title: Circulating level of gelatinase activity predicts ventricular remodeling in patients with acute myocardial infarction.
abstract: BACKGROUND
  Matrix metalloproteinase (MMP) plays an important role in the development of ventricular remodeling in an animal model of acute myocardial infarction (AMI). We examined whether circulating MMP activity can predict left ventricular (LV) remodeling after AMI in humans.
  
  
  METHODS
  We measured the circulating level of MMP-2 and MMP-9 activities (gelatinase activity) at 14 days after the onset of AMI by gelatin zymography in 52 consecutive patients (age 62+/-2). All patients underwent direct PTCA and stenting at an acute stage, and were treated subsequently with losartan or enalapril. Biplane left ventriculography was performed at admission, and 2 weeks and 6 months after the onset of AMI.
  
  
  RESULTS
  We expressed gelatinolysis activity as the ratio to MMP-2 standard. Mean gelatinase activity was 0.721+/-0.013. We divided patients into two groups, groups with gelatinolysis activity <0.72 (low group, n=27) and >0.72 (high group, n=25). Either change in LV end-diastolic volume index (LVEDVI, ml/m(2)) or end-systolic volume index (LVESVI, ml/m(2)) from admission to 2 weeks was not different between the two groups. Changes in both LVEDVI and LVESVI from 2 weeks to 6 months were greater in high gelatinolysis activity group than those in low activity group. Moreover, circulating level of gelatinolysis activity was positively correlated with changes in LVEDVI and LVESVI from 2 weeks to 6 months.
  
  
  CONCLUSIONS
  These results demonstrate that circulating level of gelatinase activity can predict LV remodeling after AMI. Inhibition of gelatinase activity at the acute phase may be a therapeutic strategy for the prevention of remodeling after AMI.
authors.affiliation: Second Department of Internal Medicine, Hirosaki University School of Medicine, 5 Zaifu, Hirosaki, Aomori, Japan.
authors.forename: Toshiro
authors.initials: T
authors.lastname: Matsunaga
authors.forename: Naoki
authors.initials: N
authors.lastname: Abe
authors.forename: Kunihiko
authors.initials: K
authors.lastname: Kameda
authors.forename: Jhoji
authors.initials: J
authors.lastname: Hagii
authors.forename: Norio
authors.initials: N
authors.lastname: Fujita
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Onodera
authors.forename: Takaatsu
authors.initials: T
authors.lastname: Kamata
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Ishizaka
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Hanada
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Osanai
authors.forename: Ken
authors.initials: K
authors.lastname: Okumura
mesh_terms: D015415:Biomarkers / Q000097:blood; D006328:Cardiac Catheterization; D017023:Coronary Angiography; D005260:Female; D005500:Follow-Up Studies; D015637:Gated Blood-Pool Imaging; D006801:Humans; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000096:biosynthesis / Q000097:blood*; D020780:Matrix Metalloproteinase 9 / Q000096:biosynthesis / Q000097:blood*; D008875:Middle Aged; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000175:diagnosis / Q000201:enzymology* / Q000503:physiopathology; D011379:Prognosis; D012720:Severity of Illness Index; D016277:Ventricular Function, Left / Q000502:physiology; D020257:Ventricular Remodeling / Q000502:physiology*
chemical_list: D015415:Biomarkers; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9