title: Role of PMN elastase on ischemic myocardial injury in evolving myocardial infarction: correlation with clinical parameters and intervention by protease inhibitor ulinastatin.
abstract: The purposes of this study were to investigate the sequential changes of PMN elastase during evolving myocardial infarction, and also to ascertain whether or not ulinastatin (UL), a clinically useful protease inhibitor, would affect the extent of ischemic myocardial injury. The levels of plasma PMN elastase (as alpha 1-proteinase inhibitor-elastase complex) were measured once in 13 normal controls, and at intervals in 30 acute myocardial infarction (AMI) patients given UL and 30 AMI controls on conventional therapy, and compared between the groups. The levels in control group on conventional therapy were significantly higher from 6 to 72 hours after the onset than those in normal controls. Maximum PMN elastase levels in non-survivors (n = 7) were significantly higher than in survivors (n = 23) at the 6-month follow-up (288.7 +/- 75.8 vs. 188.1 +/- 56.9 micrograms/l, p less than 0.01). The maximum level of PMN elastase in patients given UL was significantly lower than that in the control group (162.2 +/- 96.2 vs 207.3 +/- 70.1 micrograms/l, p less than 0.05), and the peak CK-MB in patients given UL was significantly lower than that in controls (252.3 +/- 150.9 vs 360.1 +/- 239.6 IU/l, p less than 0.05). Early mortality (seen at 6-month follow-up) in patients administered UL was significantly lower than that of the treated controls (3.3% vs 23.3%, p less than 0.05). Analysis of changes in PMN elastase levels suggested that UL would be clinically beneficial for reduction of ischemic myocardial injury.
authors.affiliation: Department of Medicine, Nippon Medical School, Tokyo, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Shimai
authors.forename: T
authors.initials: T
authors.lastname: Takano
authors.forename: Y
authors.initials: Y
authors.lastname: Seino
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
authors.forename: H
authors.initials: H
authors.lastname: Hayakawa
mesh_terms: D000368:Aged; D003327:Coronary Disease / Q000201:enzymology / Q000209:etiology / Q000517:prevention & control*; D003402:Creatine Kinase / Q000097:blood; D005260:Female; D005500:Follow-Up Studies; D006023:Glycoproteins / Q000627:therapeutic use*; D006801:Humans; D007527:Isoenzymes; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000188:drug therapy / Q000201:enzymology*; D009504:Neutrophils / Q000201:enzymology*; D010196:Pancreatic Elastase / Q000037:antagonists & inhibitors / Q000097:blood / Q000502:physiology*; D011379:Prognosis; D011480:Protease Inhibitors / Q000627:therapeutic use*
chemical_list: D006023:Glycoproteins; D007527:Isoenzymes; D011480:Protease Inhibitors; D003402:Creatine Kinase; D010196:Pancreatic Elastase; C028665:urinastatin