Department of Cardiology and Cardiovascular Diseases, University of Tübingen, Tübingen, Germany.
Department of Pathology, Institute of Pathology and Neuropathology, University of Tübingen, Tübingen, Germany.
J Am Coll Cardiol. 2017 May 2;69(17):2160-2172. doi: 10.1016/j.jacc.2017.02.049.
Tachycardiomyopathy or tachycardia-induced cardiomyopathy (TCM) has been known for decades as a reversible form of nonischemic cardiomyopathy. However, its mechanism and properties remain poorly understood.
The current study investigated endomyocardial biopsy samples from patients with TCM and compared them with samples from patients with dilated cardiomyopathy (DCM) and inflammatory cardiomyopathy (ICM).
The study included 189 patients with new-onset heart failure and severely reduced ejection fraction not caused by valvular or ischemic heart disease. Nineteen patients retrospectively fulfilled common criteria of TCM, 79 patients had a diagnosis of DCM, and 91 had a diagnosis of ICM.
Patients with TCM, on the basis of clinical criteria, had stronger myocardial expression of major histocompatibility complex class II molecule and enhanced infiltration of CD68 macrophages compared with patients with DCM. Furthermore, when compared with patients with ICM, the presence of T cells and macrophages was significantly reduced in TCM. Myocardial fibrosis was detected to a significantly lower degree in patients with TCM compared with patients with DCM and ICM. Electron microscopic examination revealed severe structural changes in patients with TCM. A disturbed distribution pattern of mitochondria was predominantly present in TCM. Quantitative assessment of myocyte morphology revealed significantly enhanced myocyte size compared with patients with ICM. Ribonucleic acid expression analysis identified changes in metabolic pathways among the patient groups.
TCM is characterized by changes in cardiomyocyte and mitochondrial morphology accompanied by a macrophage-dominated cardiac inflammation. Thus, further prospective studies are warranted to characterize patients with TCM by endomyocardial biopsy more clearly.
心动过速性心肌病（TCM）或心动过速诱导性心肌病已被人们认识数十年，它是一种非缺血性心肌病的可逆形式。然而，其机制和特征仍知之甚少。
本研究通过对 TCM 患者的心肌活检样本进行研究，并与扩张型心肌病（DCM）和炎症性心肌病（ICM）患者的样本进行比较。
该研究纳入了 189 例新发心力衰竭且射血分数严重降低的患者，这些患者的病因并非瓣膜性心脏病或缺血性心脏病。19 例患者回顾性地满足了 TCM 的常见标准，79 例患者被诊断为 DCM，91 例患者被诊断为 ICM。
基于临床标准，TCM 患者的主要组织相容性复合体Ⅱ类分子的心肌表达更强，CD68 巨噬细胞浸润增强，与 DCM 患者相比。此外，与 ICM 患者相比，TCM 患者的 T 细胞和巨噬细胞明显减少。与 DCM 和 ICM 患者相比，TCM 患者的心肌纤维化程度明显较低。电镜检查显示 TCM 患者存在严重的结构变化。线粒体的分布模式紊乱主要存在于 TCM 患者中。定量评估肌细胞形态学发现，与 ICM 患者相比，TCM 患者的肌细胞大小明显增大。核糖核酸表达分析确定了各组患者代谢途径的变化。
TCM 的特征是心肌细胞和线粒体形态发生变化，伴有巨噬细胞主导的心脏炎症。因此，需要进一步的前瞻性研究来更清楚地通过心肌活检来确定 TCM 患者的特征。
