Archana Kulasingam1, Anne-Mette Hvas2, Erik Lerkevang Grove3, Kristian Løkke Funck1, Steen Dalby Kristensen4. 1. Department of Cardiology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark. 2. Department of Clinical Biochemistry, Centre for Haemophilia and Thrombosis, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark; Department of Clinical Medicine, Faculty of Health, Aarhus University, Palle Juul-Jensens Boulevard 82, 8200 Aarhus N, Denmark. 3. Department of Cardiology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark; Department of Clinical Medicine, Faculty of Health, Aarhus University, Palle Juul-Jensens Boulevard 82, 8200 Aarhus N, Denmark. 4. Department of Cardiology, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, 8200 Aarhus N, Denmark; Department of Clinical Medicine, Faculty of Health, Aarhus University, Palle Juul-Jensens Boulevard 82, 8200 Aarhus N, Denmark. Electronic address: steendk@dadlnet.dk.
Abstract
BACKGROUND: ST-elevation myocardial infarction (STEMI) involves inflammation, activation of platelets, coagulation and changes in fibrinolysis as well as remodelling of myocardial tissue after STEMI. Recently, new proximity extension assays including panels of biomarkers for cardiovascular disease have been developed. This study investigates a wide range of cardiovascular protein biomarkers in the acute phase of STEMI compared with the stable phase three months after STEMI. We hypothesized that major changes in inflammation, haemostasis, tissue remodelling, and proteolysis are prevalent. MATERIALS AND METHODS: This was a prospective, observational study including 48 STEMI patients (mean age 60 ± 12 years, 79% men) treated with primary percutaneous coronary intervention (PPCI). Blood samples were obtained immediately prior to PPCI and again three months later. Levels of 92 biomarkers reflecting inflammation, immune response, cell adhesion, haemostasis, fibrinolysis, tissue remodelling, and proteolysis were assessed using a proximity extension assay (Olink® CARDIOVASCULAR III). RESULTS: When comparing the acute phase of STEMI with the stable phase three months later, a total of 29 biomarkers differed significantly after Bonferroni correction (p < 0.0005). In the acute phase of STEMI, we found an overall increase of biomarkers reflecting immune and inflammatory response, cell adhesion, and haemostasis. Biomarkers reflecting tissue remodelling and proteolysis were increased at three months follow-up compared with the acute phase. Out of the 29 biomarkers, six biomarkers did not confirm our predefined hypotheses. CONCLUSIONS: Using a novel proximity extension assay technique, we detected changes in several biomarkers when comparing the acute phase with three months follow-up in patients with STEMI. These biomarkers may play important roles in the pathogenesis of STEMI.
BACKGROUND: ST-elevation myocardial infarction (STEMI) involves inflammation, activation of platelets, coagulation and changes in fibrinolysis as well as remodelling of myocardial tissue after STEMI. Recently, new proximity extension assays including panels of biomarkers for cardiovascular disease have been developed. This study investigates a wide range of cardiovascular protein biomarkers in the acute phase of STEMI compared with the stable phase three months after STEMI. We hypothesized that major changes in inflammation, haemostasis, tissue remodelling, and proteolysis are prevalent. MATERIALS AND METHODS: This was a prospective, observational study including 48 STEMI patients (mean age 60 ± 12 years, 79% men) treated with primary percutaneous coronary intervention (PPCI). Blood samples were obtained immediately prior to PPCI and again three months later. Levels of 92 biomarkers reflecting inflammation, immune response, cell adhesion, haemostasis, fibrinolysis, tissue remodelling, and proteolysis were assessed using a proximity extension assay (Olink® CARDIOVASCULAR III). RESULTS: When comparing the acute phase of STEMI with the stable phase three months later, a total of 29 biomarkers differed significantly after Bonferroni correction (p < 0.0005). In the acute phase of STEMI, we found an overall increase of biomarkers reflecting immune and inflammatory response, cell adhesion, and haemostasis. Biomarkers reflecting tissue remodelling and proteolysis were increased at three months follow-up compared with the acute phase. Out of the 29 biomarkers, six biomarkers did not confirm our predefined hypotheses. CONCLUSIONS: Using a novel proximity extension assay technique, we detected changes in several biomarkers when comparing the acute phase with three months follow-up in patients with STEMI. These biomarkers may play important roles in the pathogenesis of STEMI.
Authors: Christina Christersson; Tomasz Baron; Frank Flachskampf; Lars Lindhagen; Bertil Lindahl; Agneta Siegbahn Journal: J Cardiovasc Transl Res Date: 2022-06-21 Impact factor: 4.132
Authors: Anna Dieden; Leone Malan; Catharina M C Mels; Leandi Lammertyn; Annemarie Wentzel; Peter M Nilsson; Petri Gudmundsson; Amra Jujic; Martin Magnusson Journal: Medicine (Baltimore) Date: 2021-05-21 Impact factor: 1.817