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Circulation. 2003;108:e165-e166
doi: 10.1161/01.CIR.0000109202.90989.99
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(Circulation. 2003;108:e165.)
© 2003 American Heart Association, Inc.


Images in Cardiovascular Medicine

ST-Segment Elevation in an Unresponsive Patient

Glenn A. Hirsch, MD; Alan W. Heldman, MD; Ilan S. Wittstein, MD; Steven P. Schulman, MD; Gary Gerstenblith, MD

From the Division of Cardiology, Department of Medicine, The Johns Hopkins Hospital, Baltimore, Md (G.A.H., A.W.H., I.S.W., S.P.S., G.G.), and the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md (G.A.H.).

Correspondence to Glenn A. Hirsch, MD, NIH/NHLBI, 10 Center Drive, MSC-1061, Building 10, Room B1D-416, Bethesda, MD 20892-1061. E-mail ghirsch{at}jhmi.edu

A distressed woman hailed a car for assistance several blocks from our institution. Upon arrival at the Emergency Department, she was unresponsive. Telemetry demonstrated ventricular fibrillation, and she was defibrillated to sinus rhythm with ECG, as shown in Figure 1. She was taken for emergent cardiac catheterization with a heart rate of 117 bpm and blood pressure of 95/55 mm Hg. Coronary angiography revealed no stenosis or flow abnormalities. During catheterization, ST-segment elevation resolved and recurred several times (Figure 2). Reinjection of the left coronary artery showed no change in diameter or TIMI (thrombolysis in myocardial infarction) flow during the periods of extreme elevation and near-normalization (Figure 3). Echocardiography showed anteroapical hypokinesis with a left ventricular ejection fraction of 0.25. She remained hypotensive, and an intra-aortic balloon pump was inserted. Cardiac enzymes were elevated, with a creatine kinase level of 1445 (24 to 170 IU/L), creatine kinase-MB of 177 (0 to 7 µg/L), and troponin I of 1.76 (0.3 to 0.5 ng/mL). The patient remained unresponsive. Computed tomography of the brain showed diffuse subarachnoid hemorrhage and cerebral edema (Figure 4). Further neurological testing showed brain death.



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Figure 1. ECG obtained immediately after defibrillation demonstrates sinus tachycardia with anterolateral ST-segment elevation, inferior ST-segment depression, and a prolonged QT interval.



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Figure 2. Dynamic ST-segment changes occurred over several minutes during cardiac catheterization. (Tracing shown was recorded from the same precordial lead.)



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Figure 3. No coronary stenosis or vasospasm was present during coronary angiography.



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Figure 4. A, Computed tomography of the brain revealed diffuse subarachnoid hemorrhage (arrows) and cerebral edema compared with previous head CT from the same patient (B).

This case demonstrates an electrocardiographic current of injury and serum evidence of myocardial necrosis despite angiographically normal coronary blood flow in the setting of subarachnoid hemorrhage. One important factor contributing to myocardial injury and left ventricular dysfunction in this setting is contraction band necrosis due to direct catecholamine toxicity.

Footnotes

The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke’s Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.

Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Luke’s Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.




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