Relationships between lipoprotein(a), lipids, apolipoproteins, basal and stimulated fibrinolytic regulators, and d-dimer

Plasma Lp(a) levels correlate with number, severity, and length-extension of coronary lesions in male patients undergoing coronary arteriography for clinically suspected coronary atherosclerosis.

“…41 High Lp(a) concentrations of sometimes more than 300 mg/dL have also been found in patients with myocardial infarction and angiographically normal coronary arteries, 42 which supports the idea that Lp(a) is involved in the thrombotic pathogenesis of coronary occlusion, as might be assumed by its partial homology to plasminogen and its effect of reducing tissue-type plasminogen activator-mediated clot lysis. 43 - 44 In another study, 45 however, newly referred hyperlipidemic patients exhibited no relation between Lp(a) levels and inhibition of regulators of basal and stimulated fibrinoh/tic activity or D-dimer, a measure of in vivo fibrinoh/sis.…”

Protein C and S Deficiency, Thrombophilia, and Hypofibrinolysis: Pathophysiologic Causes of Legg-Perthes Disease

“…Basal and stimulated determinants of fibrinolysis and Ddimer were quantitated as previously reported ( II,22). After the patients fasted for 12-h, blood was obtained between 0800 hand 0900 h in seated patients to minimize the influence of time of day on regulators of basal and stimulated fibrinolytic activity (11).…”

“…PAI-Fx, a major inhibitor of fibrinolysis (10, 11 ,22-24) Additional measures of fibrinolytic regulators included a2-antiplasmin (a fibrinolytic inhibitor) (S-225I , KabiVitrum, Franklin, OH), plasminogen (Spectrozyme PL, American Diagnostica), and fibrinogen (Dade Thrombin, Baxter Healthcare Corp., Miami, FL) (11,22).…”

18 Associations of Thrombophilia, Hypofibrinolysis, and Retinal Vein Occlusion.

“…Polymerase chain reaction (PCR)-cDNA coagulation measures (Table 2) were performed in cases with RVO and in healthy controls using previously published methods by laboratory staff blinded to the subjects' status (case, control, severity of cases) (1,12,(14)(15)(16)(17)(18)(19)(20)(21). The PCR analyses of four thrombophilic gene mutations (G1691A factor V Leiden, C677T MTHFR, G20210A prothrombin, platelet glycoprotein IIb/IIIa PL A1/A2 polymorphism) and the hypofibrinolytic 4G/5G mutation of the PAI-1 gene promoter were performed at the Molecular Diagnostics Laboratory in Cincinnati, using previously published methods, as summarized in the Appendix (1,12,(14)(15)(16)(17)(18)(19)(20)(21).…”