Hemodynamic and prognostic value of thallium-201 myocardial imaging in patients with dilated cardiomyopathy.

Hemodynamic and prognostic value of thallium-201 myocardial imaging in patients with dilated cardiomyopathy.
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201铊心肌显像对扩张型心肌病患者的血流动力学和预后价值。

DOI:
10.1016/0167-5273(89)90307-0
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发表时间:
1989
影响因子:
3.5
通讯作者:
Y. Nimura
Y. Nimura
中科院分区:
医学2区
文献类型:
--
作者:
J. Tamai;S. Nagata;T. Nishimura;C. Yutani;K. Miyatake;H. Sakakibara;Y. Nimura

文献摘要

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我们研究了70例扩张型心肌病患者,以确定铊显像的灌注缺损程度是否与患者的血流动力学和预后有关。根据灌注缺损的程度将患者分为三组,即,I级:无灌注缺损(n= 19),II级:心尖灌注缺损(n= 22),III级:广泛灌注缺损(n= 29)。与I级和II级患者相比,III级患者表现出明显的血流动力学恶化。三年生存率随灌注缺损程度的增加而降低(P< 0.05)。进展性心力衰竭死亡倾向于广泛灌注缺损患者(P< 0.05)。在III级患者中,灌注缺损主要延伸至后外侧段。虽然尸检研究显示这些患者左心室壁纤维化增加,但纤维化的扩展与纤维化无关。此外,在随访检查中,18例患者中有3例灌注缺损消退。提示铊显像的灌注缺损程度对扩张型心肌病的无创性评价和预后判断有一定的价值。然而,灌注缺损的分布与心肌纤维化无关。
We studied 70 patients with dilated cardiomyopathy to determine whether extent of perfusion defect on thallium imaging could be related to the hemodynamics and prognosis of the patients. Patients were divided into three groups according to the extent of perfusion defect, i.e., Grade I: no perfusion defect (n= 19), Grade II: apical perfusion defect (n= 22), and Grade III: extensive perfusion defect (n= 29). The patients of Grade III demonstrated marked hemodynamic deterioration compared with those of Grade I and II. Three-year survival rate showed lower value in proportion to the extent of perfusion defect (P< 0.05). Death from progressive heart failure tended to occur in patients with extensive perfusion defect (P< 0.05). In patients of Grade III, the perfusion defect extended mainly to the posterolateral segment. Although autopsy studies showed increased fibrosis in the left ventricular wall in these patients, the extension of the fibrosis was not related to that of fibrosis. Moreover, the perfusion defect had regressed in three of 18 patients in the follow-up examination. These results indicate that the extent of perfusion defect on thallium imaging may be of value in non-invasive evaluation and prediction of the prognosis in patients with dilated cardiomyopathy. Distribution of the perfusion defect was, however, not related to that of myocardial fibrosis.