New myocardial infarction was defined as the occurrence of a new episode of ischaemic chest pain, characteristic electrocardiographic (ECG) alterations (new ST-segment depression or elevation The outcome measurements were specified previously as the in-hospital and 180-day rates of the composite of death due to either any cause or new non-fatal myocardial infarction, and the corresponding rates of death and new non-fatal myocardial infarction individually. All case report forms were reviewed automatically and manually to ensure the consistency and quality of the data. All major events were adjudicated by a clinical event committee that did not know the results of the serum biomarker determinations or the identities of patients and centres. The Ethics Committee of each centre approved the study protocol and patients provided written informed consent. All patients were followed up from hospital admission until day 180 or death, whichever occurred first. Simultaneous levels of CK-MB (activity or mass) were measured at each centre and used for the prognostic analysis. The investigators were blinded to the test results until the study was completed. Samples were stored at −70 ☌ until they were analysed at a core laboratory (see Appendix A). \(>\) 20 min with ST-segment elevation, who had undergone coronary angioplasty during the previous six months, and patients with active cancer or autoimmune inflammatory disease.Īfter informed consent had been obtained, serum samples for a single measurement of troponin T (TnT), high-sensitivity C-reactive protein (hsCRP), myoglobin, and NT-proBNP were drawn. We excluded patients who were candidates for reperfusion therapy on admission because of ischaemic chest pain The enrolment period was from December 1999 to July 2001. We included 1483 consecutive patients admitted to coronary care units with resting chest pain within 24 h of admission. This is a prospective, multicentre (see Appendix A), cohort study. Thus, we analysed the additive value of NT-proBNP concentration in relation to the Thrombolysis in Myocardial Infarction (TIMI) risk score and the American Cardiology College/American Heart Association (ACC/AHA) classification, and studied the predictive capacity of NT-proBNP in relation to troponin T (TnT), high-sensitivity C-reactive protein (hsCRP), myoglobin, and creatine kinase-MB (CK-MB) concentrations in a large cohort of patients with NSTE-ACS. More importantly, the predictive value of BNP has not been studied over a prognostication scheme. Most of the information available comes from subsidiary analysis of randomised controlled trials. However, further assessment of the utility of NT-proBNP is required. Also, BNP was associated with the occurrence of subsequent heart failure 1,2,3 and added information to concentrations of troponin T and I, and other biomarkers. 1–6 In patients with unstable angina and non-ST-elevation myocardial infarction, high levels of these markers were accompanied by a two- to threefold greater risk of death at 10 months. N-terminal probrain natriuretic peptide, Acute coronary syndromes, Cardiac markers, Prognosis, Risk stratification Introductionīrain natriuretic peptide (BNP) and N-terminal probrain natriuretic peptide (NT-proBNP) have recently shown promise for risk stratification in patients with non-ST-elevation acute coronary syndromes (NSTE-ACS).
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |