CMR Sensitivity Varies With Clinical Presentation and Extent of Cell Necrosis in Biopsy-Proven Acute Myocarditis

Abstract

The aim of this study was to determine whether clinical presentation and type of cell death in acute myocarditis might contribute to cardiac magnetic resonance (CMR) sensitivity. Growing evidence indicates CMR is the reference noninvasive tool for the diagnosis of acute myocarditis. However, factors affecting CMR sensitivity are still unclear. We retrospectively evaluated 57 consecutive patients with a diagnosis of acute myocarditis made on the basis of clinical history (≤3 months) and endomyocardial biopsy evidence of lymphocytic infiltrates (≥14 infiltrating leukocytes/mm(2) at immunohistochemistry) in association with damage of the adjacent myocytes and absence or minimal evidence of myocardial fibrosis. CMR acquisition protocol included T2-weighted (edema), early (hyperemia), and late (fibrosis/necrosis) gadolinium enhancement sequences. Presence of ≥2 CMR criteria denoted myocarditis. Type of cell death was evaluated by using in situ ligation with hairpin probes. Three clinical myocarditis patterns were recognized: infarct-like (pattern 1, n= 21), cardiomyopathic (pattern 2, n= 21), and arrhythmic (pattern 3, n= 15). Tissue edema was observed in 81% ofpattern 1, 28% of pattern 2, and 27% of pattern 3. Early enhancement was evident in 71% of pattern 1,67% of pattern 2, and 40% of pattern 3. Late gadolinium enhancement was documented in 71% of pattern 1, 57% of pattern 2, and 47% of pattern 3. CMR sensitivity was significantly higher in pattern 1 (80%) compared with pattern 2 (57%) and pattern 3 (40%) (p < 0.05). Cell necrosis was the prevalent mechanism of death in pattern 1 compared with pattern 2 (p < 0.001) and pattern 3 (p < 0.05), whereas apoptosis prevailed in pattern 2 (p < 0.001 vs. pattern 1 and p < 0.05 vs. pattern 3). In acute myocarditis, CMR sensitivity is high for infarct-like, low for cardiomyopathic, and very low for arrhythmic clinical presentation; it correlates with the extent of cell necrosis-promoting expansion of interstitial space.