Journal ArticleDOI
Relationships between lipoprotein(a), lipids, apolipoproteins, basal and stimulated fibrinolytic regulators, and D-dimer.
TLDR
Given the absence of any relationship between Lp(a) levels and inhibition or stimulation of fibrinolysis regulators or D-dimer either in the basal or stimulated state, it is postulate that Lp (a)'s major atherogenic effects are mediated by mechanisms other than reduction of fibinolytic stimulation or in vivo fibralelysis.Abstract:
In 191 newly referred hyperlipidemic patients, our specific aim was to assess relationships between levels of lipoprotein(a) [Lp(a)], lipids, apolipoproteins, regulators of basal and stimulated fibrinolytic activity, and D-dimer, a measure of in vivo fibrinolysis. Lp(a) levels correlated with none of the measures of basal fibrinolytic regulators or D-dimer. In 25 patients, levels of stimulated regulators of fibrinolytic activity and D-dimer were measured after 10-minute cuff venous occlusion. Lp(a) levels again correlated with none of the stimulated regulators of fibrinolytic activity or D-dimer. However, both basal and stimulated levels of fibrinolytic regulators and D-dimer were closely related to other major risk factors for coronary heart disease (CHD) including triglyceride, apolipoprotein (apo) A1, apo B, Quetelet index (QI), and sex. By stepwise regression in 191 patients, the following standardized partial regression coefficients were significant (P < or = .05), and model R2 and P values were as follows: basal tissue plasminogen activator (tPA) with apo B-.18, with time .17, with QI -.28, R2 = 17%, P < or = .0001; basal plasminogen activator inhibitor (PAI) with apo B..25, with time -.15, with QI .17, R2 = 14%, P < or = .0001; basal alpha 2-antiplasmin with apo A1.14, with apo B.24, with QI.17, with sex .30, R2 = 25%, P < .0001; basal plasminogen with A1.15, with apo B.21, with QI.17, with sex.17, R2 = 15%, P < or = .0001; basal fibrinogen with Lp(a).17, with QI.21, with sex.26, R2 = 14%, P < or = .0001; D-dimer with sex.15, R2 = 21%, P < or = .048. Given the absence of any relationship between Lp(a) levels and inhibition or stimulation of fibrinolysis regulators or D-dimer either in the basal or stimulated state, we postulate that Lp(a)'s major atherogenic effects are mediated by mechanisms other than reduction of fibrinolysis stimulation or in vivo fibrinolysis.read more
Citations
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Metformin therapy is associated with a decrease in plasma plasminogen activator inhibitor-1, lipoprotein(a), and immunoreactive insulin levels in patients with the polycystic ovary syndrome.
TL;DR: Metformin decreases Izero in hyperinsulinemic PCOS patients, reverses the hyperinsulinemia-driven endocrinopathy, decreases PAI-1, and decreases Lp(a), and should thus reduce the increased risk of atherothrombosis in PCOS.
Journal ArticleDOI
Hypofibrinolysis, thrombophilia, osteonecrosis.
TL;DR: Heritable hypofibrinolysis and thrombophilia, often augmented in women by hyperestrogenemia, seem to be major pathoetiologies of osteonecrosis.
Journal ArticleDOI
Metformin reduces weight, centripetal obesity, insulin, leptin, and low-density lipoprotein cholesterol in nondiabetic, morbidly obese subjects with body mass index greater than 30.
Charles J. Glueck,Robert N. Fontaine,Ping Wang,M.T.R. Subbiah,K. Weber,Ellen Illig,Patricia Streicher,Luann Sieve-Smith,Trent Tracy,James E. Lang,P. McCullough +10 more
TL;DR: Metformin safely and effectively reduces CHD risk factors (weight, fasting insulin, leptin, LDL cholesterol, centripetal obesity) in morbidly obese, nondiabetic subjects with BMI > 30, probably by virtue of its insulin-sensitizing action.
Journal ArticleDOI
Evidence that homocysteine is an independent risk factor for atherosclerosis in hyperlipidemic patients
TL;DR: In 482 patients sequentially referred for diagnosis and therapy of hyperlipidemia, the prevalence of homocysteinemia was determined, to assess whether it was independently associated with atherosclerotic vascular disease, and to determine how effectively high homocysteine could be treated with folic acid and pyridoxine.
Journal ArticleDOI
Antifibrinolytic activity of apolipoprotein(a) in vivo: human apolipoprotein(a) transgenic mice are resistant to tissue plasminogen activator-mediated thrombolysis.
Theresa M. Palabrica,Alexander C. Liu,Mark Aronovitz,Mark Aronovitz,Bruce Furie,Richard M. Lawn,Barbara C. Furie,Barbara C. Furie +7 more
TL;DR: Results directly demonstrate an in vivo effect of apolipoprotein(a) on fibrinolysis, an effect that may contribute to the pathology associated with elevated levels of this protein.
References
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Journal ArticleDOI
Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults
DeWitt S. Goodman,Stephen B. Hulley,Luther T. Clark,Clay Davis,Valentin Fuster,John C. LaRosa,Albert Oberman,Ernst J. Schaefer,Daniel Steinberg,W. Virgil Brown,Scott M. Grundy,Diane M. Becker,Edwin L. Bierman,Jacqueline Sooter-Bochenek,Rebecca M. Mullis,Neil J. Stone,Donald B. Hunninghake,Jacqueline M. Dunbar,Henry N. Ginsberg,D. Roger Illingworth,Harold C. Sadin,Gustav Schonfeld,James I. Cleeman,H. Bryan Brewer,Nancy D. Ernst,William T. Friedewald,Jeffrey M. Hoeg,Basil M. Rifkind,David L. Gordon +28 more
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Journal ArticleDOI
cDNA sequence of human apolipoprotein(a) is homologous to plasminogen
John W. McLean,James E. Tomlinson,Wun-Jing Kuang,Dan L. Eaton,Ellson Y. Chen,Gunther M. Fless,Angelo M. Scanu,Richard M. Lawn +7 more
TL;DR: Sequencing of cloned human apolipoprotein(a) complementary DMA shows that it is very similar to human plasminogen.