title: High lipoprotein(a) level promotes both coronary atherosclerosis and myocardial infarction: a path analysis using a large number of autopsy cases.
abstract: OBJECTIVE
  To investigate whether hyper-lipoproteinaemia(a) (Lp(a)) promotes coronary atherosclerosis, acute thrombosis resulting in myocardial infarction (MI), or both.
  
  
  METHODS
  Retrospective chart review.
  
  
  METHODS
  A community-based general geriatric hospital.
  
  
  METHODS
  1062 consecutive autopsy cases (609 men, 453 women). The mean age at the time of death was 80 years.
  
  
  METHODS
  A semiquantitative evaluation of the coronary stenosis on cut sections and pathological definition of MI. Lp(a) levels of fresh serum taken antemortem, measured by a latex-enhanced turbidimetric immunoassay.
  
  
  RESULTS
  The prevalence of severe coronary stenosis and pathological MI increased linearly with increasing Lp(a) levels with no apparent threshold. The odds ratios (95% CI) of hyper-Lp(a) (2.99 (1.70 to 5.28) for 200-299 mg/l and 3.25 (1.90 to 5.54) for >300 mg/l) for severe coronary stenosis were larger than those of hypertension (2.61 (1.88 to 3.63)), diabetes mellitus (2.09 (1.41 to 3.11)) and hypercholesterolaemia (2.05 (1.31 to 3.21)). The severe coronary sclerosis was much stronger risk of MI (6.28 (4.33 to 9.11)) than hyper-Lp(a), hypertension and diabetes mellitus. A path analysis showed that the Lp(a) levels affected both coronary sclerosis and MI, with path coefficients of 0.15 and 0.07 (direct effect), respectively. In cases with severe coronary sclerosis Lp(a) affected only MI (0.15).
  
  
  CONCLUSIONS
  Lp(a) levels have distinct effects on coronary sclerosis and MI, with about half of the overall effect on MI being via coronary sclerosis. This result supports the prothrombotic and a probable proinflammatory role of Lp(a) in coronary events.
authors.affiliation: Department of Pathology, Tokyo Metropolitan Geriatric Hospital, Itabashi, Tokyo 173-0015, Japan. sawabe@tmig.or.jp
authors.forename: M
authors.initials: M
authors.lastname: Sawabe
authors.forename: N
authors.initials: N
authors.lastname: Tanaka
authors.forename: K
authors.initials: K
authors.lastname: Nakahara
authors.forename: A
authors.initials: A
authors.lastname: Hamamatsu
authors.forename: K
authors.initials: K
authors.lastname: Chida
authors.forename: T
authors.initials: T
authors.lastname: Arai
authors.forename: K
authors.initials: K
authors.lastname: Harada
authors.forename: T
authors.initials: T
authors.lastname: Inamatsu
authors.forename: T
authors.initials: T
authors.lastname: Ozawa
authors.forename: M M
authors.initials: MM
authors.lastname: Naka
authors.forename: S
authors.initials: S
authors.lastname: Matsushita
mesh_terms: D000208:Acute Disease; D000369:Aged, 80 and over; D001344:Autopsy; D002908:Chronic Disease; D003324:Coronary Artery Disease / Q000209:etiology*; D003328:Coronary Thrombosis / Q000209:etiology*; D005260:Female; D006801:Humans; D006951:Hyperlipoproteinemias / Q000150:complications*; D017270:Lipoprotein(a) / Q000378:metabolism*; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology*; D012189:Retrospective Studies; D012307:Risk Factors
chemical_list: D017270:Lipoprotein(a)