American Journal of Emergency Medicine xxx (2015) xxx–xxx
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Diagnosing acute pulmonary embolism masquerading as inferior myocardial infarction Acute pulmonary embolism (APE) masquerading as inferior myocardial infarction was sporadically reported by several authors. We analyzed the clinical and electrocardiographic characteristics of the 8 patients reported in the English literature. The clinical manifestations included chest pain (37.5%), dyspnea (37.5%), sweating (25%), sinus tachycardia (62.5%), and hemodynamic instability (50%). Most patients (62.5%) presented the right ventricular strain pattern. In conclusion, patients presenting with chest pain and/or dyspnea can be experiencing a range of syndromes, including acute myocardial infarction and APE. The clinician should consider APE in patients with findings consistent with both inferior wall ST-segment elevation myocardial infarction and APE when the electrocardiogram (ECG) demonstrates findings consistent with right ventricular strain. Acute pulmonary embolism (APE) masquerading as inferior wall ST-segment elevation myocardial infarction (STEMI) was sporadically reported by several authors [1-8] and was frequently misdiagnosed as inferior wall STEMI. Considering these misdiagnoses, we found 8 reports in the English literature presenting STsegment elevation (STE) in the inferior leads and summarized the clinical and ECG characteristics of these patients to reduce the misdiagnosis. The clinical and ECG manifestations are listed in Table. Regarding the clinical manifestations, there were 5 patients (62.5%) presenting sinus tachycardia; 4 patients (50%) presenting hemodynamic instability including cardiogenic shock, hypotension, or cardiac arrest; and 3 patients (37.5%) presenting dyspnea or sweating or chest pain. Regarding the ECG manifestations, there were 5 patients (62.5%) with ST-segment depression (STD) in leads I and V4/V5 to V6; 5 patients (62.5%) with right ventricular strain (RVS) pattern including QR sign or right bundle branch block in lead V1 or S1Q3 or S1Q3T3; 5 patients (62.5%) with a late R-wave amplitude greater than 1.5 mm in lead aVR; and 3 patients (37.5%) with STE in lead V1. In addition, V3R or V3R to V5R was recorded in 2 patients, and all showed STE. The amplitude of the STE in the inferior leads was found less than or equal to 0.1 mV in 5 patients and less than or equal to 0.2 mV in 3 patients. The ECG example is presented in Figure. Although the amplitude of the STE in the inferior leads was not prominent (≤ 0.2 mV), the clinical manifestations included dyspnea (37.5%), sweating (25%), sinus tachycardia (62.5%), and hemodynamic instability (50%). The clinical manifestations were not consistent with the amplitude of the STE in the inferior leads in patients with inferior myocardial infarction. In these conditions, the presentation was suggestive of APE, or the diagnosis of inferior STEMI was uncertain [1].
ST-segment elevation confined to the inferior leads is a very rare ECG manifestation of APE. However, STE in leads V1 to V3/V4 is a common ECG manifestation of patients with submassive to massive APE [9]; parts of these patients are simultaneously with STE in the inferior leads [10]. We described the dynamic ECG changes in a patient with APE [2], who presented initially STE in the right precordial leads and followed by STE in the inferior leads after onset of APE, and finally simultaneously STE in the right precordial and inferior leads during cardiogenic shock. Thus, we speculate that STE confined to the inferior leads is a transient ECG manifestation of APE and is also a response to a specific degree of right ventricular (RV) transmural ischemia [2]. If V3R to V5R leads are recorded, these leads may simultaneously present STE [5,7]. Hence, STE in the inferior leads represent RV transmural ischemia in APE. We previously described 3 specific ischemic ECG patterns [10], indicating different manifestations of myocardial ischemia in APE: left ventricular (LV) subendocardial ischemic pattern of STE in lead aVR with concomitant STD in leads I and V 4 to V 6 , RV transmural ischemic pattern of STE in leads V 1 to V 3 /V 4 with or without STE in inferior leads, and LV subendocardial ischemic plus RV transmural ischemic pattern of STE in leads III and/or V1 / V 2 with concomitant STD in leads V 4 /V 5 to V 6 . Of the 8 patients, 5 showed LV subendocardial ischemic plus RV transmural ischemic pattern, and the remaining 3 patients should be categorized as RV transmural ischemic pattern. Right ventricular strain pattern, including abnormal QRS morphology in lead V1 (notched S wave, right bundle branch block or QR sigh) and/or S1Q3 or S1Q3T3, is also a common ECG manifestation in APE [10]. A late R-wave amplitude greater than or equal to 1.5 mm in lead aVR is found to be more commonly present in patients with APE than without [11]. This sign indicates that the depolarization vector of the QRS terminal portion points to the right superior possibly because of RV enlargement or strain. Most patients (62.5%) presented the RVS pattern or a late R-wave amplitude greater than or equal to 1.5 mm in lead aVR. Hence, specific ischemic ECG pattern with concomitant RVS pattern or a late R-wave amplitude greater than or equal to 1.5 mm in lead aVR is highly suggestive of APE. In conclusion, patients presenting with chest pain and/or dyspnea can be experiencing a range of syndromes, including acute myocardial infarction and APE. The ECG can be of value in ruling in certain diagnoses, such as STEMI. Unfortunately, as noted in our discussion, the ECG can demonstrate findings consistent with inferior wall STEMI when the patient is experiencing APE. The clinician should consider APE in patients with findings consistent with both inferior wall STEMI and APE when the ECG also demonstrates findings consistent with RVS.
0735-6757/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Zhan Z-Q, et al, Diagnosing acute pulmonary embolism masquerading as inferior myocardial infarction, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.01.036
2
Z-Q. Zhan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Table Clinical and ECG manifestations of ST-segment elevation in the inferior leads associated with APE First author
S/A
Clinical condition
CAG results
ST-segment deviation pattern
Other ECG manifestation
Omar et al [1], 2015
M/57
Profuse sweating
Not performed
ST, abnormal Q waves in III and aVF
Zhan et al [2], 2014 Emren et al [3], 2014 Obiagwu et al [4], 2014
M/79 M/69 F/85
Dyspnea, hypotension Chest pain and sweating Dyspnea and chest pain
Noncritical plaques Noncritical plaques 60% stenosis in RCA
Bozorgi et al [5], 2013
F/66
Dyspnea and chest pain
Normal RCA
Alsidawi et al [6], 2013
M/73
Cardiac arrest
30%-50% stenosis in LAD
Zhan et al [7], 2013
F/65
Cardiogenic shock
Not performed
Lu et al [8], 2010
M/47
Cardiogenic shock
Not performed
STE (≤0.1 mV) in III, aVF, and V1; STD in I, aVL, and V4-V6 STE (≤0.1 mV) in II, III, and aVF STE (≤0.1 mV) in II, III, and aVF STE (≤0.1 mV) in II, III, aVF, and aVR; STD in I, aVL, and V5-V6 STE (≤0.1 mV) in III, aVF, aVR, V1, and V3R-V5R; STD in I, aVL, and V5-V6 STE (≤0.2 mV) in II, III, and aVF; STD in I and aVL STE (≤0.2 mV) in III, aVF, aVR, and V3R; STD in I, aVL, and V4-V6 STE (≤0.2 mV) in II, III, aVF, aVR, and V1; STD in leads I, aVL, and V2-V6
ST, S1Q3, RBBB, LRA N1.5 mm in aVR – RBBB, LRA N1.5 mm in aVR ST; NTW in II, III, aVF, and V1 Junctional escape rhythm, RBBB, S1Q3, LRA N1.5 mm in aVR ST; QR sign in V1; S1Q3T3; NTW in II, III, aVF, and V1-V6; LRA N1.5 mm in aVR ST, QR sign in V1, S1Q3, LRA N1.5 mm in aVR
Abbreviations: S/A, sex/age; CAG, coronary artery angiography; M, male; ST, sinus tachycardia; RBBB, right bundle branch block; LRA, late R-wave amplitude; F, female; RCA, right coronary artery; NTW, negative T wave; LAD, left anterior descending coronary artery.
Zhong-Qun Zhan, MD Chong-Quan Wang, MD Zhi-Xiao Wang, MD Department of Cardiology, Shiyan Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China ⁎ Corresponding author at: Department of Cardiology, Shiyan Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China. E-mail addresses: [email protected], [email protected], [email protected]
http://dx.doi.org/10.1016/j.ajem.2015.01.036 References
Figure. Electrocardiogram of a patient with acute pulmonary embolism during cardiogenic shock shows sinus tachycardia, S1Q3T3, QR sign in lead V1, a late R-wave amplitude greater than or equal to 1.5 mm in lead aVR, ST-segment elevation in leads III and aVF, and ST-segment depression in leads I and V4 to V6.
[1] Omar HR, Mangar D, Camporesi EM. Acute pulmonary embolism masquerading as inferior myocardial infarction. Am J Emerg Med 2015. http://dx.doi.org/10.1016/j. ajem.2014.11.036. [2] Zhan ZQ, Wang CQ, Baranchuk A. Acute pulmonary embolism with ST-segment elevation in the inferior leads. Int J Cardiol 2014;177(2):718–9. [3] Emren SV, Arikan ME, Senoz O, Varis E, Akan E. Acute pulmonary embolism mimicking inferior myocardial infarction. Turk Kardiyol Dern Ars 2014;42(3):290–3. [4] Obiagwu C, John J, Mastrine L, Borgen E, Shani J. Acute pulmonary embolism masquerading as acute inferior myocardial infarction. J Med Cases 2014;5(2):73–5. [5] Bozorgi A, Rahnamoun Z. Pulmonary thromboembolism initially mistaken for inferior STEMI. Herz 2013;38(5):553–5. [6] Alsidawi S, Abdalla M, Helmy T. Massive pulmonary embolism with ST-elevation in the inferior leads and other interesting ECG findings. J Biomed Graph Comput 2013; 3(1):43–50. [7] Zhong-Qun Z, Chong-Quan W, Nikus KC, Sclarovsky S, Chao-Rong H. A new electrocardiogram finding for massive pulmonary embolism: ST elevation in lead aVR with ST depression in leads I and V(4) to V(6). Am J Emerg Med 2013;31(2):456.e5–8. [8] Lu CR, Chen JY, Hsu CH, Chang KC, Huang SK. Acute massive pulmonary embolism after radiofrequency catheter ablation: a rare but devastating complication. Tex Heart Inst J 2010;37(4):498–9. [9] Grand A, Taine B, Huret JF, Pernot F, Lagabrielle D. An overlooked electrocardiographic sign of acute embolic cor pulmonale: elevation of the ST segment in right precordial leads. Ann Cardiol Angeiol (Paris) 1985;34(5):361–2. [10] Zhan ZQ, Wang CQ, Nikus KC, He CR, Wang J, Mao S, et al. Electrocardiogram patterns during hemodynamic instability in patients with acute pulmonary embolism. Ann Noninvasive Electrocardiol 2014;19(6):543–51. [11] Kireyev D, Arkhipov MV, Zador ST, Paris JA, Boden WE. Clinical utility of aVR-The neglected electrocardiographic lead. Ann Noninvasive Electrocardiol 2010;15(2):175–80.
Please cite this article as: Zhan Z-Q, et al, Diagnosing acute pulmonary embolism masquerading as inferior myocardial infarction, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.01.036
Contents lists available at ScienceDirect
American Journal of Emergency Medicine journal homepage: www.elsevier.com/locate/ajem
Case Report
Diagnosing acute pulmonary embolism masquerading as inferior myocardial infarction Acute pulmonary embolism (APE) masquerading as inferior myocardial infarction was sporadically reported by several authors. We analyzed the clinical and electrocardiographic characteristics of the 8 patients reported in the English literature. The clinical manifestations included chest pain (37.5%), dyspnea (37.5%), sweating (25%), sinus tachycardia (62.5%), and hemodynamic instability (50%). Most patients (62.5%) presented the right ventricular strain pattern. In conclusion, patients presenting with chest pain and/or dyspnea can be experiencing a range of syndromes, including acute myocardial infarction and APE. The clinician should consider APE in patients with findings consistent with both inferior wall ST-segment elevation myocardial infarction and APE when the electrocardiogram (ECG) demonstrates findings consistent with right ventricular strain. Acute pulmonary embolism (APE) masquerading as inferior wall ST-segment elevation myocardial infarction (STEMI) was sporadically reported by several authors [1-8] and was frequently misdiagnosed as inferior wall STEMI. Considering these misdiagnoses, we found 8 reports in the English literature presenting STsegment elevation (STE) in the inferior leads and summarized the clinical and ECG characteristics of these patients to reduce the misdiagnosis. The clinical and ECG manifestations are listed in Table. Regarding the clinical manifestations, there were 5 patients (62.5%) presenting sinus tachycardia; 4 patients (50%) presenting hemodynamic instability including cardiogenic shock, hypotension, or cardiac arrest; and 3 patients (37.5%) presenting dyspnea or sweating or chest pain. Regarding the ECG manifestations, there were 5 patients (62.5%) with ST-segment depression (STD) in leads I and V4/V5 to V6; 5 patients (62.5%) with right ventricular strain (RVS) pattern including QR sign or right bundle branch block in lead V1 or S1Q3 or S1Q3T3; 5 patients (62.5%) with a late R-wave amplitude greater than 1.5 mm in lead aVR; and 3 patients (37.5%) with STE in lead V1. In addition, V3R or V3R to V5R was recorded in 2 patients, and all showed STE. The amplitude of the STE in the inferior leads was found less than or equal to 0.1 mV in 5 patients and less than or equal to 0.2 mV in 3 patients. The ECG example is presented in Figure. Although the amplitude of the STE in the inferior leads was not prominent (≤ 0.2 mV), the clinical manifestations included dyspnea (37.5%), sweating (25%), sinus tachycardia (62.5%), and hemodynamic instability (50%). The clinical manifestations were not consistent with the amplitude of the STE in the inferior leads in patients with inferior myocardial infarction. In these conditions, the presentation was suggestive of APE, or the diagnosis of inferior STEMI was uncertain [1].
ST-segment elevation confined to the inferior leads is a very rare ECG manifestation of APE. However, STE in leads V1 to V3/V4 is a common ECG manifestation of patients with submassive to massive APE [9]; parts of these patients are simultaneously with STE in the inferior leads [10]. We described the dynamic ECG changes in a patient with APE [2], who presented initially STE in the right precordial leads and followed by STE in the inferior leads after onset of APE, and finally simultaneously STE in the right precordial and inferior leads during cardiogenic shock. Thus, we speculate that STE confined to the inferior leads is a transient ECG manifestation of APE and is also a response to a specific degree of right ventricular (RV) transmural ischemia [2]. If V3R to V5R leads are recorded, these leads may simultaneously present STE [5,7]. Hence, STE in the inferior leads represent RV transmural ischemia in APE. We previously described 3 specific ischemic ECG patterns [10], indicating different manifestations of myocardial ischemia in APE: left ventricular (LV) subendocardial ischemic pattern of STE in lead aVR with concomitant STD in leads I and V 4 to V 6 , RV transmural ischemic pattern of STE in leads V 1 to V 3 /V 4 with or without STE in inferior leads, and LV subendocardial ischemic plus RV transmural ischemic pattern of STE in leads III and/or V1 / V 2 with concomitant STD in leads V 4 /V 5 to V 6 . Of the 8 patients, 5 showed LV subendocardial ischemic plus RV transmural ischemic pattern, and the remaining 3 patients should be categorized as RV transmural ischemic pattern. Right ventricular strain pattern, including abnormal QRS morphology in lead V1 (notched S wave, right bundle branch block or QR sigh) and/or S1Q3 or S1Q3T3, is also a common ECG manifestation in APE [10]. A late R-wave amplitude greater than or equal to 1.5 mm in lead aVR is found to be more commonly present in patients with APE than without [11]. This sign indicates that the depolarization vector of the QRS terminal portion points to the right superior possibly because of RV enlargement or strain. Most patients (62.5%) presented the RVS pattern or a late R-wave amplitude greater than or equal to 1.5 mm in lead aVR. Hence, specific ischemic ECG pattern with concomitant RVS pattern or a late R-wave amplitude greater than or equal to 1.5 mm in lead aVR is highly suggestive of APE. In conclusion, patients presenting with chest pain and/or dyspnea can be experiencing a range of syndromes, including acute myocardial infarction and APE. The ECG can be of value in ruling in certain diagnoses, such as STEMI. Unfortunately, as noted in our discussion, the ECG can demonstrate findings consistent with inferior wall STEMI when the patient is experiencing APE. The clinician should consider APE in patients with findings consistent with both inferior wall STEMI and APE when the ECG also demonstrates findings consistent with RVS.
0735-6757/© 2015 Elsevier Inc. All rights reserved.
Please cite this article as: Zhan Z-Q, et al, Diagnosing acute pulmonary embolism masquerading as inferior myocardial infarction, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.01.036
2
Z-Q. Zhan et al. / American Journal of Emergency Medicine xxx (2015) xxx–xxx
Table Clinical and ECG manifestations of ST-segment elevation in the inferior leads associated with APE First author
S/A
Clinical condition
CAG results
ST-segment deviation pattern
Other ECG manifestation
Omar et al [1], 2015
M/57
Profuse sweating
Not performed
ST, abnormal Q waves in III and aVF
Zhan et al [2], 2014 Emren et al [3], 2014 Obiagwu et al [4], 2014
M/79 M/69 F/85
Dyspnea, hypotension Chest pain and sweating Dyspnea and chest pain
Noncritical plaques Noncritical plaques 60% stenosis in RCA
Bozorgi et al [5], 2013
F/66
Dyspnea and chest pain
Normal RCA
Alsidawi et al [6], 2013
M/73
Cardiac arrest
30%-50% stenosis in LAD
Zhan et al [7], 2013
F/65
Cardiogenic shock
Not performed
Lu et al [8], 2010
M/47
Cardiogenic shock
Not performed
STE (≤0.1 mV) in III, aVF, and V1; STD in I, aVL, and V4-V6 STE (≤0.1 mV) in II, III, and aVF STE (≤0.1 mV) in II, III, and aVF STE (≤0.1 mV) in II, III, aVF, and aVR; STD in I, aVL, and V5-V6 STE (≤0.1 mV) in III, aVF, aVR, V1, and V3R-V5R; STD in I, aVL, and V5-V6 STE (≤0.2 mV) in II, III, and aVF; STD in I and aVL STE (≤0.2 mV) in III, aVF, aVR, and V3R; STD in I, aVL, and V4-V6 STE (≤0.2 mV) in II, III, aVF, aVR, and V1; STD in leads I, aVL, and V2-V6
ST, S1Q3, RBBB, LRA N1.5 mm in aVR – RBBB, LRA N1.5 mm in aVR ST; NTW in II, III, aVF, and V1 Junctional escape rhythm, RBBB, S1Q3, LRA N1.5 mm in aVR ST; QR sign in V1; S1Q3T3; NTW in II, III, aVF, and V1-V6; LRA N1.5 mm in aVR ST, QR sign in V1, S1Q3, LRA N1.5 mm in aVR
Abbreviations: S/A, sex/age; CAG, coronary artery angiography; M, male; ST, sinus tachycardia; RBBB, right bundle branch block; LRA, late R-wave amplitude; F, female; RCA, right coronary artery; NTW, negative T wave; LAD, left anterior descending coronary artery.
Zhong-Qun Zhan, MD Chong-Quan Wang, MD Zhi-Xiao Wang, MD Department of Cardiology, Shiyan Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China ⁎ Corresponding author at: Department of Cardiology, Shiyan Taihe Hospital, Hubei University of Medicine, Shiyan City, Hubei Province, China. E-mail addresses: [email protected], [email protected], [email protected]
http://dx.doi.org/10.1016/j.ajem.2015.01.036 References
Figure. Electrocardiogram of a patient with acute pulmonary embolism during cardiogenic shock shows sinus tachycardia, S1Q3T3, QR sign in lead V1, a late R-wave amplitude greater than or equal to 1.5 mm in lead aVR, ST-segment elevation in leads III and aVF, and ST-segment depression in leads I and V4 to V6.
[1] Omar HR, Mangar D, Camporesi EM. Acute pulmonary embolism masquerading as inferior myocardial infarction. Am J Emerg Med 2015. http://dx.doi.org/10.1016/j. ajem.2014.11.036. [2] Zhan ZQ, Wang CQ, Baranchuk A. Acute pulmonary embolism with ST-segment elevation in the inferior leads. Int J Cardiol 2014;177(2):718–9. [3] Emren SV, Arikan ME, Senoz O, Varis E, Akan E. Acute pulmonary embolism mimicking inferior myocardial infarction. Turk Kardiyol Dern Ars 2014;42(3):290–3. [4] Obiagwu C, John J, Mastrine L, Borgen E, Shani J. Acute pulmonary embolism masquerading as acute inferior myocardial infarction. J Med Cases 2014;5(2):73–5. [5] Bozorgi A, Rahnamoun Z. Pulmonary thromboembolism initially mistaken for inferior STEMI. Herz 2013;38(5):553–5. [6] Alsidawi S, Abdalla M, Helmy T. Massive pulmonary embolism with ST-elevation in the inferior leads and other interesting ECG findings. J Biomed Graph Comput 2013; 3(1):43–50. [7] Zhong-Qun Z, Chong-Quan W, Nikus KC, Sclarovsky S, Chao-Rong H. A new electrocardiogram finding for massive pulmonary embolism: ST elevation in lead aVR with ST depression in leads I and V(4) to V(6). Am J Emerg Med 2013;31(2):456.e5–8. [8] Lu CR, Chen JY, Hsu CH, Chang KC, Huang SK. Acute massive pulmonary embolism after radiofrequency catheter ablation: a rare but devastating complication. Tex Heart Inst J 2010;37(4):498–9. [9] Grand A, Taine B, Huret JF, Pernot F, Lagabrielle D. An overlooked electrocardiographic sign of acute embolic cor pulmonale: elevation of the ST segment in right precordial leads. Ann Cardiol Angeiol (Paris) 1985;34(5):361–2. [10] Zhan ZQ, Wang CQ, Nikus KC, He CR, Wang J, Mao S, et al. Electrocardiogram patterns during hemodynamic instability in patients with acute pulmonary embolism. Ann Noninvasive Electrocardiol 2014;19(6):543–51. [11] Kireyev D, Arkhipov MV, Zador ST, Paris JA, Boden WE. Clinical utility of aVR-The neglected electrocardiographic lead. Ann Noninvasive Electrocardiol 2010;15(2):175–80.
Please cite this article as: Zhan Z-Q, et al, Diagnosing acute pulmonary embolism masquerading as inferior myocardial infarction, Am J Emerg Med (2015), http://dx.doi.org/10.1016/j.ajem.2015.01.036
