Begieneman Mark P V, Emmens Reindert W, Rijvers Liza, Kubat Bela, Paulus Walter J, Vonk Alexander B A, Rozendaal Lawrence, Biesbroek P Stefan, Wouters Diana, Zeerleder Sacha, van Ham Marieke, Heymans Stephane, van Rossum Albert C, Niessen Hans W M, Krijnen Paul A J
Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands; ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands; Dutch Forensic Institute, The Hague, the Netherlands.
Department of Pathology, VU University Medical Center, Amsterdam, the Netherlands; ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands; Department of Immunopathology, Sanquin Research, Amsterdam, the Netherlands.
Cardiovasc Pathol. 2016 Mar-Apr;25(2):141-8. doi: 10.1016/j.carpath.2015.12.001. Epub 2015 Dec 4.
Atrial fibrillation (AF) is a common complication in myocarditis. Atrial inflammation has been suggested to play an important role in the pathophysiology of AF. However, little is known about the occurrence of atrial inflammation in myocarditis patients. Here, we analyzed inflammatory cell numbers in the atria of myocarditis patients without symptomatic AF.
Cardiac tissue was obtained postmortem from lymphocytic myocarditis patients (n=6), catecholamine-induced myocarditis patients (n=5), and control patients without pathological evidence of heart disease (n=5). Tissue sections of left and right ventricle and left and right atrium were stained for myeloperoxidase (neutrophilic granulocytes), CD45 (lymphocytes), and CD68 (macrophages). These cells were subsequently quantified in atrial and ventricular myocardium and atrial adipose tissue.
In lymphocytic myocarditis patients, a significant increase was observed for lymphocytes in the left atrial adipose tissue. In catecholamine-induced myocarditis patients, significant increases were found in the atria for all three inflammatory cell types. Infiltrating inflammatory cell numbers in the atrial myocardium correlated positively with those in the ventricles, especially in catecholamine-induced myocarditis patients.
To a varying extent, atrial myocarditis occurs concurrently with ventricular myocarditis in patients diagnosed with myocarditis of different etiology. This provides a substrate that potentially predisposes myocarditis patients to the development of AF and subsequent complications such as sudden cardiac death and heart failure.
心房颤动（AF）是心肌炎的常见并发症。已有研究表明心房炎症在AF的病理生理学中起重要作用。然而，对于心肌炎患者心房炎症的发生情况知之甚少。在此，我们分析了无症状AF的心肌炎患者心房中的炎症细胞数量。
从淋巴细胞性心肌炎患者（n = 6）、儿茶酚胺诱导性心肌炎患者（n = 5）以及无心脏病病理证据的对照患者（n = 5）的尸体中获取心脏组织。对左、右心室及左、右心房的组织切片进行髓过氧化物酶（中性粒细胞）、CD45（淋巴细胞）和CD68（巨噬细胞）染色。随后对心房和心室心肌以及心房脂肪组织中的这些细胞进行定量分析。
在淋巴细胞性心肌炎患者中，左心房脂肪组织中的淋巴细胞显著增加。在儿茶酚胺诱导性心肌炎患者中，所有三种炎症细胞类型在心房中均显著增加。心房心肌中浸润的炎症细胞数量与心室中的炎症细胞数量呈正相关，尤其是在儿茶酚胺诱导性心肌炎患者中。
在诊断为不同病因心肌炎的患者中，心房心肌炎在不同程度上与心室心肌炎同时发生。这为心肌炎患者易发生AF及随后的并发症如心源性猝死和心力衰竭提供了潜在基础。
