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題名 | Changes of Endothelin-1 and Atrial Natriuretic Peptide during Dobutamine Stress Echocardiography=在Dobutamine壓力心臟超音波檢查時內皮素-1和心房利鈉胜之變化 |
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作者 | 程文俊; 王兆弘; 洪明銳; Cherng, Wen-jin; Wang, Chao-hung; Hung, Ming-jui; |
期刊 | 臺灣醫學會雜誌 |
出版日期 | 19981200 |
卷期 | 97:12 1998.12[民87.12] |
頁次 | 頁812-818 |
分類號 | 415.3024 |
語文 | eng |
關鍵詞 | Dobutamine壓力; 心臟超音波檢查; 內皮素-1; 心房利鈉胜; Endothelin-1; Dobutamine; Echocardiography; Atrial natriuretic peptide; |
英文摘要 | The aim of this study was to test the hypothesis that plasma endothelin-1 (ET-1) and atrial natriuretic peptide (ANP) concentrations in patients with ischemic heart disease are related either to myocardial ischemia or left ventricular (LV) dysfunction during dobutamine stress echocardiography. plasma concentrations of ET-1 and ANP were measured in three patient groups. Group I (n=21) patients had normal stress echocardiography and a resting LV ejection fraction (LVEF) of 40% or more. Group II (n=32) had positive stress echocardiography and a resting LVEF of more than 40%. Group III (n=18) had positive stress echocardiography with a resting LVEF of less than 40%. All three groups were subjected to thallium 201 scintigraphy and coronary angiography studies. The resting LV end-diastolic pressure was significantly higher in groups II and III than in Group I. The LVEF decreased significantly in group III compared to groups I and II. In the resting state, groups II and III had higher ET-1 concentrations than Group I (p=0.021 and p=0.039, respectively). The plasma ANP concentration was higher in group III than in group I and II (p=0.005 and p=0.054, respectively). During peak doubutamine infusion, the ET-1 concentration dropped 8.7% from the baseline in group I, 10.2% in group II, and 10.5% in group III. The AVP concentrations were increased in all three groups but only the increse in Group II reached statical significance. In conclusion, in patients with suspected ischemic heart disease, the concentrations of ET-1 and ANP may predict significant anatomic and functional coronary artery disease. However, ET-1 does not play a pathophysiologic role during an ischemic attack. |
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