title: Pentraxin 3, ficolin-2 and lectin pathway associated serine protease MASP-3 as early predictors of myocardial infarction - the HUNT2 study.
abstract: The lectin complement pathway is suggested to play a role in atherogenesis. Pentraxin-3 (PTX3), ficolin-1, ficolin-2, ficolin-3, MBL/ficolin/collectin-associated serine protease-3 (MASP-3) and MBL/ficolin/collectin-associated protein-1 (MAP-1) are molecules related to activation of the lectin complement pathway. We hypothesized that serum levels of these molecules may be associated with the incidence of myocardial infarction (MI). In a Norwegian population-based cohort (HUNT2) where young to middle-aged relatively healthy Caucasians were followed up for a first-time MI from 1995-1997 through 2008, the 370 youngest MI patients were matched by age (range 29-62 years) and gender to 370 controls. After adjustments for traditional risk factors, the two highest tertiles of PTX3 and the highest tertiles of ficolin-2 and MASP-3 were associated with MI, with odds ratios (95% confidence interval) of 1.65 (1.10-2.47) and 2.79 (1.83-4.24) for PTX3, 1.55 (1.04-2.30) for ficolin-2, and 0.63 (0.043-0.94) for MASP-3. Ficolin-1, ficolin-3 and MAP-1 were not associated with MI. In a multimarker analysis of all associated biomarkers, only PTX3 and MASP-3 remained significant. PTX-3 and MASP-3 enhanced prediction of MI compared to the traditional Framingham risk score alone (AUC increased from 0.64 to 0.68, p = 0.006). These results support the role of complement-dependent inflammation in the pathophysiology of cardiovascular disease.
authors.affiliation: Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Inga Thorsen
authors.initials: IT
authors.lastname: Vengen
authors.affiliation: Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.
authors.forename: Tone Bull
authors.initials: TB
authors.lastname: Enger
authors.affiliation: Department of Laboratory Medicine, Children's and Women's Health, Norwegian University of Science and Technology, Trondheim, Norway.|Department of Immunology and Transfusion Medicine, St Olavs University Hospital, Trondheim, Norway.
authors.forename: Vibeke
authors.initials: V
authors.lastname: Videm
authors.affiliation: Laboratory of Molecular Medicine, Department of Clinical Immunology, Sect. 7631, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Trondheim, Norway.
authors.forename: Peter
authors.initials: P
authors.lastname: Garred
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D016022:Case-Control Studies; D015331:Cohort Studies; D037582:Complement Pathway, Mannose-Binding Lectin; D005260:Female; D006801:Humans; D007249:Inflammation; D037102:Lectins / Q000097:blood; D008297:Male; D050606:Mannose-Binding Protein-Associated Serine Proteases / Q000032:analysis*; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000175:diagnosis* / Q000378:metabolism; D011379:Prognosis; D000683:Serum Amyloid P-Component / Q000032:analysis*; D000097604:Ficolins; D000099153:Pentraxins
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D037102:Lectins; D050606:Mannose-Binding Protein-Associated Serine Proteases; D000683:Serum Amyloid P-Component; D000097604:Ficolins; D000099153:Pentraxins; C084067:MASP1 protein, human