title: [The influence of hereditary thrombophilic mechanisms on the degree of permanent intravascular coagulation in patients with artificial heart valves].
abstract: The genotyping of 40 patients with artificial heart valves (AHV) was performed after prosthesis of the mitral and aotic valves with bicuspid AHV (Medinzh-2 and CarboMedics). The patients took phenylin and varfarin. The patients' genotype was estimated by the thrombophylic genes: factor V Leiden (FVL), prothrombin G20210A, methylene tetrahydrofolate reductase C677T, G/A--455FGB, 4G/5G PAI-1, PI A1/A2 GPIIIa. The genes determining the thrombocytic activity or the vascular wall state substantially influence the third degree of the intensity of the permanent intravascular coagulation (PIC-3) independent of the degree of correction of hemostasis of oral anticoagulants. The addition of anti-aggregants to therapy is the only that can normalize functional activity of thrombocytes in patients with AHV having such defects. The laboratory detection of the genetic defects is of great practical importance for the determination of risk groups of formation of PIC-3 and the strategy of antithrombotic protection of patients with AHV.
authors.forename: T V
authors.initials: TV
authors.lastname: Vavilova
authors.forename: O V
authors.initials: OV
authors.lastname: Sirotkina
authors.forename: G I
authors.initials: GI
authors.lastname: Razorenov
authors.forename: T S
authors.initials: TS
authors.lastname: Razorenova
authors.forename: V L
authors.initials: VL
authors.lastname: Emanuél'
authors.forename: V V
authors.initials: VV
authors.lastname: Gritsenko
authors.forename: P I
authors.initials: PI
authors.lastname: Orlovskiĭ
authors.forename: D N
authors.initials: DN
authors.lastname: Doĭnikov
authors.forename: V E
authors.initials: VE
authors.lastname: Sharafutdinov
authors.forename: S A
authors.initials: SA
authors.lastname: Karpov
authors.forename: A A
authors.initials: AA
authors.lastname: Kuznetsov
authors.forename: M I
authors.initials: MI
authors.lastname: Kadinskaia
mesh_terms: D000925:Anticoagulants / Q000627:therapeutic use; D001777:Blood Coagulation / Q000187:drug effects / Q000235:genetics*; D001779:Blood Coagulation Factors / Q000235:genetics*; D001792:Blood Platelets / Q000187:drug effects; D005165:Factor V / Q000235:genetics; D005260:Female; D005838:Genotype; D019918:Heart Valve Prosthesis Implantation / Q000009:adverse effects; D006801:Humans; D008297:Male; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D010630:Phenindione / Q000627:therapeutic use; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011516:Prothrombin / Q000235:genetics; D013923:Thromboembolism / Q000097:blood* / Q000235:genetics / Q000517:prevention & control; D019851:Thrombophilia / Q000235:genetics*; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D000925:Anticoagulants; D001779:Blood Coagulation Factors; D010975:Platelet Aggregation Inhibitors; C095381:factor V Leiden; D010630:Phenindione; D014859:Warfarin; D005165:Factor V; D011516:Prothrombin; D042965:Methylenetetrahydrofolate Reductase (NADPH2)