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首页> 外文期刊>JACC. Cardiovascular imaging. >CMR sensitivity varies with clinical presentation and extent of cell necrosis in biopsy-proven acute myocarditis
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CMR sensitivity varies with clinical presentation and extent of cell necrosis in biopsy-proven acute myocarditis

机译:在经活检证实的急性心肌炎中,CMR敏感性随临床表现和细胞坏死程度而异

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摘要

Objectives: 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. Background: Growing evidence indicates CMR is the reference noninvasive tool for the diagnosis of acute myocarditis. However, factors affecting CMR sensitivity are still unclear. Methods: 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/mm2 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 (fibrosisecrosis) gadolinium enhancement sequences. Presence of ≥2 CMR criteria denoted myocarditis. Type of cell death was evaluated by using in situ ligation with hairpin probes. Results: 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% of pattern 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). Conclusions: 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.
机译:目的:本研究的目的是确定急性心肌炎的临床表现和细胞死亡类型是否可能对心脏磁共振(CMR)敏感性产生影响。背景:越来越多的证据表明CMR是诊断急性心肌炎的参考非侵入性工具。但是,影响CMR敏感性的因素仍不清楚。方法:我们回顾性评估了57例根据临床病史(≤3个月)和心内膜活检的淋巴细胞浸润(免疫组织化学检查≥14个浸润白细胞/ mm2)与邻近组织损害相关的诊断为急性心肌炎的连续患者。心肌细胞和心肌纤维化的缺乏或极少证据。 CMR采集方案包括T2加权(水肿),早期(充血)和晚期(纤维化/坏死)g增强序列。 ≥2CMR标准的存在表示为心肌炎。通过使用与发夹探针的原位连接来评估细胞死亡的类型。结果:识别出三种临床心肌炎模式:梗死样(模式1,n = 21),心肌病(模式2,n = 21)和心律不齐(模式3,n = 15)。在模式1的81%,模式2的28%和模式3的27%中观察到组织水肿。在模式1的71%,模式2的67%和模式3的40%中,早期增强明显。在模式1的71%,模式2的57%和模式3的47%中记录到增强。模式1(80%)的CMR敏感性显着高于模式2(57%)和模式3(40%) (p <0.05)。与模式2(p <0.001)和模式3(p <0.05)相比,细胞坏死是模式1的主要死亡机制,而模式2则细胞凋亡普遍存在(模式1的p <0.001,模式2的p <0.05 3)。结论:在急性心肌炎中,CMR敏感性对于梗死样的敏感性高,对心肌病的敏感性低,而对于心律不齐的临床表现则非常低。它与细胞坏死促进间隙空间扩展的程度有关。

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