Pulmonary embolism causes endomyocarditis in the human heart
Pulmonary embolism causes endomyocarditis in the human heart
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DOI：
10.1136/hrt.2007.118638
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发表时间：
2008-04-01
期刊：
影响因子：
5.7
通讯作者：
Niessen, H. W. M.
中科院分区：
文献类型：
--
作者：
Begieneman, M. P. V.;de Goot, F. R. W. van;Niessen, H. W. M.
背景：肺栓塞（PE）是发病率和死亡率的重要原因。在最近的一项研究中，在PE患者中，巨噬细胞的水平增加被发现在右ventriculard.Objective：为了评估存在的炎性细胞，肌细胞溶解和腔内血栓在左，右ventriculard.Patients死亡，因为PE作为一个假定的新的来源的heartfailure.Methods：22例PE患者进行了研究。为了比较，使用了8名对照和11名死于慢性肺动脉高压（PHT）的患者。用抗体对左心室和右心室的载玻片进行染色，鉴定嗜中性粒细胞、淋巴细胞和巨噬细胞，随后对其进行定量。使用补体染色观察肌细胞溶解。血栓被确定为常规staining.Results：与对照组相比，在PE患者的血管外定位的所有三个炎性细胞的显着增加被发现在右心室和左心室，符合myocytolysis，指示心肌炎。PHT患者中未发现炎性细胞增加。结论：PE患者存在左、右心室内膜心肌炎和腔内血栓，这些异常可能是PE患者心肌酶释放和心脏功能异常的一个新的解释，并可能与PE的发病率和死亡率有关。
Background: Pulmonary embolism (PE) is a significant cause of morbidity and mortality. In a recent study in patients with PE, an increased level of macrophages was found in the right ventricle.Objective: To evaluate the presence of inflammatory cells, myocytolysis and intracavitary thrombi in the left and right ventricle of patients who died because of PE as a putative new source of heart failure.Patients and methods: 22 patients with PE were studied. For comparison, eight controls and 11 patients who died of chronic pulmonary hypertension (PHT) were used. Slides of the left and right ventricle were stained with antibodies, identifying neutrophilic granulocytes, lymphocytes and macrophages, which were subsequently quantified. Myocytolysis was visualised using complement staining. Thrombi were identified by conventional staining.Results: Compared with controls, in patients with PE a significant increase in extravascular localisation of all three inflammatory cells was found both in the right and left ventricle, coinciding with myocytolysis, indicative for myocarditis. No increase in inflammatory cells was found in patients with PHT. Endocardial cellular infiltration was also found, partly coinciding with the presence of ventricular thrombi.Conclusions: In patients with PE, endomyocarditis and intracavitary thrombi in the left and right ventricle were found. These abnormalities may be an additional new explanation for the observed cardiac enzyme release and functional abnormalities of the heart in these patients and may contribute to the morbidity and mortality of the disease.