title: Relation of plasma lipoprotein(a) to infarct artery patency in survivors of myocardial infarction.
abstract: BACKGROUND
  In the minutes to days after myocardial infarction, endogenous lysis of an occlusive coronary arterial thrombus occurs in most subjects. Compared with those in whom thrombolysis does not occur, those with antegrade flow in the infarct artery have improved left ventricular performance, less left ventricular dilatation, and improved survival. This study was performed to assess intrinsic hemostasis and fibrinolysis in survivors of myocardial infarction with or without antegrade perfusion of the infarct artery.
  
  
  RESULTS
  In 105 survivors of infarction (75 men, 30 women; age, 30 to 80 years) not given thrombolytic therapy, coronary angiography revealed a patent (group 1, n = 52) or occluded (group 2, n = 53) infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, infarct artery. Plasma concentrations of plasminogen, fibrinogen, tissue plasminogen activator activity, plasminogen activator inhibitor activity, cholesterol, triglycerides, and lipoproteins, including lipoprotein(a) (Lp[a]), were measured in blood procured 23 +/- 13 (mean +/- SD) months after infarction. Groups 1 and 2 were similar in age, sex, race, cardioactive medications, infarct artery, extent of coronary artery disease, and left ventricular performance. Of the plasma constituents assayed, the groups were similar except that Lp(a) averaged 18.5 +/- 21.7 mg/dL in group 1 and 49.1 +/- 44.8 mg/dL in group 2 (P < .001). This difference was evident in both Caucasian (n = 65) (P = .009) and African American (n = 40) (P = .01) subjects.
  
  
  CONCLUSIONS
  Survivors of myocardial infarction who failed to recanalize the infarct artery have higher plasma Lp(a) concentrations than those with a patent infarct artery. Lp(a) may inhibit intrinsic fibrinolysis.
authors.affiliation: Department of Internal Medicine (Cardiovascular Division), University of Texas, Southwestern Medical Center, Dallas 75235.
authors.forename: D J
authors.initials: DJ
authors.lastname: Moliterno
authors.forename: R A
authors.initials: RA
authors.lastname: Lange
authors.forename: R S
authors.initials: RS
authors.lastname: Meidell
authors.forename: J E
authors.initials: JE
authors.lastname: Willard
authors.forename: C C
authors.initials: CC
authors.lastname: Leffert
authors.forename: R D
authors.initials: RD
authors.lastname: Gerard
authors.forename: E
authors.initials: E
authors.lastname: Boerwinkle
authors.forename: H H
authors.initials: HH
authors.lastname: Hobbs
authors.forename: L D
authors.initials: LD
authors.lastname: Hillis
mesh_terms: D017023:Coronary Angiography; D003328:Coronary Thrombosis / Q000097:blood* / Q000208:ethnology / Q000503:physiopathology; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005342:Fibrinolysis / Q000502:physiology*; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000208:ethnology / Q000503:physiopathology; D012307:Risk Factors; D014654:Vascular Patency / Q000502:physiology*
chemical_list: D017270:Lipoprotein(a)