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Acute Myocardial Infarction With Wide Complex RhythmWhat Is the Culprit Artery?

Educational Objective
To identify the key insights or developments described in this article
1 Credit CME

A man in his 70s presented to the emergency department with sudden-onset chest pain and profuse sweating, which had been persistent for 2 hours. His medical history was notable for hyperlipidemia but no other cardiac history. The patient’s heart rate was 88 beats/min, respiratory rate was 20 breaths/min, and blood pressure was 90/42 mm Hg. A 12-lead electrocardiogram (ECG) obtained at presentation is shown in the Figure, A. The initial myoglobin level was 247.50 ng/mL (reference range, <154.9 ng/mL), creatine kinase MB isoform level was 2.2 ng/mL (reference range, <7.2 ng/mL), and serum high-sensitivity cardiac troponin I level was 0.0144 ng/mL (reference range, <0.0342 ng/mL). The repeated serum myoglobin level was more than 1200 ng/mL, creatine kinase MB isoform level was more than 300 ng/mL, and high-sensitivity cardiac troponin I level was more than 50 ng/mL.

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The ECG showing new RBBB should prompt a primary percutaneous coronary intervention strategy in patients with ongoing symptoms consistent with myocardial ischemia.2 It often suggests a proximal LAD lesion with larger infarct size, which is related to many complications, including heart failure and increased mortality rate.3 The Figure, A shows the ST-segment elevation MI (STEMI) pattern associated with RBBB and LAFB resembling proximal LAD occlusion. However, there is absence of ST-segment elevation in lead V1. A plausible explanation may be an acute total LMT occlusion without collateral circulation.

In patients with MI caused by LMT obstruction, there are 2 prominent electrocardiographic presentations. First, when a subtotal occlusion or acute total LMT occlusion accompanying well-developed collateral circulation occurs, there may be a non-STEMI (NSTEMI). The presence of ST-segment depression in 8 or more surface leads, coupled with ST-segment elevation in lead aVR and/or lead V1, suggests multivessel ischemia or LMT obstruction.2 Second, the electrocardiographic manifestation is a STEMI due to an acute LMT occlusion without collateral circulation. In 2012, Fiol et al1 first reported the STEMI pattern in conjunction with RBBB and LAFB of proximal LAD occlusion without ST-segment elevation in lead V1, which had been recorded in patients with acute total occlusion of LMT without collateral circulation. In this condition, the absence of ST-segment elevation in lead V1 may be related to acute occlusion of the left circumflex artery, which results in ST-segment depression in the right precordial leads, counteracting ST-segment elevation in lead V1 induced by the occlusion of LAD.1,4 Therefore, the presence of ST-segment elevation in lead V1 indicates isolated proximal LAD occlusion, whereas its absence supports acute total occlusion of the LMT without collateral circulation or its equivalent.4

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CME Disclosure Statement: Unless noted, all individuals in control of content reported no relevant financial relationships. If applicable, all relevant financial relationships have been mitigated.

Article Information

Corresponding Author: Yuanzhe Jin, MD, Department of Cardiology of the Fourth Affiliated Hospital of China Medical University, Fourth Chongshan E Rd, Shenyang 110032, Liaoning, China (yzjin@cmu.edu.cn).

Published Online: March 14, 2022. doi:10.1001/jamainternmed.2022.0122

Conflict of Interest Disclosures: None reported.

Additional Contributions: We thank the patient’s daughter for granting permission to publish this information.

References
1.
Fiol  M , Carrillo  A , Rodríguez  A , Pascual  M , Bethencourt  A , Bayés de Luna  A .  Electrocardiographic changes of ST-elevation myocardial infarction in patients with complete occlusion of the left main trunk without collateral circulation.   J Electrocardiol. 2012;45(5):487-490.PubMedGoogle ScholarCrossref
2.
Ibanez  B , James  S , Agewall  S ,  et al; ESC Scientific Document Group.  2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation.   Eur Heart J. 2018;39(2):119-177.PubMedGoogle ScholarCrossref
3.
Xiang  L , Zhong  A , You  T , Chen  J , Xu  W , Shi  M .  Prognostic significance of right bundle branch block for patients with acute myocardial infarction.   Med Sci Monit. 2016;22:998-1004.PubMedGoogle ScholarCrossref
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Bayés de Luna  A , Fiol-Sala  M .  Where is the culprit lesion?   Circulation. 2016;134(19):1507-1509.PubMedGoogle ScholarCrossref
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Gutiérrez-Barrios  A , Gheorghe  L , Camacho-Freire  S ,  et al.  Primary angioplasty in a catastrophic presentation.   J Interv Cardiol. 2020;2020:5246504.PubMedGoogle Scholar
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González-Bravo  DH , Escabí-Mendoza  J .  Electrocardiographic recognition of unprotected left main ST-segment elevation myocardial infarction.   JACC Case Rep. 2021;3(5):754-759.PubMedGoogle ScholarCrossref
7.
Yamaji  H , Iwasaki  K , Kusachi  S ,  et al.  Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography.   J Am Coll Cardiol. 2001;38(5):1348-1354.PubMedGoogle ScholarCrossref
8.
Fujii  T , Hasegawa  M , Miyamoto  J , Ikari  Y .  Differences in initial electrocardiographic findings between ST-elevation myocardial infarction due to left main trunk and left anterior descending artery lesions.   Int J Emerg Med. 2019;12(1):12.PubMedGoogle ScholarCrossref
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Wagner  GS , Macfarlane  P , Wellens  H ,  et al.  AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram.   J Am Coll Cardiol. 2009;53(11):1003-1011.PubMedGoogle ScholarCrossref
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