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Title: | Noninvasive diagnosis of ruptured peripheral atherosclerotic lesions and myocardial infarction by antibody profiling | Authors: | Cleutjens, KBJM Faber, BCG Rousch, M van Doorn, R Hackeng, TM Vink, C GEUSENS, Piet ten Cate, H Waltenberger, J Tchaikovski, V Lobbes, M SOMERS, Veerle Sijbers, A Black, D Kitslaar, PJEHM Daemen, MJAP |
Issue Date: | 2008 | Publisher: | AMER SOC CLINICAL INVESTIGATION INC | Source: | JOURNAL OF CLINICAL INVESTIGATION, 118(8). p. 2979-2985 | Abstract: | Novel biomarkers, such as circulating (auto)antibody signatures, may improve early detection and treatment of ruptured atherosclerotic lesions and accompanying cardiovascular events, such as myocardial infarction. Using a phage-display library derived from cDNAs preferentially expressed in ruptured peripheral human atherosclerotic plaques, we performed serological antigen selection to isolate displayed cDNA products specifically interacting with antibodies in sera from patients with proven ruptured peripheral atherosclerotic lesions. Two cDNA products were subsequently evaluated on a validation series of patients with peripheral atherosclerotic lesions, healthy controls, and patients with coronary artery disease at different stages. Our biomarker set was able to discriminate between patients with peripheral ruptured lesions and patients with peripheral stable plaques with 100% specificity and 76% sensitivity. Furthermore, 93% of patients with an acute myocardial infarction (AMI) tested positive for our biomarkers, whereas all patients with stable angina pectoris tested negative. Moreover, 90% of AMI patients who initially tested negative for troponin T, for which a positive result is known to indicate myocardial infarction, tested positive for our biomarkers upon hospital admission. In conclusion, antibody profiling constitutes a promising approach for noninvasive diagnosis of atherosclerotic lesions, because a positive serum response against a set of 2 cDNA products showed a strong association with the presence of ruptured peripheral atherosclerotic lesions and myocardial infarction. | Notes: | Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Pathol, NL-6200 MD Maastricht, Netherlands. Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Biochem, NL-6200 MD Maastricht, Netherlands. Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Med Microbiol, NL-6200 MD Maastricht, Netherlands. Univ Maastricht, Subdiv Rheumatol, Dept Internal Med, NL-6200 MD Maastricht, Netherlands. Hasselt Univ, Biomed Res Inst, Diepenbeek, Belgium. Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Internal Med, NL-6200 MD Maastricht, Netherlands. Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Cardiol, NL-6200 MD Maastricht, Netherlands. NV Organon, Dept Mol Design & Informat, NL-5340 BH Oss, Netherlands. Univ Maastricht, Cardiovasc Res Inst Maastricht, Dept Gen Surg, NL-6200 MD Maastricht, Netherlands. | Document URI: | http://hdl.handle.net/1942/8449 | ISSN: | 0021-9738 | e-ISSN: | 1558-8238 | DOI: | 10.1172/JCI32767 | ISI #: | 000258146800034 | Category: | A1 | Type: | Journal Contribution | Validations: | ecoom 2009 |
Appears in Collections: | Research publications |
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