A cute myocarditis often is demonstrated on cardiac MRI (CMR) as increased signal on T2-weighted imaging and late gadolinium enhancement (LGE) in either a midwall or a subepicardial distribution. Previous reports have demonstrated a similar pattern of enhancement on delayed postcontrast CT. 1-3 We present 2 cases of edema demonstrated on arterial phase CT coronary angiography (CTCA) in patients with clinical features that suggest acute myocarditis as confirmed by CMR.CT examinations were performed on a dual-source 64-detector CT scanner (SOMATOM Definition; Siemens Medical Solutions; Forchheim, Germany). Iomeron 350 (Iomoprol 71.4%; Bracco-Eisai; Tokyo, Japan) was injected at 6.5 mL/second into the cubital fossa through an 18-gauge cannula followed by a 50-mL saline flush. Scans were performed in the arterial phase, with triggering from the ascending aorta with a threshold of 100 Hounsfeld units. Both studies were acquired with dose-modulated, retrospective ECG gating. The tube voltage was set at 120 kV (peak) for the first case and 100 kV for the second case.CMR was performed with a 1.5-T GE Signa Twinspeed system (GE Healthcare; Milwaukee, WI) with an 8-element cardiac phased-array coil.LGE imaging was performed using a segmented inversion recovery fast-gradient echo sequence between 10 and 20 minutes after intravenous administration of 0.2 mmol/kg of gadolinium-diethylene triamine pentaacetic acid.
Case 1A 27-year-old man with no significant medical history presented with chest pain. Troponin I level was elevated at 4.4 g/L, and the ECG showed a sinus bradycardia. Echocardiography was normal. CTCA showed normal epicardial coronary arteries. There was a small area of subepicardial and midwall low attenuation within the mid anterolateral left ventricular wall ( Figure 1A and 1B). CMR demonstrated high signal on both steady-state free precession imaging and fat-suppressed T2-weighted imaging ( Figure 1C), with LGE corresponding to the areas of low attenuation on CT ( Figure 1D). A diagnosis of myocarditis was made on the basis of the MRI and clinical findings in the presence of normal coronary arteries. Estimated dose from CTCA was 8.3 mSv.
Case 2A 24-year-old male smoker with no significant medical history presented with sudden onset of sharp chest pain radiating to the left arm that was not pleuritic in nature. Troponin I level was elevated at 8.0 g/L; other laboratory results were normal. There were nonspecific inferolateral ECG changes. CMR demonstrated midwall LGE within the basal septum and adjacent inferior wall ( Figure 2B). Corresponding high signal was demonstrated on both steady-state free precession imaging and fat-suppressed T2-weighted imaging (Figure 2A). CTCA was performed to evaluate the coronary arteries, which were normal. Decreased attenuation was demonstrated within the interventricular septum and inferior wall corresponding to the areas of abnormal signal intensity on CMR ( Figure 2C and 2D). Estimated dose from CTCA was 2.45 mSv.A third patient later presented with chest pain and elevated...
Complications of intracardiac tumours can carry significant morbidity and mortality. This article depicts the case of a female who presented with multiple oncotic intracranial aneurysms secondary to a left atrial myxoma. The clinical manifestations and pathogenesis of cardiac myxoma, as well as the imaging pathway, management and prognosis of myxomatous aneurysms will be discussed. Excision of the cardiac mass is mandatory both for symptomatic improvement and to prevent further embolic complications. Local recurrence and delayed onset cerebral complications do occur, and necessitate ongoing patient follow-up. Our report highlights several important features of the diagnostic and treatment pathway for atrial myxoma—in particular, the potentially non-specific clinical presentation, the pivotal role of cardiac MRI in the multimodality diagnostic imaging work up and the need for multidisciplinary communication to identify the diagnosis and guide appropriate management.
patient it seemed to resolve post-op Day 2, responding only to surgery having been refractory medically prior to that.In summary, cardiogenic pulmonary oedema remains a possible and sufficient explanation for asymmetric right upper lobe pulmonary abnormalities in a patient with significant mitral valve regurgitation. Transthoracic and/or transoesophageal echocardiography with particular attention to mitral regurgitation jet direction and demonstration of regurgitant systolic reversal of flow into right pulmonary vein(s) would corroborate this diagnosis. Clinical judgment may mandate the need to exclude other coexisting pulmonary pathology, but indeed the sole underlying pathology may be cardiac. Such pulmonary oedema may persist despite aggressive medical measures and resolve only after surgical correction of the valve dysfunction.
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