Platelet Function and Platelet Phospholipids in Patients With Hyperbetalipoproteinemia

ABSTRACT. Platelet function, intra‐vascular coagulation (IVC) and fibrinolysis were studied in 85 patients with Type II hyperlipo‐proteinaemia, 36 with Type IV hypertriglyce‐ridaemia and 36 normal subjects. The effects of clofibrate and nicotinic acid therapy on their plasma lipid concentrations, platelet behaviour, IVC and fibrinolysis were also evaluated. Untreated Type II patients had platelet hyperreactivity to aggregating agents and increased nucleotide release. Their platelet phospholipid content was quantitatively and qualitatively altered. The mechanism of platelet hyperreactivity appears to be related to their ability to convert AA to cyclic endoperoxides and thromboxanes. Although both groups of common hyperlipidaemias had accelerated activation of the blood coagulation systems, the Type II patients had worse blood alterations than the Type IV patients did. Furthermore, our data also suggests that in hypercholesterolaemia platelets appear to mediate these blood changes. Clofibrate treatment in Type II patients improved the platelet reactivity, reversed IVC and stimulated fibrinolysis without altering their plasma lipid levels. In contrast, in Type IV patients, clofibrate therapy significantly lowered plasma triglycerides but did not alter the blood coagulation changes nor did it stimulate fibrinolysis. Thrombo‐embolic complications were common in both groups of hyperlipida etnias but more so in Type II patients. A correlation therefore appears to exist between laboratory evidence of platelet reactivity and IVC and increased incidence of thromboembolic complications. Taken together, these observations suggest that anti‐platelet drugs may be useful in the prevention of thrombo‐embolic complications in Type II patients. In contrast, in hypertriglyceridaemia, impairment of the fibrinolytic system is the likely mechanism by which these thrombotic events occur. Unfortunately, simple preventive treatments to stimulate fibrinolysis are not yet available.

Section: Discussionsupporting

confidence: 92%

Platelets, Intravascular Coagulation and Fibrinolysis in Hyperlipidaemias: Relationship to Thrombo‐Embolic Complications

Carvalho

Lees

1980

“…Changes in the coagulation system have been related to increased tendency to thrombosis and to activation of this system during ongoing thrombosis. We observed a moderate but not significant shortening of the whole blood clotting time possibly associated with an increased platelet activity in the coagulation process (1,11). The other coagulation factors and activities which have been associated with a "hypercoagulable" state were normal, and we could not demonstrate the tendency to hyperfibrinogenemia reported by others in such patients (7).…”

Section: Inhibitory Effect Of Prostacyclin (Pg12) On Collagen-induccontrasting

confidence: 68%

“…PF-3 measured in PRP has been reported to be increased (1,3) and normal (2) in patients with hypercholesterolemia. It may be suggested that, owing to abnormalities in the platelet membrane (8), the isolation procedure used induced more release of PF-3 in the patients, leaving less PF-3 to be detected in the isolated platelets.…”

Section: Inhibitory Effect Of Prostacyclin (Pg12) On Collagen-inducmentioning

confidence: 97%

Platelets and Coagulation in Patients with Familial Hypercholesterolemia (Type Ha)

Nordøy

Brox

Holme

et al. 1983

Self Cite

Seventeen subjects with hypercholesterdemia (type IIa) were compared with 11 normocholesterolemic family members (controls) with similar dietary habits. The type IIa subjects had a shorter bleeding time. Beta-thromboglobulin in plasma and thromboxane B2 and malondialdehyde released from platelets before and after stimulation with collagen or thrombin were similar. No differences in platelet sensitivity to adenosine diphosphate, thrombin or collagen were observed. Gel-filtered platelets from type IIa subjects had a tendency to spontaneous aggregation and lower procoagulant activity. Platelet sensitivity to prostacyclin was slightly higher in type IIa subjects. No differences in a seriea of coagulation parameters were observed b e tween the groups. This study has shown some deviations from normal in platelets from subjects with familial hyperchdelstemlemla. These changes may contribute to tbe increased tendency to occlusive vascular in such subjects.Abbreviations: BTG = B-thromboglobulin, MDA = malondialdehyde, TXB, = thromboxane B2, ADP = adenosine diphosphate, PGI, = prostacyclin, W E , = prostaglandin E,, CAMP = cyclic adenosine monophosphate, PRP = platelet-rich plasma, PPP= platelet-poor plasma, PA = platelet aggregation, SPA = spontaneous platelet aggregation, ~0 1 1 ,~~ = the lowest concentration of collagen giving about 70% platelet aggregation, IDso = the concentration of prostacyclin needed to reduce collagen-induced platelet aggregation by 50%, PPCA = platelet procoagulant activity, PF-3 = platelet factor 3, HDL = high density lipoprotein, LDL = low density lipoprotein.

“…However, the concentration of arachidonic acid was low compared to that of Danes. The daily consumption of eicosapentaenoic acid of Eskimos was 2-6 g (1) while that of Danes is about one tenth. In the Eskimos, Dyerberg and Bang (4) found a decreased platelet aggregability after stimulation with ADP and collagen and an increased bleeding time.…”

Section: H 0 Bang Andj Dyerhergmentioning

confidence: 95%

Personal Reflections on the Incidence of Ischaemic Heart Disease in Oslo during the Second World War

Bang

Dyerberg

1981

The dietary changes in Norway and especially in Oslo during the Second World War, with reduced fat intake and increased consumption of fish and fish products, was paralleled by a reduced incidence of and mortality from IHD. This was prohably caused to a high degree by reduced platelet aggregability leading to a reduced tendency to thrombosis. We suggest that the mechanism behind this reduction was a changed balance between proand anti-aggregatory prostaglandins towards the anti-aggregatory side, caused by eicosapentaenoic acid from fish lipids. Furthermore, hypocholesterolaemia due to reduced fat intake and increased consumption of polyunsaturated fatty acids certainly contributed to this effect by reducing platelet aggregability . K c~y icwrds: diet, fish oil, ischaemic heart disease, platelet aggregation, Second World War. Acta Med Scand 210: 245, 1981.