title: Clinical and biochemical factors associated with prognosis after myocardial infarction at a young age.
abstract: OBJECTIVE
  This study examined the effect of metabolic disturbances, hemostatic function, coronary artery disease severity and left ventricular function on the long-term prognosis after myocardial infarction in men < 45 years old.
  
  
  BACKGROUND
  Heavy smoking; dyslipoproteinemias involving very low density lipoprotein (VLDL), low density lipoprotein (LDL) and high density lipoprotein (HDL); a family history of premature coronary artery disease; hyperinsulinemic responses to oral and intravenous glucose challenges; and defective fibrinolytic function characterize the young postinfarction patient, but the influence of these features on the long-term prognosis is virtually unknown.
  
  
  METHODS
  Measurements of hemostatic function and metabolic and angiographic indicators of risk were included in a prospective cohort study of variables predictive of reinfarction, cardiac death and major coronary events within 6 to 9 years in 108 unselected nondiabetic men with a first myocardial infarction before age 45 years.
  
  
  RESULTS
  During follow-up, 20 patients had sudden cardiac death, and 53 had a major coronary event (reinfarction, sudden cardiac death, bypass surgery or intervention by catheterization). In multivariate analysis, VLDL and global coronary atherosclerosis score predicted reinfarction; plasma plasminogen activator inhibitor-1 (PAI-1) activity and global coronary stenosis score predicted cardiac death; and VLDL triglyceride levels, global coronary atherosclerosis score and age predicted any major coronary event.
  
  
  CONCLUSIONS
  This prospective cohort study shows that hypertriglyceridemia, impaired fibrinolytic capacity secondary to plasma PAI-1 activity elevation and extensive coronary artery disease increase the risk of recurrences in men with a first myocardial infarction before age 45 and contribute to the relatively poor long-term prognosis in this patient group.
authors.affiliation: Department of Cardiology, Karolinska Hospital, Karolinska Institute, Stockholm, Sweden.
authors.forename: K
authors.initials: K
authors.lastname: Malmberg
authors.forename: P
authors.initials: P
authors.lastname: Båvenholm
authors.forename: A
authors.initials: A
authors.lastname: Hamsten
mesh_terms: D000328:Adult; D000367:Age Factors; D001786:Blood Glucose / Q000378:metabolism; D015331:Cohort Studies; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging; D016757:Death, Sudden, Cardiac / Q000209:etiology; D005342:Fibrinolysis; D005500:Follow-Up Studies; D005951:Glucose Tolerance Test; D006801:Humans; D015228:Hypertriglyceridemia / Q000150:complications; D007328:Insulin / Q000097:blood; D008074:Lipoproteins / Q000097:blood; D008079:Lipoproteins, VLDL / Q000097:blood; D008297:Male; D015999:Multivariate Analysis; D009203:Myocardial Infarction / Q000097:blood* / Q000000981:diagnostic imaging / Q000401:mortality; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood; D011379:Prognosis; D016016:Proportional Hazards Models; D011446:Prospective Studies; D012008:Recurrence; D016019:Survival Analysis; D014280:Triglycerides / Q000097:blood; D016277:Ventricular Function, Left
chemical_list: D001786:Blood Glucose; D007328:Insulin; D008074:Lipoproteins; D008079:Lipoproteins, VLDL; D017395:Plasminogen Activator Inhibitor 1; D014280:Triglycerides