Acute Pericarditis Assessed With Magnetic Resonance Imaging
A New Approach
A 19-year-old man with the diagnosis of acute pericarditis based on the classic clinical syndrome and an ECG (Figure 1A) was referred to our cardiac magnetic resonance (CMR) unit 1 month after his hospital admission because of suspected associated acute myocarditis. A follow-up ECG within the time frame of referral showed essentially significant regression of ST elevation (Figure 1B). An echocardiogram performed at the referring hospital on the same day (Figure 2A and 2B) was reported as showing mild concentric left ventricular (LV) hypertrophy with good LV systolic function (ejection fraction 75%).
The combination of 3 CMR sequences (cine imaging with the new balanced steady-state free-precession technique [shown in Figure 3, first row]; contrast-enhancement inversion recovery CMR imaging in the late phase after gadolinium injection [shown in Figure 3, second row], and short τ-inversion recovery T2-weighted imaging [Figure 3, third row]) confirmed the diagnosis of acute pericarditis (columns 1 and 3, Figure 3). With the same approach, associated acute myocarditis or myocardial fibrosis was excluded. The pericardium was of normal thickness, with no evidence of constrictive physiology or significant effusion. There was mild LV dilatation, borderline increased LV mass, and no regional wall-motion abnormality, with an LV ejection fraction of 73%. The patient was treated with nonsteroidal antiinflammatory medication for persistent symptoms over a 6-week period and remained asymptomatic thereafter. Echocardiography performed 2 months after initial presentation (Figure 2C and 2D) showed no significant change compared with the echocardiogram performed at the time of the initial CMR scan. A follow-up CMR scan after 6 months (columns 2 and 4, Figure 3) showed normal LV size, borderline increased LV mass, and resolution of pericardial inflammatory process.
Short τ-inversion recovery T2-weighted imaging demonstrated hyperintense signal from the pericardium (arrowed in both images labeled E in Figure 3) in the initial scan. This imaging technique is particularly sensitive for tissue edema, a substantial feature of an acute inflammatory reaction, because an increase of free-water content due to lymphocyte infiltration causes T2 relaxation time prolongation. The contrast-enhancement inversion recovery MRI sequences also demonstrated hyperenhancement of the pericardium (arrowed visceral and parietal pericardium in both images labeled C in Figure 3), which can be due to severe edema that leads to an increased distribution volume of gadolinium contrast and/or cellular necrosis. The reversibility of the hyperenhancement is consistent with no significant necrosis and healing of the inflammatory process in this case.
There was significant improvement of the clinical picture and of the ECG changes at the time of the initial CMR scan. Interestingly, although the echocardiogram showed no specific abnormality, the ECG still showed approximately 1 mm of ST elevation, and the combined approach of the 3 described CMR techniques proved to be a valuable noninvasive tool in the diagnosis of acute pericarditis. It demonstrated the exact cardiac region affected in this syndrome, which can be a diagnostic challenge in a significant number of patients, on occasion even mimicking acute myocardial infarction. Additionally, CMR enabled monitoring of the inflammatory process and thus provided prognostic information, because even subclinical persistence of the inflammatory process can be related to the development of pericardial constriction and impaired left ventricular function, which is unlikely in this case.