title: Aggregation of lipoprotein and inflammatory parameters in families with a history of premature myocardial infarction: the Tallinn myocardial infarction study.
abstract: BACKGROUND
  The offspring of individuals with a history of premature myocardial infarction are at increased risk of premature coronary attacks. The aim of this study was to determine parent/offspring associations of coronary risk factors in families affected by premature myocardial infarction and to compare these to corresponding control families.
  
  
  METHODS
  The cohort of cases consisted of 71 male survivors of myocardial infarction and their 128 descendants (aged 7-18 years). As control families, 85 randomly selected healthy males with their 66 descendants were investigated. Besides traditional risk factors, serum high sensitive C-reactive protein (hsCRP), apolipoprotein (apo) E phenotypes and lipoprotein(a) were analyzed.
  
  
  RESULTS
  In the offspring of the patients, fibrinogen and atherogenic lipoprotein parameters were higher than in the corresponding controls, but hsCRP, lipoprotein(a) and anthropometric data did not differ between the groups. The adult-offspring positive correlations were detected in fibrinogen and in almost all measured lipoprotein fractions in the affected families; amongst the controls, the association was observed only for triglyceride levels. Multiple logistic regression analysis demonstrated independent association of offspring apoB, apoA-I and fibrinogen levels with a family history of premature myocardial infarction.
  
  
  CONCLUSIONS
  The most informative predictors of future coronary attacks during childhood are apoB-100 and apoB/apoA-I ratio; serum hsCRP and lipoprotein(a) do not have predictive value in childhood.
authors.affiliation: Department of Chronic Disease Prevention, National Institute for Health Development, Tallinn, Estonia. katrin.aasvee@tai.ee
authors.forename: Katrin
authors.initials: K
authors.lastname: Aasvee
authors.forename: Elvira
authors.initials: E
authors.lastname: Kurvinen
authors.forename: Jouko
authors.initials: J
authors.lastname: Sundvall
authors.forename: Matti
authors.initials: M
authors.lastname: Jauhiainen
authors.forename: Inna
authors.initials: I
authors.lastname: Tur
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism*; D000293:Adolescent; D000328:Adult; D000367:Age Factors; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D001057:Apolipoproteins E / Q000235:genetics; D002097:C-Reactive Protein / Q000378:metabolism; D002648:Child; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D005192:Family Health; D005260:Female; D005387:Finland; D006801:Humans; D017270:Lipoprotein(a) / Q000097:blood; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood* / Q000235:genetics*; D011110:Polymorphism, Genetic; D012307:Risk Factors; D012737:Sex Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D000209:Acute-Phase Proteins; D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D017270:Lipoprotein(a); D008074:Lipoproteins; D014280:Triglycerides; D002097:C-Reactive Protein; D002784:Cholesterol