Effect of Three Fibrate Derivatives and of Two HMG-CoA Reductase Inhibitors on Plasma Fibrinogen Level in Patients with Primary Hypercholesterolemia

1993 ◽  
Vol 70 (02) ◽  
pp. 241-243 ◽  
Author(s):  
Adriana Branchi ◽  
Angelo Rovellini ◽  
Domenico Sommariva ◽  
Angelo G Gugliandolo ◽  
Angelo Fasoli
Keyword(s):  
Slow Release ◽  
Fibrinogen Level ◽  
Plasma Fibrinogen ◽  
Fibrinogen Concentration ◽  
Plasma Fibrinogen Level ◽  
Primary Hypercholesterolemia ◽  
Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitors ◽  
Coa Reductase ◽  
Hypocholesterolemic Drugs

SummaryIn order to evaluate the effects of hypocholesterolemic drugs on plasma fibrinogen concentration, six groups of subjects with primary hypercholesterolemia have been put on treatment with diet alone or diet plus fenofibrate (100 mg t.i.d.), slow release bezafibrate (400 mg once a day), gemfibrozil (600 mg b.i.d.), simvastatin (20 mg once a day) or pravastatin (20 mg once a day) respectively. After 1 month of therapy, plasma fibrinogen significantly decreased by 9% and 15% in fenofibrate and bezafibrate groups respectively and increased by 19% in gemfibrozil treated patients. After 4 months of therapy the changes were −16% with fenofibrate, −10% with bezafibrate and +20% with gemfibrozil. No significant changes were observed in patients treated with diet alone, simvastatin or pravastatin. The fibrinogen lowering effect of fenofibrate and bezafibrate does not seem to be related to the hypolipidemic activity of the drugs.

The Relationship of Plasma Fibrinogen, Erythrocyte Flexibility and Blood Viscosity

1977 ◽  
Vol 38 (03) ◽  
pp. 0660-0667 ◽  
Author(s):  
P. A Dupont ◽  
J. A Sirs
Keyword(s):  
Blood Viscosity ◽  
Fibrinogen Level ◽  
Plasma Viscosity ◽  
Plasma Fibrinogen ◽  
Fibrinogen Concentration ◽  
Plasma Fibrinogen Level ◽  
Shear Rates ◽  
High Shear Rates ◽  
Direct Measurements ◽  
Relationship Of

SummaryMeasurements have been made of plasma fibrinogen concentration, erythrocyte flexibility and blood viscosity at shear rates from 5.75 to 230 sec−1 during and following surgery. In the post-operative period the plasma fibrinogen level in the patient rose to over 1,000 mg/dl and because there were subsequent complications, only returned to normal after 4 weeks. There was an associated change of erythrocyte flexibility, with a correlation coefficient of 0.98. The blood viscosity also varied with the plasma fibrinogen level, the effect being more pronounced at low shear rates. The internal viscosity of the red blood cell, calculated from the plasma viscosity and whole blood viscosity at 230 sec−1, decreases with increasing plasma fibrinogen concentration, in agreement with the direct measurements made of erythrocyte flexibility. It is proposed that at high shear rates an increase in plasma viscosity due to an elevation of fibrinogen concentration, is offset by a decrease in the rigidity of the erythrocytes, and these 2 effects counter-balance.

Comparative Evaluation of the Safety and Efficacy of HMG-CoA Reductase Inhibitor Monotherapy in the Treatment of Primary Hypercholesterolemia

1995 ◽  
Vol 29 (7-8) ◽  
pp. 743-759 ◽  
Author(s):  
Irene Hsu ◽  
Sarah A Spinier ◽  
Nelda E Johnson
Keyword(s):  
Clinical Trials ◽  
Reductase Inhibitor ◽  
Efficacy And Safety ◽  
Comparative Efficacy ◽  
Hmg Coa Reductase ◽  
Primary Hypercholesterolemia ◽  
Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitor ◽  
Coa Reductase

Objective: To evaluate the comparative efficacy and safety of the 4 currently available hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors, fluvastatin, lovastatin, pravastatin, and simvastatin, in the treatment of primary hypercholesterolemia. Data Sources: English-language clinical studies, abstracts, and review articles identified from MEDLINE searches and bibliographies of identified articles. Unpublished data were obtained from the Food and Drug Administration in accordance with the Freedom of Information Act. Study Selection: Placebo-controlled and comparative studies of HMG-CoA reductase inhibitor monotherapy in the treatment of primary hypercholesterolemia. Data Extraction: Pertinent studies were selected and the data were synthesized into a review format. Data Synthesis: The chemistry, pharmacology, and pharmacokinetics of the 4 HMG-CoA reductase inhibitors are reviewed. Clinical trials evaluating the hypocholesterolemic efficacy of the HMG-CoA reductase inhibitors are examined, and results on the comparative efficacy and safety of these agents are summarized. On a milligram-per-milligram basis, simvastatin is twice as potent as lovastatin and pravastatin. The hypocholesterolemic effects of fluvastatin appear to be approximately 30% less than that of lovastatin. In posttransplant patients receiving cyclosporine, safety has been documented for low doses of lovastatin and simvastatin, but when a higher dosage of an HMG-CoA reductase inhibitor is warranted, pravastatin should be considered the drug of choice because of a lower incidence of myopathy. Relevant data on the incidence of adverse effects are presented. Pertinent outcomes data from clinical trials evaluating the effect of HMG-CoA reductase inhibitors on atherosclerosis regression and coronary mortality, as well as published economic analyses of cholesterol-lowering agents, are summarized. Recommendations on the selection of an HMG-CoA reductase inhibitor in various clinical situations are provided. Conclusions: The literature supports the comparable safety and tolerability of all 4 currently available HMG-CoA reductase inhibitors. Therefore, the choice of an HMG-CoA reductase inhibitor should depend on the extent of cholesterol lowering needed to meet the recommended treatment goal established by the National Cholesterol Education Program. Direct comparative studies are needed to confirm the relative, long-term cost-effectiveness of the various HMG-CoA reductase inhibitors in the treatment of primary hypercholesterolemia.

Determination of Fibrinogen and Fibrinogenolytic Activity

1962 ◽  
Vol 08 (02) ◽  
pp. 297-310 ◽  
Author(s):  
Inga Marie Nilsson ◽  
Bertil Olow
Keyword(s):  
Thrombolytic Therapy ◽  
Fibrinolytic Activity ◽  
Fibrinogen Level ◽  
Plasma Fibrinogen ◽  
Fibrinogen Concentration ◽  
Plasma Fibrinogen Level ◽  
Fibrinogenolytic Activity ◽  
The Difference ◽  
The Moment

SummaryA method for determining plasma fibrinogen and fibrinogenolytic activity, with epsilonaminocaproic acid (ε-ACA) as an inhibitor of fibrinolysis, in patients with high fibrinolytic activity, is described in detail.The fibrinogen was determined by a modification of Morrison’s syneresis method in parallel in 1. citrated plasma that was incubated for 2 hours at 37° C, after which further digestion was prevented by addition of ε-ACA and is referred to as fibrinogen A, and 2. in citrated plasma prepared from blood collected in tubes containing ε-ACA to prevent activation of plasminogen and is referred to as fibrinogen B. The difference between fibrinogen B and fibrinogen A gives the amount of lysed fibrinogen in 2 hours at 37° C. Fibrinogen B gives the fibrinogen concentration at the moment of sampling.The method is recommended to be used for evaluation of the true plasma fibrinogen level and the degree of fibrinogenolytic activity. This is particularly important during thrombolytic therapy.

scholarly journals Effect of the HMG-CoA Reductase Inhibitors on Blood Pressure in Patients With Essential Hypertension and Primary Hypercholesterolemia

Hypertension ◽  
1999 ◽  
Vol 34 (6) ◽  
pp. 1281-1286 ◽  
Author(s):  
Nicola Glorioso ◽  
Chiara Troffa ◽  
Fabiana Filigheddu ◽  
Francesco Dettori ◽  
Aldo Soro ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Hmg Coa Reductase ◽  
Primary Hypercholesterolemia ◽  
Reductase Inhibitors ◽  
Hmg Coa Reductase Inhibitors ◽  
Coa Reductase

Platelet Adhesiveness and Fibrinolysis after Recent Cerebro-Vascular Accidents and their Relationship with Subsequent Deep Venous Thrombosis of the Legs

1976 ◽  
Vol 36 (01) ◽  
pp. 127-132 ◽  
Author(s):  
C. P Warlow ◽  
J. A. N Rennie ◽  
D Ogston ◽  
A. S Douglas
Keyword(s):  
Platelet Count ◽  
Venous Thrombosis ◽  
Deep Venous Thrombosis ◽  
Plasminogen Activator ◽  
Fibrinogen Level ◽  
Plasma Fibrinogen ◽  
Platelet Adhesiveness ◽  
Plasma Fibrinogen Level ◽  
Vascular Accidents ◽  
Subsequent Rise

SummaryIn fifteen patients with a cerebro-vascular accident resulting in an acute hemiplegia there was a subsequent rise in the platelet count and plasma fibrinogen level. There were no significant alterations in platelet adhesiveness, plasminogen activator, plasminogen, FR-antigen and haematocrit. Patients diagnosed as developing deep venous thrombosis with the 125I-fibrinogen technique had a significantly lower platelet adhesiveness and plasminogen level than those who were not.

Variation in the Promoter Region of the β Fibrinogen Gene Is Associated with Plasma Fibrinogen Levels in Smokers and Non-Smokers

1991 ◽  
Vol 65 (05) ◽  
pp. 487-490 ◽  
Author(s):  
A E Thomas ◽  
F R Green ◽  
C H Kelleher ◽  
H C Wilkes ◽  
P J Brennan ◽  
...  
Keyword(s):  
Heart Disease ◽  
Promoter Region ◽  
Fragment Length Polymorphism ◽  
Fibrinogen Level ◽  
Plasma Fibrinogen ◽  
Plasma Fibrinogen Level ◽  
Healthy Men ◽  
History Of ◽  
General Practices ◽  
Restriction Fragment Length

SummaryWe investigated the association between fibrinogen levels and a HaeIII restriction fragment length polymorphism located at −453 bp from the start of transcription of the β fibrinogen gene. 292 healthy men aged 45 to 69 years, recruited from general practices throughout Britain, were studied. None had a history of ischaemic heart disease. 41.1% (120) were smokers and fibrinogen levels were higher in this group. The frequency of the noncutting allele (designated H2) was 0.19 and was the same in smokers and non-smokers. The H2 allele was associated with elevated levels of fibrinogen in both smokers and non-smokers and the effect of genotype was similar in both groups. After smoking, HaeIII genotype was the strongest predictor of fibrinogen levels and explained 3.1% of the variance in fibrinogen levels. These results confirm earlier studies that variation at the fibrinogen locus contributes to the between-individual differences in plasma fibrinogen level.

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