Richard G Jung1,2,3, Trevor Simard1,2,3,4, Pietro Di Santo1,2,4,5, Alisha Labinaz1,2, Robert Moreland1,6, Anne-Claire Duchez7, Kamran Majeed1,2,4,8, Pouya Motazedian1,9, Rebecca Rochman1,2, Young Jung10, Benjamin Hibbert1,2,3,4. 1. 1 CAPITAL Research Group, University of Ottawa Heart Institute, Ottawa, ON, Canada. 2. 2 Vascular Biology and Experimental Medicine Laboratory, University of Ottawa Heart Institute, Ottawa, ON, Canada. 3. 3 Department of Cellular and Molecular Medicine, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. 4. 4 Division of Cardiology, University of Ottawa Heart Institute, Ottawa, ON, Canada. 5. 5 School of Epidemiology and Public Health, University of Ottawa, Ottawa, ON, Canada. 6. 6 Department of Radiology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. 7. 7 Department of Biochemistry, Microbiology and Immunology, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada. 8. 8 University of Western Australia, Perth, WA, Australia. 9. 9 Department of Medicine, Cumming School of Medicine, Calgary, AB, Canada. 10. 10 Department of Health Research Methods, Evidence, and Impact, McMaster University, Hamilton, ON, Canada.
Abstract
INTRODUCTION AND OBJECTIVE: Target lesion failure continues to limit the efficacy of percutaneous coronary intervention despite advancements in stent design and medical therapy. Identification of biomarkers to risk stratify patients after percutaneous coronary intervention has the potential to focus therapies on cohorts with increased benefits. Plasminogen activator inhibitor-1 has been identified as a candidate biomarker. Herein, we evaluate biological variables which impact plasminogen activator inhibitor-1 levels and analytical characteristics which impact its utility as a biomarker in humans. METHODS: Plasma plasminogen activator inhibitor-1 was measured in 689 patients undergoing coronary angiography. Plasminogen activator inhibitor-1 levels were measured. Clinical and procedural characteristics were collected in a prospective registry. RESULTS: Plasma plasminogen activator inhibitor-1 analytical (CVa = 4.1%), intra-individual (CVi = 44.0%) and inter-individual (CVg = 118.6%) variations with reference change value of 122.3% were calculated. Plasminogen activator inhibitor-1 levels were elevated in patients with cardiovascular risk factors, including type 2 diabetes, pre-diabetes, smokers, obesity, hypertension, and daytime variation in procedure and blood draw. CONCLUSION: Variation in plasma plasminogen activator inhibitor-1 levels is influenced by multiple biological and procedural characteristics. The performance of plasma plasminogen activator inhibitor-1 is consistent with biomarkers in clinical use (N-terminal pro-B-type natriuretic peptide and C-reactive protein) and its applicability is promising.
INTRODUCTION AND OBJECTIVE: Target lesion failure continues to limit the efficacy of percutaneous coronary intervention despite advancements in stent design and medical therapy. Identification of biomarkers to risk stratify patients after percutaneous coronary intervention has the potential to focus therapies on cohorts with increased benefits. Plasminogen activator inhibitor-1 has been identified as a candidate biomarker. Herein, we evaluate biological variables which impact plasminogen activator inhibitor-1 levels and analytical characteristics which impact its utility as a biomarker in humans. METHODS: Plasma plasminogen activator inhibitor-1 was measured in 689 patients undergoing coronary angiography. Plasminogen activator inhibitor-1 levels were measured. Clinical and procedural characteristics were collected in a prospective registry. RESULTS: Plasma plasminogen activator inhibitor-1 analytical (CVa = 4.1%), intra-individual (CVi = 44.0%) and inter-individual (CVg = 118.6%) variations with reference change value of 122.3% were calculated. Plasminogen activator inhibitor-1 levels were elevated in patients with cardiovascular risk factors, including type 2 diabetes, pre-diabetes, smokers, obesity, hypertension, and daytime variation in procedure and blood draw. CONCLUSION: Variation in plasma plasminogen activator inhibitor-1 levels is influenced by multiple biological and procedural characteristics. The performance of plasma plasminogen activator inhibitor-1 is consistent with biomarkers in clinical use (N-terminal pro-B-type natriuretic peptide and C-reactive protein) and its applicability is promising.
Authors: Adil Rasheed; Sarah A Shawky; Ricky Tsai; Richard G Jung; Trevor Simard; Michael F Saikali; Benjamin Hibbert; Katey J Rayner; Carolyn L Cummins Journal: Stem Cells Transl Med Date: 2020-11-24 Impact factor: 6.940
Authors: Trevor Simard; Richard G Jung; Pietro Di Santo; David T Harnett; Omar Abdel-Razek; F Daniel Ramirez; Pouya Motazedian; Simon Parlow; Alisha Labinaz; Robert Moreland; Jeffrey Marbach; Anthony Poulin; Amos Levi; Kamran Majeed; Paul Boland; Etienne Couture; Kiran Sarathy; Steven Promislow; Juan J Russo; Aun Yeong Chong; Derek So; Michael Froeschl; Alexander Dick; Marino Labinaz; Michel Le May; David R Holmes; Benjamin Hibbert Journal: Mayo Clin Proc Innov Qual Outcomes Date: 2021-12-04
Authors: Trevor Simard; Richard Jung; Alisha Labinaz; Mohammad Ali Faraz; F Daniel Ramirez; Pietro Di Santo; Dylan Perry-Nguyen; Ian Pitcher; Pouya Motazedian; Chantal Gaudet; Rebecca Rochman; Jeffrey Marbach; Paul Boland; Kiran Sarathy; Saleh Alghofaili; Juan J Russo; Etienne Couture; Steven Promislow; Rob S Beanlands; Benjamin Hibbert Journal: J Am Heart Assoc Date: 2019-08-05 Impact factor: 5.501