ectopic tachycardia due to an atrial tumor. Am Heart J. 1988;115: 606-610. 10. Castellanos A Jr, Lemberg L, Arcebal AG. Mechanisms of slow ventricular tachycardias in acute myocardial infarction. Dis Chest. 1969;56:470-476.