title: Risk Factors, biochemical markers, and genetic polymorphisms in early coronary artery disease.
abstract: OBJECTIVE
  To assess the risk factors, lipid and apolipoprotein profile, hemostasis variables, and polymorphisms of the apolipoprotein AI-CIII gene in early coronary artery disease (CAD).
  
  
  METHODS
  Case-control study with 112 patients in each group controlled by sex and age. After clinical evaluation and nutritional instruction, blood samples were collected for biochemical assays and genetic study.
  
  
  RESULTS
  Familial history of early CAD (64 vs 39%), arterial hypertension (69 vs 36%), diabetes mellitus (25 vs 3%), and previous smoking (71 vs 46%) were more prevalent in the case group (p<0.001). Hypertension and diabetes were independent risk factors. Early CAD was characterized by higher serum levels of total cholesterol (235 +/-6 vs 209 +/- 4 mg/dL), of LDL-c (154 +/- 5 vs 135 +/- 4 mg/dL), triglycerides (205 +/- 12 vs 143 +/- 9 mg/dL), and apolipoprotein B (129 +/- 3 vs 105 +/- 3 mg/dL), and lower serum levels of HDL-c (40 +/- 1 vs 46 +/- 1 mg/dL) and apolipoprotein AI (134 +/- 2 vs 146 +/- 2mg/dL) [p<0.01], in addition to an elevation in fibrinogen and D-dimer (p<0.02). The simultaneous presence of the rare alleles of the APO AI-CIII genes in early CAD are associated with hypertriglyceridemia (p=0.03).
  
  
  CONCLUSIONS
  Of the classical risk factors, hypertension and diabetes mellitus were independently associated with early CAD. In addition to an unfavorable lipid profile, an increase in the thrombotic risk was identified in this population. An additive effect of the APO AI-CIII genes was observed in triglyceride levels.
authors.affiliation: Disciplina de Cardiologia, UNIFESP/EPM, Universidade Federal de São Paulo, Sao Paulo, SP. lipides.dmed@unifesp.epm.br
authors.forename: Maria Cristina
authors.initials: MC
authors.lastname: Izar
authors.forename: Francisco Antonio Helfenstein
authors.initials: FA
authors.lastname: Fonseca
authors.forename: Sílvia Saiuli Miki
authors.initials: SS
authors.lastname: Ihara
authors.forename: Nelson
authors.initials: N
authors.lastname: Kasinski
authors.forename: Won Han
authors.initials: WH
authors.lastname: Sang
authors.forename: Ieda Edite Lanzarini
authors.initials: IE
authors.lastname: Lopes
authors.forename: Leonor do Espírito Santo de Almeida
authors.initials: Ldo E
authors.lastname: Pinto
authors.forename: Waldir Gabriel Miranda
authors.initials: WG
authors.lastname: Relvas
authors.forename: Daisy
authors.initials: D
authors.lastname: Lourenço
authors.forename: Sérgio
authors.initials: S
authors.lastname: Tufik
authors.forename: Angelo Amato Vincenzo
authors.initials: AA
authors.lastname: de Paola
authors.forename: Antonio Carlos Camargo
authors.initials: AC
authors.lastname: Carvalho
mesh_terms: D000328:Adult; D016632:Apolipoprotein A-I / Q000235:genetics; D053305:Apolipoprotein C-III; D001056:Apolipoproteins C / Q000235:genetics; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood / Q000209:etiology* / Q000235:genetics; D005260:Female; D006487:Hemostasis; D006801:Humans; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D016632:Apolipoprotein A-I; D053305:Apolipoprotein C-III; D001056:Apolipoproteins C; D015415:Biomarkers; D008055:Lipids