European Heart Journal Advance Access originally published online on October 21, 2005
European Heart Journal 2006 27(4):468; doi:10.1093/eurheartj/ehi523
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Diagnosing acute myocarditis using cardiac MRI
Western Infirmary Glasgow, Glasgow G11 6NT, UK
* Corresponding author. E-mail address: t.martin{at}clinmed.gla.ac.uk
A 35-year-old man attended the Emergency Room with his first episode of central chest pain. The pain began 8 h prior to presentation and the 12-lead ECG showed ST-segment elevation of >1 mm in leads II, III, and aVF (Figure, lower panel). He was treated with thrombolysis and transferred to the Coronary Care Unit. Troponin I was 60.9 pg/mL (normal <0.2 pg/mL), and creatinine kinase and MB fraction were 2888 and 235 IU, respectively. No abnormality was demonstrated on transthoracic echocardiography. CMR examination was carried out the following day on a 1.5 T scanner (Siemens Sonata) with a phased-array chest coil, during breath hold and gated to the electrocardiogram. A steady-state free-precession (true FISP) sequence was used to acquire a short-axis cinematographic (CINE) stack of the left ventricle (field of view=340 mm, slice thickness=8 mm, interslice gap=2 mm, TR=47.4 ms, TE=1.58 ms, flip-angle=60°). Delayed contrast-enhanced cardiac magnetic resonance imaging was then performed using the standard turboFLASH inversion-recovery sequence. Briefly, gadolinium-DTPA (Amersham Health), 0.2 mmol/kg, was administered intravenously and delayed enhancement short-axis images were recorded 10–20 min later [field of view=340 mm, slice-thickness=8 mm, interslice gap=2 mm, TE=4.3 ms, flip-angle=30°, optimum inversion time adjusted to null normal myocardium (range 200–300 ms)].
An extensive area of hyper-enhancement that spares the subendocardium and does not match a coronary artery territory is demonstrated (Figure, upper left: four-chamber and upper right: mid-ventricular short axis). There is a preserved left ventricular function with no regional wall motion abnormality on the corresponding CINE images, and the patient has neither cardiovascular risk factors nor previous history of chest pain. Subsequent coronary angiography did not demonstrate a culprit lesion. Therefore, the myocardial damage should not be secondary to coronary artery disease (including emboli or spasm). A right ventricular endomyocardial biopsy was performed and was in keeping with an evolving cardiomyopathy. Correct diagnosis of myocardial infarction is always of clinical importance, and this case illustrates a novel use for CMR in the non-invasive determination of the aetiology of myocardial damage.
Delayed enhancement images on cardiac MRI shown in upper panels and admission 12-lead ECG in the lower panel. Upper left panel: four-chamber and upper right panel: mid-ventricular short-axis views.
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