Increased Plasma Fibrinogen and Platelet-Aggregates in Type II Hyperlipoproteinaemia

SummaryPlasma fibrinogen and platelet-aggregates (method of Wu and Hoak) were measured in 21 patients with familial Type II hyperlipoproteinaemia and 21 matched control subjects. Patients with hyperlipoproteinaemia had increased levels of fibrinogen and platelet- aggregates (p<0.01). Young patients with hyperlipoproteinaemia had prematurely high fibrinogen levels, and the normal rise in fibrinogen during adult life was abolished. There were no statistically significant correlations within the patient group between fibrinogen, platelet-aggregates, and plasma lipids. High fibrinogen and platelet-aggregate levels may play a part in the development of the premature arterial disease associated with Type II hyperlipoproteinaemia, or may be markers of arterial injury.

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Increased Plasma Fibrinogen and Platelet-Aggregates in Type II Hyperlipoproteinaemia

10.1055/s-0039-1687455 ◽

1979 ◽

Author(s):

J.L.H.C. Third ◽

G.D.O. Lowe ◽

M.M. Drummond ◽

W.F. Bremner ◽

T.D.V. Lawrie ◽

...

Keyword(s):

Plasma Lipids ◽

Young Patients ◽

Adult Life ◽

Arterial Disease ◽

Arterial Injury ◽

Plasma Fibrinogen ◽

Type Ii ◽

Platelet Aggregate ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates

Plasma-fibrinogen and circulating platelet-aggregates (method of Wu and Hoak1) were measured in 21 patients with Type II hyperlipoproteinaeima and 21 matched control subjects. Patients with hyperlipoproteinaemia had increased levels of fibrinogen (3.5 g/l ± SEM 0.2 vs. 2.5 g/l±0.1, p(0.01) and platelet-aggregates (platelet aggregate ratio 0.71 vs. 0.65, p(0.01). Young patients with hyperlipoproteinaemia had prematurely high fibrinogen levels, and the normal fibrinogen rise durina adult life was abolished. There were no significant correlations between fibrinogen, platelet-aggregates, and plasma lipids (cholesterol, cholesterol fractions, or triglyceride). High librinogen and platelet-aggregate levels may play a part in the development of the premature arterial disease associated with Type II hyperlipoproteinaemia, or may be markers of arterial injury. 1Wu, K.K., Hoak, J.C.Lancet, 1974, ii, 924.

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Increased Plasma Fibrinogen and Circulating Platelet-Aggregates in Type II Hyperlipoproteinaemia

Clinical Science ◽

10.1042/cs056021pb ◽

1979 ◽

Vol 56 (3) ◽

pp. 21P-21P ◽

Cited By ~ 2

Author(s):

G. D. O. Lowe ◽

M. M. Reavey ◽

J. L. H. C. Third ◽

W. F. Bremner ◽

C. D. Forbes ◽

...

Keyword(s):

Plasma Fibrinogen ◽

Type Ii ◽

Circulating Platelet Aggregates ◽

Platelet Aggregates

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PLATELET AGGREGATE-ASSOCIATED FIBRIN FORMATION AS A FUNCTION OF AGGREGATE SIZE AND HEPARIN CONCENTRATION

10.1055/s-0038-1644857 ◽

1987 ◽

Author(s):

L J Wurzinger ◽

K Herbst ◽

H Schmid-Schonbein

Keyword(s):

Whole Blood ◽

Aggregate Size ◽

Arterial Disease ◽

Amidolytic Activity ◽

Protein Assay ◽

Heparin Concentration ◽

Platelet Aggregate ◽

Minimum Number ◽

Platelet Aggregates

The in vitro observation that fibrin forms withina few minutes in the crevices and niches inside and on the surface of platelet aggregates (PA), preparedfrom heparinized (5 U/ml) blood is consistent with the doubtful efficiency of heparin in the treatment of occlusive arterial disease (Thrcmb. Haemost. 46: 666,1981). Release of heparin- neutralizing proteins into limited and largely disclosed plasma compartments between aggregated platelets was held responsible for this remarkable phenomenon. However, the minimum number of aggregated platelets necessary to overcome the heparin inhibition remained undetermined then.PRP prepared from whole blood ant^coagulated with 0.5, 1 and 5 U/ml of mucosal heparin (Liquemin ), was aggregated with 10 or 100 pM ADP for 2 min at 37°C. Single PAs of various dimensions were withdrawn, washed, and incubated with a chromogenic substrate (S-2238, Kabi AB) to measure their thrombin content. Subsequently the number of platelets contained in the PA was evaluated by assaying the protein content of the aggregates. Microscopic PAs, their mass being toosmall to be determined precisely by a protein assay, were isolated with a filter technique, their extension was documented on photomicrographs for later calculation of aggregate volume and platelet content, before they were incubated with S-2238. Aggregates toosmall to develop detectable amidolytic activity, were checked microscopically for fibrin formed.S 2238 amidolytic activity (thrombin) in heparinizedPRP samples evolved as a linear function of the logarithm of PA mass. For a given heparin concentration (in whole blood) the following lowerthreshold platelet numbers of aggregates were found sufficient to allow the formation of detectable quantities of thrombin:These results suggest a fatal role platelet aggregates of minute dimensions may well play as a nidus of coagulation in fully heparinized blood.

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Long-term effects of colestipol (U-26,597 A) on plasma lipids in familial type II hyperbetalipoproteinaemia

Atherosclerosis ◽

10.1016/0021-9150(75)90023-4 ◽

1975 ◽

Vol 22 (3) ◽

pp. 431-445 ◽

Cited By ~ 11

Author(s):

R. Fellin ◽

G. Briani ◽

P. Balestrieri ◽

G. Baggio ◽

M.R. Baiocchi ◽

...

Keyword(s):

Plasma Lipids ◽

Type Ii ◽

Long Term Effects ◽

Familial Type

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Effects of Short-term Treatment with Eptastatin (CS-514), a New Inhibitor of HMG CoA Reductase, on Plasma Lipids, Lipoproteins, and Apolipoproteins in Patients with Non-familial Type II Hyperlipoproteinemia

The Journal of Japan Atherosclerosis Society ◽

10.5551/jat1973.14.6_1305 ◽

1987 ◽

Vol 14 (6) ◽

pp. 1305-1307 ◽

Cited By ~ 1

Author(s):

Tsutomu KAZUMI ◽

Gen YOSHINO ◽

Toshio KASAMA ◽

Ippei IWATANI ◽

Masahide IWAI ◽

...

Keyword(s):

Plasma Lipids ◽

Term Treatment ◽

Type Ii ◽

Short Term ◽

Short Term Treatment ◽

Hmg Coa Reductase ◽

Familial Type ◽

Coa Reductase

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Diet and probucol in lowering cholesterol concentrations. Additive effects on plasma cholesterol concentrations in patients with familial type ii hyperlipoproteinemia

Archives of Internal Medicine ◽

10.1001/archinte.137.10.1429 ◽

1977 ◽

Vol 137 (10) ◽

pp. 1429-1434 ◽

Cited By ~ 23

Author(s):

J. LeLorier

Keyword(s):

Plasma Cholesterol ◽

Type Ii ◽

Additive Effects ◽

Familial Type

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In Vivo Effect of Suloctidil as an Antiplatelet Agent

Thrombosis and Haemostasis ◽

10.1055/s-0038-1646799 ◽

1979 ◽

Vol 41 (03) ◽

pp. 465-474 ◽

Cited By ~ 7

Author(s):

Marcia R Stelzer ◽

Thomas S Burns ◽

Robert N Saunders

Keyword(s):

Ex Vivo ◽

Antiplatelet Agent ◽

Ratio Method ◽

Platelet Aggregate ◽

Permanent Effect ◽

Platelet Aggregates ◽

5 Ht Uptake ◽

High Doses

SummaryThe relationship between the effects of suloctidil in vivo as an antiplatelet agent and in vitro as a modifier of platelet serotonin (5-HT) parameters was investigated. Suloctidil was found to be effective in reducing platelet aggregates formation in the retired breeder rat as determined using the platelet aggregate ratio method (PAR) with an ED50 of 16.1 mg/kg 24 hours post administration. In contrast to the hypothesis that 5-HT depletion is involved in the anti-aggregatory mechanism of suloctidil, no correlation was found between platelet 5- HT content and this antiplatelet activity. Reduction of platelet 5-HT content required multiple injections of high doses (100 mg/kg/day) of suloctidil. Suloctidil administration for 8 days at 100 mg/kg/day, which lowered platelet 5-HT content by 50%, resulted in no permanent effect on ex vivo platelet 5-HT uptake or thrombin-induced release, nor alteration in the plasma 5-HT level. However, these platelets exhibited a short-lived, significant increase in percent leakage of 5-HT after 30 minutes of incubation. Therefore, suloctidil treatment at high doses may with time result in platelet 5-HT depletion, however this effect is probably not related to the primary anti-aggregatory activity of the drug.

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Association of Variables of Coagulation, Fibrinolysis and Acute-phase with Atherosclerosis in Coronary and Peripheral Arteries and those Arteries Supplying the Brain

Thrombosis and Haemostasis ◽

10.1055/s-0038-1653783 ◽

1995 ◽

Vol 73 (03) ◽

pp. 374-379 ◽

Cited By ~ 140

Author(s):

Jürgen Heinrich ◽

Helmut Schulte ◽

Rainer Schönfeld ◽

Ekkehart Köhler ◽

Gerd Assmann

Keyword(s):

Acute Phase ◽

Coronary Atherosclerosis ◽

Plasminogen Activator Inhibitor ◽

Arterial Disease ◽

Plasma Fibrinogen ◽

Base Line ◽

Peripheral Arteries ◽

Brain Vessels ◽

The Brain ◽

D Dimer

SummaryWe investigated the vessel status of coronary and peripheral arteries and those arteries supplying the brain in 929 consecutive male patients admitted to a coronary rehabilitation unit. The severity of coronary atherosclerosis was scored using coronary angiography. Changes in extracranial brain vessels and manifest cerebrovascular disease (CVD) were determined by B-mode ultrasound and Doppler examination. Peripheral arterial disease (PAD) was diagnosed using base-line and stress oscillography. We assessed variables of coagulation, fibrinolysis, and the acute phase response.There was a significant increase in plasma fibrinogen, plasminogen, d-dimer and C-reactive protein (CRP) with increasing severity of coronary heart disease. Compared to men with unaffected arteries, men with 3 diseased coronary arteries had 58% greater d-dimer concentrations. Patients with CVD and PAD, respectively, also had significantly higher fibrinogen, d-dimer and CRP concentrations. We did not find an association between plasminogen activator inhibitor activity and the severity of coronary atherosclerosis.In conclusion, plasma fibrinogen, d-dimer and CRP concentrations were significantly related to atherosclerosis in the coronary, peripheral and extracranial brain arteries.

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A Six Year Prospective Study of Fibrinogen and Other Risk Factors Associated with Mortality in Stable Claudicants

Thrombosis and Haemostasis ◽

10.1055/s-0038-1656361 ◽

1992 ◽

Vol 68 (03) ◽

pp. 261-263 ◽

Cited By ~ 71

Author(s):

A K Banerjee ◽

J Pearson ◽

E L Gilliland ◽

D Goss ◽

J D Lewis ◽

...

Keyword(s):

Risk Factors ◽

Intermittent Claudication ◽

Fibrinogen Level ◽

Past History ◽

Fold Increase ◽

Arterial Disease ◽

Plasma Fibrinogen ◽

Plasma Fibrinogen Level ◽

Factors Associated ◽

Probability Of Death

SummaryA total of 333 patients with stable intermittent claudication at recruitment were followed up for 6 years to determine risk factors associated with subsequent mortality. Cardiovascular diseases were the underlying cause of death in 78% of the 114 patients who died. The strongest independent predictor of death during the follow-up period was the plasma fibrinogen level, an increase of 1 g/l being associated with a nearly two-fold increase in the probability of death within the next 6 years. Age, low ankle/brachial pressure index and a past history of myocardial infarction also increased the probability of death during the study period. The plasma fibrinogen level is a valuable index of those patients with stable intermittent claudication at high risk of early mortality. The results also provide further evidence for the involvement of fibrinogen in the pathogenesis of arterial disease.

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