Sato Takuma, Ikeda Yoshihiko, Seguchi Osamu, Fukushima Satsuki, Tsukamoto Yasumasa
Department of Transplant Medicine, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan.
Department of Pathology, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Suita, Osaka 564-8565, Japan.
Eur Heart J Case Rep. 2025 May 20;9(6):ytaf248. doi: 10.1093/ehjcr/ytaf248. eCollection 2025 Jun.
An accurate and rapid pathologic diagnostic in fulminant myocarditis is crucial for appropriate therapeutic decision-making. Since giant cells can appear in various conditions, careful judgment based on repeated imaging, pathological analysis, and close clinical follow-up is essential to make precise decisions.
A previously healthy 36-year-old woman was admitted to the hospital with haemodynamic compromise requiring mechanical circulatory support. Pathologic findings of left ventricular (LV) at the time of left ventricular assist device (LVAD) implantation confirmed the diagnosis of lymphocytic myocarditis. Cardiac function had gradually recovered, and LVAD was successfully weaned on post-operative day (POD) 10. However, surgical biopsy of LV at the time of LVAD removal revealed multinucleated giant cell formation, resulting in administered prednisolone for 2 weeks. After the withdrawal of prednisolone, pathologic findings of the right ventricle (RV) endomyocardial biopsy (EMB) specimens obtained on POD 21 showed continuous resolving myocarditis without any giant cell formation. Several additional examinations showed no evidence of an autoimmune-related disease background. The cardiac catheterisation performed on POD 85 showed normal hemodynamics with preserved LV function and EMB of the RV showed resolving myocarditis without giant cells. One year later, the patient was well without immunosuppressive therapy.
The multinucleated giant cell formation might be the accidental result of the fusion of macrophages that had ingested myocardial calcifications or degenerative macromolecules formed by the severe inflammatory process of lymphocytic myocarditis. The massive calcium deposition in both ventricles on CT and the positivity of monocytic markers in giant cells support this hypothesis.
暴发性心肌炎的准确快速病理诊断对于做出恰当的治疗决策至关重要。由于巨细胞可出现在多种情况中，基于反复成像、病理分析及密切临床随访进行仔细判断对于做出精确决策至关重要。
一名既往健康的36岁女性因血流动力学不稳定入院，需要机械循环支持。左心室辅助装置（LVAD）植入时左心室（LV）的病理结果确诊为淋巴细胞性心肌炎。心功能逐渐恢复，LVAD在术后第10天成功撤机。然而，LVAD移除时LV的手术活检显示有多核巨细胞形成，因此给予泼尼松龙治疗2周。泼尼松龙停药后，术后第21天获取的右心室（RV）心内膜心肌活检（EMB）标本的病理结果显示心肌炎持续缓解，无任何巨细胞形成。多项额外检查未发现自身免疫相关疾病背景的证据。术后第85天行心导管检查显示血流动力学正常，LV功能保留，RV的EMB显示心肌炎缓解，无巨细胞。一年后，患者未接受免疫抑制治疗，情况良好。
多核巨细胞形成可能是巨噬细胞融合的意外结果，这些巨噬细胞吞噬了心肌钙化或由淋巴细胞性心肌炎的严重炎症过程形成的变性大分子。CT上两心室的大量钙沉积以及巨细胞中单核细胞标志物的阳性支持这一假说。
