title: Factors involved in sudden coagulation observed in patients with acute myocardial infarction.
abstract: Coronary artery diseases (CAD) evolving into acute myocardial infarction (AMI) is associated with coagulation and thrombotic occlusion of coronary vessels in the presence of unstable atheroma. The atheromatous plaque becomes unstable when it is infiltrated by monocytes, macrophages and neutrophils capable of secreting proteases that induce plaque erosion, rupture and initialize the coagulation process. The aim of this study was (a) to analyse the plasma of patients with AMI for the presence of proteases that may activate rapid coagulation, (b) to evaluate coagulation markers as prothrombin fragment (F1+2) and antithrombin III and (c) to find an interrelation between proteases and coagulation markers. The examined plasma showed high values of prothrombin fragment (F1+2) and low levels of antithrombin III. These markers showed a highly significant negative-correlation. The plasma also exhibited increased levels of matrix metalloproteinase-9 (MMP-9) which were positively-correlated with the prothrombin fragment (F1+2). MMP-9 seems to cause the coagulation activity by increasing the level of prothrombin fragment (F1+2) and the consumption of antithrombin III. The examined plasma also exhibited high levels of neutrophil gelatinase-associated lipocalin (NGAL), which is known to modulate MMP-9 activity. The high plasma levels of MMP-9 and NGAL can be attributed to plaque instability and appear to activate sudden coagulation. MMP-9 and NGAL, in the presence of altered values of prothrombin fragment (F1+2) and antithrombin III in AMI patients, seem to be suitable markers to be studied in unstable plaque patients, for the prediction and prevention of acute coronary syndrome.
authors.affiliation: Department of Medical Biotechnology and Translational Medicine, Research Unit Iraklis Galatoulas, University of Milan, Italy. arnaldo.pinelli@unimi.it
authors.forename: Arnaldo
authors.initials: A
authors.lastname: Pinelli
authors.forename: Silvio
authors.initials: S
authors.lastname: Trivulzio
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Rossoni
authors.forename: Rosaria
authors.initials: R
authors.lastname: Redaelli
authors.forename: Sergio
authors.initials: S
authors.lastname: Brenna
mesh_terms: D000209:Acute-Phase Proteins; D000368:Aged; D000990:Antithrombin III / Q000378:metabolism; D001777:Blood Coagulation; D003324:Coronary Artery Disease / Q000097:blood / Q000378:metabolism / Q000473:pathology; D006801:Humans; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood; D008297:Male; D020780:Matrix Metalloproteinase 9 / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000378:metabolism / Q000473:pathology; D010446:Peptide Fragments / Q000097:blood; D010447:Peptide Hydrolases / Q000097:blood; D058226:Plaque, Atherosclerotic / Q000378:metabolism / Q000473:pathology; D011379:Prognosis; D011498:Protein Precursors / Q000097:blood; D011516:Prothrombin; D011518:Proto-Oncogene Proteins / Q000097:blood
chemical_list: D000209:Acute-Phase Proteins; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D010446:Peptide Fragments; D011498:Protein Precursors; D011518:Proto-Oncogene Proteins; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D000990:Antithrombin III; D011516:Prothrombin; D010447:Peptide Hydrolases; D020780:Matrix Metalloproteinase 9