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肥厚型心肌病患者出现急性临床恶化时的心肌炎。

Myocarditis in hypertrophic cardiomyopathy patients presenting acute clinical deterioration.

作者信息

Frustaci Andrea, Verardo Romina, Caldarulo Marina, Acconcia Maria Cristina, Russo Matteo A, Chimenti Cristina

机构信息

Heart and Great Vessels Attilio Reale Department, La Sapienza University, Viale del Policlinico 155, Rome, Italy.

出版信息

Eur Heart J. 2007 Mar;28(6):733-40. doi: 10.1093/eurheartj/ehl525. Epub 2007 Feb 19.

Abstract

AIM

We sought to determine whether myocarditis can be a major cause of acute electrical instability or clinical deterioration in HCM patients.

METHODS AND RESULTS

A total of 119 HCM patients (69 M/50F, mean age 41 +/- 8), 42 with acute clinical deterioration and 77 clinically stable, underwent cardiac catheterization with left ventricular endomyocardial biopsy and gene analysis of major sarcomeric proteins. Endomyocardial tissue was processed for histology, immunohistochemistry, and polymerase chain reaction for the most common cardiotropic viruses. Controls were surgical samples from 50 patients with mitral stenosis. All 119 patients showed histological findings suggestive of HCM. In addition, CD45RO+ lymphocytes (> or =14/mm(2)) with focal necrosis of the adjacent severely hypertrophied and often disorganized myocytes, consistent with an overlapping active myocarditis, were observed in 28 of 42 unstable and none of 77 stable HCM patients. A viral genome was detected in 14 of 28 patients with myocarditis and in none of HCM patients without and in none of controls. No correlation between sarcomeric protein gene mutations and HCM clinical profile was observed.

CONCLUSION

Myocarditis, often viral, represents a common cause of acute clinical deterioration in HCM. Its recognition can potentially affect disease prognosis and treatment.

摘要

目的

我们试图确定心肌炎是否可能是肥厚型心肌病(HCM)患者急性电不稳定或临床恶化的主要原因。

方法与结果

总共119例HCM患者(69例男性/50例女性,平均年龄41±8岁),其中42例有急性临床恶化,77例临床稳定,接受了心脏导管检查及左心室心内膜活检,并对主要肌节蛋白进行基因分析。心内膜组织进行组织学、免疫组织化学检查以及针对最常见嗜心肌病毒的聚合酶链反应。对照组为50例二尖瓣狭窄患者的手术样本。所有119例患者均显示出提示HCM的组织学表现。此外,在42例不稳定的HCM患者中有28例观察到CD45RO+淋巴细胞(≥14/mm²),其相邻的严重肥厚且常排列紊乱的心肌细胞有局灶性坏死,这与重叠性活动性心肌炎相符,而77例稳定的HCM患者中均未观察到。在28例心肌炎患者中有14例检测到病毒基因组,无心肌炎的HCM患者及对照组均未检测到。未观察到肌节蛋白基因突变与HCM临床特征之间存在相关性。

结论

心肌炎,通常由病毒引起,是HCM患者急性临床恶化的常见原因。对其识别可能会影响疾病的预后和治疗。

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