Circulation Journal
Online ISSN : 1347-4820
Print ISSN : 1346-9843
ISSN-L : 1346-9843
Images in Cardiovascular Medicine
Clinical Implications of Cardiac Magnetic Resonance Imaging for Identifying Culprit Lesions in Patients With Suspected Multivessel Acute Myocardial Infarction
Riku AraiAkimasa YamadaSaki MizobuchiNaotaka AkutsuToshihiko NishidaDaisuke FukamachiYasuo Okumura
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2020 Volume 84 Issue 7 Pages 1195-

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A 67-year-old woman with diabetes presented to the emergency department because of syncope. She was in shock with blood pressure of 70/55 mmHg. A synthesized 18-lead ECG showed sinus rhythm with ST-segment elevation in leads II, III, aVF, aVR, V1, syn-V3R-to-syn-V5R, and V5-to-syn-V9, with ST-segment depression in leads I, aVL, and V2-to-V4 (Figure A), suggesting extensive left ventricular (LV) infarction with right ventricular infarction. Enhanced CT for ruling out aortic dissection showed a focal transmural myocardial perfusion defect in the LV in the inferoseptal-posterolateral region (Figure B,C). The ECG and CT findings suggested multivessel acute myocardial infarction (MVAMI). Coronary angiography (CAG) showed subtotal occlusion of both the proximal left circumflex artery (LCX) and proximal right coronary artery (RCA) (Figure D,E: arrows), and significant stenosis of the left anterior descending artery (LAD) (Figure F: arrow). Percutaneous coronary intervention to these 3 vessels immediately recovered the cardiogenic shock (Figure G–I). Thrombosuction of the LCX and RCA revealed fresh thrombus from only the LCX. Intravascular ultrasound showed the thrombus in LCX (Figure J: arrow) and mixed plaque in both the RCA and LAD without thrombus (Figure K,L).

Figure.

See the text for a description of the corresponding figures.

The patient’s clinical course was uneventful. T2-weighted cardiac magnetic resonance (CMR) 47 days after MVAMI revealed myocardial oedema remained only in the lateral LV wall (Figure M,N: arrowheads) with subendocardial late-gadolinium enhancement in only part of the transmural retention of contrast (Figure M,N: arrow). The patient did not have any potential sources of hypercoagulability.

This case was initially suspected to be MVAMI but the multimodality findings generated 2 other possible mechanisms: (1) the first culprit was the LCX and the associated hemodynamic changes caused transmural RCA ischemia, or (2) the first culprit was the LAD. The short duration of LAD ischemia caused hemodynamic collapse and the LCX occlusion. CMR did not detect anterior LV infarction because the LAD self-recanalized after short duration of ischemia. In suspected MVAMI, subsequent CMR is effective in accurately depicting the myocardial condition.

Disclosures

Y.O. received research funding from Boston Scientific Japan.

 
© 2020 THE JAPANESE CIRCULATION SOCIETY
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