Abstract
We report the case of a 67-year-old man with no significant medical history who experienced sudden cardiac arrest at home. Emergency medical services performed electrical defibrillation for ventricular fibrillation and restored spontaneous circulation. A postresuscitation 12-lead electrocardiogram showed ST-elevation in the precordial leads and frequent premature ventricular contractions. Although these findings are common in daily clinical practice, an immediate detailed differential diagnosis and investigation are required. This case clearly demonstrates that in such circumstances, a broad differential diagnostic knowledge and prompt decision-making can improve the patient's prognosis.
Key words: acute coronary syndrome, electrocardiogram, ventricular fibrillation
Graphical Abstract
Case Presentation
A 67-year-old man with well-controlled hypertension and diabetes mellitus was found unconscious at home. He had been well 5 minutes earlier. Emergency medical services performed 2 defibrillations for ventricular fibrillation (VF), successfully restoring circulation. On admission, he was unconscious but hemodynamically stable (blood pressure 110/87 mm Hg, heart rate 90 beats/min). Cardiovascular and respiratory physical examinations were unremarkable. VF recurred multiple times, requiring repeated defibrillation. A postresuscitation 12-lead electrocardiogram (ECG) was performed (Figure 1).
Take-Home Messages
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Precordial ST-segment elevation with ventricular fibrillationshould prompt broad differential diagnosis.
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Precordial ST-segment elevation with ventricular fibrillation, especially with maximal elevation in V1 to V3, may reflect right ventricular infarction such as conus branch occlusion, which can mimic anterior myocardial infarction.
Figure 1.
A Postresuscitation 12-Lead Electrocardiogram
What Is the Most Likely Mechanism Underlying VF in This Patient?
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A)
Early repolarization syndrome
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B)
Brugada syndrome
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C)
Broad anterior myocardial infarction (MI)
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D)
MI of the nondominant right coronary artery (RCA) or its branches
Discussion
The ECG showed ST-segment elevation in leads V1 to V4 and frequent premature ventricular contractions (VPCs). Several differential diagnoses were considered:
Choice A typically shows J-point elevation in inferior or lateral leads and may cause idiopathic VF. These findings were absent.
Choice B features J-point elevation (≥0.2 mV) in leads V1 to V3 with coved or saddleback morphology. It does not typically show reciprocal changes. Differentiation from MI is essential, and serial ECGs may be required.
Choice C typically presents with anterior and lateral ST-segment elevation accompanied by reciprocal ST-segment depression in inferior leads. In the present case, subtle reciprocal ST-segment depression was observed in inferior leads. When reciprocal ST-segment depression is present, a proximal left anterior descending artery (LAD) occlusion should be suspected. In contrast, in mid or distal LAD occlusion, approximately half of the patients may not show such reciprocal changes, particularly in lead III, and this should be considered during interpretation.
Choice D is supported by the presence of ST-segment elevation in leads V1 to V3 and frequent VPCs originating from the right ventricular outflow tract (RVOT). Right ventricular infarction mimicking anterior MI is referred to as “pseudoanteroseptal MI.” Geft et al1 reported 5 such RV infarction cases among 69 patients with ST-segment elevation in V1 to V5, where the LAD was patent. Khan and Chou2 described 4 cases of isolated right ventricular infarction with maximal ST-segment elevation in V1 to V3, mimicking anteroseptal MI, but without evidence of left ventricular involvement.
In this case, coronary angiography revealed occlusion of the conus branch of the RCA (Figure 2A), with no significant stenosis in the LAD or main RCA. The ST-segment elevation resolved after balloon angioplasty to the conus branch, and no further ventricular arrhythmias occurred. Cardiac magnetic resonance imaging performed on day 8 demonstrated edema and late gadolinium enhancement localized to the RVOT (Figures 2B and 2C), consistent with MI. The presence of frequent VPCs with RVOT morphology and ST-segment depression in posterior leads (V7-V9) further supported the diagnosis (Figure 2D).
Figure 2.
Coronary Angiography, Cardiac Magnetic Resonance Imaging, and Electrocardiogram in Posterior Leads
(A) Post-treatment angiography demonstrated visualization of the conus branch (pink arrow). (B, C) Cardiac magnetic resonance imaging demonstrated edema on T2-weighted imaging and an infarct area on late gadolinium enhancement in the RVOT (yellow arrow). (D) ST-segment depression in posterior leads was presented as a mirror image of conus branch MI. RVOT = right ventricular outflow tract.
These clinical features and imaging findings are consistent with previous reports demonstrating that conus branch occlusion can lead to isolated RVOT infarction and ventricular arrhythmias.3
Funding Support and Author Disclosures
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Acknowledgments
The authors would like to express their sincere appreciation to Fumiya Uchida for his valuable support and insightful advice throughout the preparation of this case report. Written permission to include this acknowledgment has been obtained from Fumiya Uchida.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
References
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