[雙語(yǔ)翻譯]醫(yī)學(xué)外文翻譯--急性肺動(dòng)脈栓塞心肌肌鈣蛋白i釋放與癥狀的持續(xù)時(shí)間的相關(guān)性研究（原文）

1、Cardiac troponin I release in acute pulmonary embolism in relation to the duration of symptomsGopikrishna Punukollua, Ijaz A. Khanb,*, Ramesh M. Gowdaa, Gaurav Lakhanpala, Balendu C. Vasavadaa, Terrence J. SacchiaaDivisi

2、on of Cardiology, Long Island College Hospital, Brooklyn, NY, USA bDivision of Cardiology, University of Maryland School of Medicine, 22 South Greene Street-S3B06, Baltimore, MD 21201, USAReceived 24 June 2003; received

3、in revised form 5 January 2004; accepted 8 January 2004 Available online 2 April 2004AbstractPurpose: To evaluate the release of cardiac troponin I in normotensive patients with acute pulmonary embolism in relation to th

4、e duration of symptoms. Methods: Fifty-seven normotensive patients with acute pulmonary embolism were included in the study. Patients were divided into two groups based on the duration of symptoms at presentation: sympto

5、ms of V 72 h, group A; symptoms of > 72 h, group B. Serum cardiac troponin I levels were measured at presentation. Results: Mean age was 63 F 18 years and 23 (40%) patients were males. Thirty-three (58%) patients had

6、symptoms of V 72 h (group A) and 24 (42%) had symptoms of >72 h (group B). Both groups had similar prevalence of right ventricular dysfunction on echocardiography (55% [n = 18] in group A vs. 42% [n = 10] in group B,

7、p = NS). Sixteen patients had elevated serum cardiac troponin I (mean F S.D. 3.3 F 2.3 ng/ml, range 0.6–8.3 ng/ml). Elevated serum cardiac troponin I was strongly associated with right ventricular dysfunction ( p = 0.015

8、). All patients with elevated serum cardiac troponin I (n = 16) were in group A ( p 72 h (group B) (Table 2). There was no difference in the severity of pulmonary embolism between the two groups and both groups had simil

9、ar prevalence of right ventricular dysfunction (55% [n = 18] in group A vs. 42% [n = 10]). The prevalence of cardiovascular factors was similar in both groups. Sixteen patients had elevated serum cardiac troponin I (mean

10、 F S.D. 3.3 F 2.3 ng/ml, range 0.6– 8.3 ng/ml). Elevated cardiac troponin I was strongly asso- ciated with right ventricular dysfunction ( p = 0.015). All patients with elevated serum cardiac troponin I levels (n = 16) w

11、ere in group A; none of the patients in group B had elevated serum cardiac troponin I levels ( p < 0.0001). Among group A, 12 of 18 (67%) patients with ( p = 0.0005) and 4 of 15 (27%) patients without ( p = NS) right

12、ventric- ular dysfunction had elevated serum cardiac troponin I. Thirteen of 16 (81%) patients with elevated serum cardiac troponin I had duration of symptoms V 24 h at presentation. (Table 3). In patients presenting wit

13、hin 8 h after symptom onset (n = 7), the peak serum troponin I levels were found at clinical presentation in 50% (n = 4) of the patients.4. Discussion4.1. BackgroundCardiac troponin elevation in acute pulmonary embolism

14、is associated with both massive and submassive pulmonary embolism. Pacouret et al. [15] initially reported that cardiac troponin I levels were elevated in submassive pulmonary embolism. Subsequent studies confirmed that

15、serum cardiac troponin I and T levels could be elevated in both massive and submassive pulmonary embolism with a strong corre- lation with right ventricular dysfunction [5,6,11,12,16–18]. The elevated cardiac troponins h

16、ave independent prognostic value for in-hospital death, hypotension and cardiogenic shock in patients with pulmonary embolism [5,11]. Similar relation was reported by Konstantinides et al. [12] where elevated cardiac tro

17、ponin I levels were associated with increased overall mortality and complicated in-hospital course. The risk of complicated in-hospital course wasreported to be five times higher in the high cardiac tropo- nin-I group co

18、mpared with patients with moderate cTnI elevation.4.2. Cardiac troponin I for risk stratification in pulmonary embolismEven though elevated levels of cardiac troponin I and T have prognostic significance in acute pulmona

19、ry embolism, the clinical utility of elevated cardiac troponin levels in the risk stratification of hemodynamically stable patients is unknown and it is appealing to speculate that troponins could function as a discrimin

20、ator for thrombolytic therapy in pulmonary embolism patients who are hemodynamically stable but have right ventricular dysfunction. Large multi- center studies are needed to prove that elevated levels of cardiac troponin

21、s may be useful in therapeutic triage of normotensive patients with right ventricular dysfunction in acute pulmonary embolism, whereas equally important would be to evaluate the release of troponins in acute pulmonary em

22、bolism especially in relation to duration of symptoms as the window period for thrombolytic therapy in acute pulmonary embolism can extend up to 14 days [19–21].4.3. Release kinetics of cardiac troponin IThe majority of

23、cardiac troponins are bound to myofila- ments, and the remainder is free in the cytosol. In acute myocardial infarction sufficient myocardial necrosis occurs to sustain an abnormally elevated levels of troponins, which b

24、egin to rise in 4–6 h and peak at about 24 h after the onset of symptoms to reach levels of about 20–50 times the upper reference limit. The concentration of these subunits remain elevated in blood for many days, about 4

25、–7 days for cardiac troponin I and 10–14 days for cardiac troponin T, due to protracted release from stores bound to deteriorating myo- filaments [22,23]. It is estimated that 3–4% of cardiac troponin I and 6–8% of cardi

26、ac troponin T is found as free cytoplasmic components [24,25]. In microinfarctions and initial stages of myocardial injury, it has been thought that release of the cytoplasmic troponin occurs with the detect- able levels

27、 of cardiac troponins in peripheral blood [22]. In addition, other forms of cardiac troponin I and T have been shown to be released into the blood after myocardial infarction [26]. So the release and clearance mechanisms

28、 of cardiac troponin I and T are still incompletely understood. There are no studies where cardiac troponins have been evaluated in relation to the onset of symptoms in acute pulmonary embolism, although studies have eva

29、luated these markers in relation to the time of presentation [11,12]. Konstantinides et al. [12] included 126 patients with 51% of them presenting with symptoms of less than 24 h, but data on proportion of patients with

30、elevated troponin levels in relation to the duration of symptoms was not evaluated. The peak troponin levels were observed within the first 4Table 3 Elevated cardiac markers based on the duration of symptomsElevated card

31、iac marker Duration of symptoms V 24 h (n = 21)Duration of symptoms 24–48 h (n = 6)Duration of symptoms 48–72 h (n = 6)Cardiac troponin I 13 (62%) 2 (33%) 1 (17%) Creatine kinase 2 (10%) None None Creatine kinase-MB 6 (2