Viral acute inflammatory pericarditis

CLINICAL HISTORY

A 15-year-old girl was admitted to the emergency room for acute chest pain, fever, and progressive asthenia. Laboratory investigations revealed mild increases in inflammatory markers (e.g., erythrocyte sedimentation rate and troponin I). Chest radiography revealed moderate cardiac enlargement, and an ECG showed elevation in the ST segment with T-wave inversion. A 2D transthoracic echocardiogram revealed moderate pericardial effusion with normal regional and global left ventricular function. Cardiac MRI was performed one month later to exclude concomitant myocardial pathology (e.g., myocarditis or other cardiomyopathies) due to persistent elevation of the inflammatory markers.

FINDINGS

Cardiac MRI was performed on a 1.5T system (Avanto, Siemens Medical Solutions). The acquisition protocol included cine MRI using balanced steady-state free precession (SSFP), morphological black-blood T2-weighted turbo spin-echo short-tau inversion-recovery (STIR) imaging, and delayed enhancement imaging after IV administration of 0.1 mmol/kg body weight Gd-BOPTA (Multihance, Bracco) using an inversion-recovery gradient-echo technique.

T2-weighted STIR (Figure 1) showed a diffuse hyperintense appearance in the entire pericardium related to the presence of pericardial fluid and/or edema in both layers (thickness 5 to 6 mm; arrows). Cardiac function was normal with no focal alteration of contractility. Left ventricular ejection fraction was estimated at 65%. Late Gd-enhanced imaging using the inversion-recovery gradient-echo technique (Figure 2) showed strong and homogeneous enhancement of both layers (arrows) without signs of underlying myocardial involvement.

DIAGNOSIS

Viral acute inflammatory pericarditis was established on the basis of both clinical and imaging data. Medical therapy was based on nonsteroidal anti-inflammatory drugs. Complete regression was observed at six-month follow-up.

DISCUSSION

Most cases of acute pericarditis in children (90%) are idiopathic. Other common causes are infection, collagen vascular disease, genetic factors, metabolic disease, neoplasms, postpericardiotomy syndrome, and post-acute myocardial infarction.1 The acute inflammatory response in pericarditis can produce serous, purulent fluid or dense, fibrinous material. The pericardial fluid in viral pericarditis is most commonly serous, of low volume, and resolves spontaneously. Neoplastic, tuberculous, and purulent pericarditis may be associated with large effusions that are exudative and hemorrhagic and have a high leukocyte content.2,3

Transthoracic echocardiography is used as the first-line modality when studying patients with suspected pericardial pathology because it is noninvasive and economical. It can be difficult, however, to visualize loculated effusion and identify focal thickenings when using this modality.4,5

MRI, which is traditionally regarded as a secondary diagnostic technique for cardiac imaging, can compensate for many of these shortcomings, providing both morphological and functional information in a single examination.6 T2-weighted sequences show the presence of inflammation as intermediate to high signal. Inversion recovery sequences may be useful for identifying acute and subacute inflammation of the membrane, differentiating the purely inflammatory form from the chronic form (by indicating fibrous tissue), and identifying the different pericardial components.7,8

Based on the clinical history of the patient, elevation of inflammatory markers, and MRI findings, the condition seems to be viral subacute pericarditis. Evidence for this diagnosis includes persistent pathological en-hancement of the serosal layers and the presence of serous effusion.

Case submitted by Marco Francone, M.D., Ph.D., Ilaria Iacucci, M.D., Federica Ciolina, M.D., and Roberto Passariello, M.D. All are radiologists at the University Sapienza of Rome in Italy.