A patient in their 30s with no known medical history presented to the emergency department with 6 hours of vertigo, vomiting, dysarthria, and left-sided weakness. They denied any chest pain or shortness of breath. Vital signs were normal. A brain computed tomographic scan (CT) was consistent with a large infarction of the left cerebellar hemisphere and left pontine. An electrocardiogram (ECG) obtained on admission is shown in Figure, A. Subsequent investigation revealed a troponin T level of 1349 pg/mL (reference range, <14 pg/mL) and an N-terminal probrain natriuretic peptide level of 1674 pg/mL (reference range, <125 pg/mL). Test results for thrombophilia, vasculitis, and antiphospholipid syndrome were all negative. Echocardiogram showed regional wall-motion abnormalities of the left ventricle with a reduced ejection fraction of 36%. The patient was initially diagnosed with acute ischemic stroke and ST-segment elevation myocardial infarction (STEMI).
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Stroke-heart syndrome has been considered a perfect storm for patients with stroke, which could be classified into 5 categories (1) ischemic and nonischemic acute myocardial injury presenting with elevated troponin levels, which is usually asymptomatic; (2) acute myocardial infarction; (3) left ventricular dysfunction; (4) neurogenic sudden cardiac death; and (5) ECG changes.2 It has been reported2 that nearly 91% of patients with acute ischemic stroke (AIS) could present with new ECG abnormalities in unselected populations, and 32% for those without preexisting cardiac diseases. Various ECG changes may occur in the setting of AIS, including ST-segment elevation, ST-segment depression, unspecified ST-T changes, QT prolongation, T inversion, abnormal T-wave morphology, bundle branch block and pathologic Q waves, among which unspecified ST changes and ST depression represent the 2 most common types.3 To our knowledge, de Winter ECG pattern induced by SIHI has never been reported previously.
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Corresponding Author: Tong Liu, MD, PhD, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, No. 23, Pingjiang Rd, Hexi District, Tianjin 300211, People’s Republic of China (email@example.com).
Published Online: September 12, 2022. doi:10.1001/jamainternmed.2022.3707
Conflict of Interest Disclosures: None reported.
Funding/Support: The work was funded by National Natural Science Foundation of China (81900301), Science and Technology Planning Project of Guangzhou (201904010451).
Role of the Funder/Sponsor: The National Natural Science Foundation of China had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.
Additional Contributions: We thank Chuan-Hai Zhang, MD, from Department of Cardiology, The First Affiliated Hospital of Jinzhou Medical University, and Nan Zhang, MD, from Second Hospital of Tianjin Medical University, for their helpful comments. They were not compensated.
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