Central Retinal Vein Occlusion and Prothrombotic Factors

Retinal vein occlusion (RVO) is an important cause of visual loss. Known risk factors are hypertension, diabetes mellitus, hyperlipidaemia, open angle glaucoma and abnormalities of haemostatic factors and blood viscosity. The aim of our study was to identify any relationships between RVO and fibrinolytic-coagulative pattern in patients affected either by metabolic disorders or not Methods: 50 patients (22 male, 28 female) affected by RVO underwent a study of metabolic, coagulative and fibrinolytic parameters. All patients were not submitted to any previous ocular theraphy before the episode of RVO. After a complete ophtalmologic evaluation, blood was collected to perform various laboratory tests: Enzymatic-colorimetric: glicaemia, total-cholesterol (TC), HDL-cholesterol (HDL-C), Tryglicerides (TG), Antitrombin III (ATIII), Protein C and S (PC, PS), Alpha-2-antiplasmin (A2P), Plasminogen (PL). ELISA: D-dimer (DD), tissue plasminogen activator and inhibitor (t-PA, PAI-1), thrombin activable fibrinolysis inhibitor (TAFI), Soluble P and E selectin (sP-sel, sE-sel), vonWillebrand factor (vWF), fragment 1+2 (F1+2), lipoprotein (a) [lp(a)]. Coagulative: Protein C resistance (APCR), Factor VII and VIII (VII, VIII). HPLC: Homocysteine. Our data show a decreased fibrinolytic power in 43/50 subjects (86%) (ELT 318±36 min, PAP 107±19 ug/l). PAI-1 was 21.4±4.2 UI/l in the general population with differences between diabetic and dyslipidaemic subjects and not-metabolic patients. 1 patients suffered from low ATIII levels (60%), none had PC, PS deficiency or APCR. 2 not-metabolic subjects had increased Lp (a) and impairment of fibrinolysis. Hyper Hc (21.6±3.1umol/l) was detected in 4 subjects TAFI and sP-sel were increased in patients (4) with type IIa hyperlipidemia. sE-sel and vWF were particularly increased in dysmetabolic subjects (diabetes and Hyper TG or low HDL-C). A prothrombotic state involving defects in coagulative and fibrinolytic factors has been previously associated with the onset of RVO. Our data show that a fibrinolytic impairment is the most common feature in such patients regardless dysmetabolic or not associated diseases. Moreover mechanisms leading to fybrinolysis alterations vary between subjects in order to associated metabolic conditions. Defects in anticoagulant natural proteins or platelet hyperactivity are very rare conditions detected in our population. Such data suggest that the fibrinolytic system may be an important target of acute treatment and profilaxys in RVO affected patients.