生物谷：七月出版的《心臟》雜志上有一篇報道說，髓過氧化物酶（MPO）水平有助于評定急性ST段抬高的心肌梗塞患者的預(yù)后。
英國萊斯特大學(xué)的Sohail Q． Khan博士說,，MPO可以用于找出有生命危險或者再次心梗的高危患者,。通過識別出這些患者,，他們希望能夠修正他們的治療，避免這些災(zāi)難性的不良后果,。Khan博士及其同事對384名急性ST段抬高的心肌梗塞患者進(jìn)行研究，看MPO能否增加急性心肌梗塞患者的預(yù)后評定,，比較MPO的使用與N端前B型尿鈉排泄肽（NT-BNP）的預(yù)后意義,。結(jié)果發(fā)現(xiàn)，急性ST段抬高的心肌梗塞患者血漿MPO水平高于對照,。與沒有再次發(fā)生心梗的存活者相比，那些死亡或者再次心梗的患者M(jìn)PO水平尤其高,。研究的初步結(jié)果表明,，中位MPO對數(shù)值和中位NT-BNP對數(shù)值是死亡或者心梗復(fù)發(fā)的獨(dú)立預(yù)后因素。MPO水平不能獨(dú)立預(yù)測死亡,，非致死性心梗，或者心衰,，而NT-BNP是死亡的獨(dú)立預(yù)后指標(biāo),。
Khan博士說,，MPO可用于對高危患者做進(jìn)一步的危險度評定,，危險度分級比目前使用的臨床和生化危險預(yù)測指標(biāo)如年齡,、腎功能,、肌鈣蛋白和NT－BNP要好,，也優(yōu)于超聲心動評價的射血分?jǐn)?shù)。聯(lián)合使用MPO和NT-BNP可以找出特別高危的患者,。
Khan博士說,，他們正在進(jìn)行一些研究,，找新的標(biāo)志，并試圖找出急性心梗后新的神經(jīng)體液途徑。他們正在招募非ST段抬高的心?；颊?，看我們的早期結(jié)果是否適合這些患者。（中國公眾科技網(wǎng)）
原始出處:
Published Online First: 28 December 2006. doi:10.1136/hrt.2006.091041
Heart 2007;93:826-831
ACUTE CORONARY SYNDROMES
Myeloperoxidase aids prognostication together with N-terminal pro-B-type natriuretic peptide in high-risk patients with acute ST elevation myocardial infarction
Sohail Q Khan, Dominic Kelly, Paulene Quinn, Joan E Davies and Leong L Ng
Department of Cardiovascular Sciences, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, Leicester, UK
Correspondence to:
Dr S Q Khan
Department of Cardiovascular Medicine, University of Leicester, Clinical Sciences Building, Leicester Royal Infirmary, Leicester LE2 7LX, UK; [email protected]
ABSTRACT
Background: Inflammation plays a critical role in acute myocardial infarction (MI). One such inflammatory marker is myeloperoxidase (MPO). Its role as a predictor of death or MI in patients with ST segment elevation myocardial infarction (STEMI) is unclear.
Aim: To investigate the role of MPO as a predictor of death or MI in patients with STEMI and to compare it with N-terminal pro-B-type natriuretic peptide (NT-BNP).
Method: 384 post STEMI patients were studied. Patients were followed up for the combined end point of death or readmission with non-fatal MI.
Results: There were 40 deaths and 37 readmissions with MI. Median MPO was raised in patients experiencing death or MI than in survivors (median (range), 50.6 (15.3–124.1) ng/ml vs 33.5 (6.6–400.2) ng/ml, p = 0.001). Using a Cox proportional hazards model, log median MPO (HR 6.91, 95% CI 1.79 to 26.73, p = 0.005) and log median NT-BNP (HR 4.21, 95% CI 1.53 to 11.58, p = 0.005) independently predicted death or non-fatal MI. MPO had predictive power in both below and above median NT-BNP levels (log rank 5.60, p = 0.020 and log rank 5.12, p = 0.024, respectively). The receiver-operating curve for median NT-BNP yielded an area under the curve (AUC) of 0.72 (95% CI 0.65 to 0.79, p<0.001); for median MPO, the AUC was 0.62 (95% CI 0.55 to 0.69, p = 0.001). The logistic model combining the two markers yielded an AUC of 0.76 (95% CI 0.69 to 0.82, p<0.001).
Conclusion: MPO and NT-BNP may be useful tools for risk stratification of all acute coronary syndromes, including patients with STEMI at higher risk.
