Saito Kazumasa, Kinjo Takahiko, Goto Shintaro, Sasaki Shingo, Tomita Hirofumi
Department of Cardiology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Department of Pathology and Bioscience, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
J Cardiol Cases. 2024 Feb 15;29(5):226-230. doi: 10.1016/j.jccase.2024.02.001. eCollection 2024 May.
The pathogenesis of chronic active myocarditis remains unclear. A 65-year-old man underwent permanent pacemaker implantation for sick sinus syndrome and pulmonary vein isolation for paroxysmal atrial fibrillation. Four years later, the left ventricular ejection fraction decreased from 51 % to 35 %, and the apical left ventricular inferior wall developed akinesis. Isolated cardiac sarcoidosis was suspected; however, prednisolone and optimal medical therapy failed to improve the symptoms. Even after cardiac resynchronization therapy followed by atrioventricular junction ablation for untreatable atrial tachycardia, the patient died of heart failure eight years after referral. An autopsy revealed inflammatory cell infiltration accompanied by cardiac myocytolysis in both atria and ventricles. He was diagnosed with chronic active myocarditis based on pathological findings and a persistent increase in the blood high-sensitivity cardiac troponin levels before death. The myocardium around the sinus node showed extensive and severe fibrosis with mild inflammation, suggesting a chronic inflammatory phase. In contrast, the left atrium and both ventricles showed active myocardial inflammation with fibrosis, suggesting a persistently active inflammatory phase. This case demonstrated that atrial inflammation caused intractable atrial arrhythmia, while ventricular inflammation led to biventricular heart failure, and highlighted the presence of spatially and temporally heterogeneous inflammation in chronic active myocarditis.
We describe a case of chronic active myocarditis with spatially and temporally heterogeneous lesions throughout the four cardiac chambers. Inflammatory cell infiltration was observed in both atria and ventricles. Extensive fibrosis replaced the myocardium around the sinus node, suggesting a chronic phase. The left atrium and ventricles showed active inflammation, suggesting an active phase. Atrial and ventricular inflammation led to atrial arrhythmia and heart failure, respectively.
慢性活动性心肌炎的发病机制尚不清楚。一名65岁男性因病态窦房结综合征接受了永久性起搏器植入术，并因阵发性心房颤动接受了肺静脉隔离术。四年后，左心室射血分数从51%降至35%，左心室心尖下壁出现运动减弱。怀疑为孤立性心脏结节病；然而，泼尼松龙和最佳药物治疗未能改善症状。即使在心脏再同步治疗后因无法治疗的房性心动过速进行了房室结消融，该患者在转诊八年后仍死于心力衰竭。尸检显示心房和心室均有炎症细胞浸润并伴有心肌细胞溶解。根据病理结果以及死亡前血液高敏心肌肌钙蛋白水平持续升高，他被诊断为慢性活动性心肌炎。窦房结周围的心肌显示广泛而严重的纤维化并伴有轻度炎症，提示处于慢性炎症期。相比之下，左心房和两个心室显示有活动性心肌炎症并伴有纤维化，提示处于持续活跃的炎症期。该病例表明，心房炎症导致难治性房性心律失常，而心室炎症导致双心室心力衰竭，并突出了慢性活动性心肌炎中存在空间和时间上异质性的炎症。
我们描述了一例慢性活动性心肌炎病例，其在四个心腔中存在空间和时间上异质性的病变。在心房和心室均观察到炎症细胞浸润。窦房结周围的心肌被广泛纤维化取代，提示处于慢性期。左心房和心室显示有活动性炎症，提示处于活跃期。心房和心室炎症分别导致房性心律失常和心力衰竭。
