Clot lipids in ischaemic heart disease

Kúnz, F; Zwierzina, Wolf-Dieter; Hörtnagl, Heide

doi:10.1016/0021-9150(83)90197-1

Cited by 4 publications

(2 citation statements)

References 21 publications

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“…Two milliliters of the lipid phase of the extracts was taken for estimation of total phospholipids by a modification 20 of the original method. 21 Thin-layer chromatography and elution of neutral lipids were carried out by a modification 12 of the original method. 22 The eluates were dried, and analyses of cholesterol, 23 glycerides, 24 and free fatty acids 25 were performed in the respective fractions.…”

Section: Lipid Extraction Chromatography and Estimationmentioning

confidence: 99%

“…As viable platelets play an important role in thrombus formation, we produced thrombi from citrated plateletrich plasma (PRP) and observed in CAD an increased content of triglycerides in these thrombi. 12 To examine whether this was a reproducible finding under more physiologically similar experimental conditions, we developed a method for preparing and examining thrombi from native (i.e., not anticoagulated) PPP and PRP to avoid nonphysiological influences of citrate on platelet function, 1314 coagulation, 15 and their interactions. 16 In addition, we had to take into account the fact that the test system and the number of additional examinations were limited by the amount of blood that could be taken from the patients.…”

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confidence: 99%

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Increased lipid binding to thrombi in coronary artery disease. Findings in patients without premedication in native (not anticoagulated) test systems.

Kúnz

Pechlaner

Erhart

et al. 1992

Arterioscler Thromb

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Thrombi and clots were produced from native (i.e., not anticoagulated) platelet-rich and platelet-poor plasma from patients with coronary artery disease and control subjects who had not taken any medication known to influence plasma lipids, coagulation, or platelet aggregation. The clotting times were recorded, and the lipid content of clots, thrombi, platelets, plasma, and high density lipoprotein was analyzed. Thrombi produced from native platelet-rich plasma were 46% heavier in coronary artery disease patients and contained about 20% more phospholipids and free cholesterol and about twice the amount of triglycerides and esterifled cholesterol in both absolute and relative amounts with respect to the corresponding lipids of plasma plus platelets. The elevated content of lipids not only increases the size of the thrombi but also changes their quality because of an increased content in plasmatic lipids, as platelets contain only trace amounts of triglycerides and cholesterol esters. In agreement herewith, fibrinogen and maximal amplitude on the thrombelastogram were increased in coronary artery disease patients, whereas the thrombus-forming time and clotting times of platelet-poor and platelet-rich plasma were shortened, indicating accelerated coagulation and activation of platelets. Analysis of these results suggests a disturbed interrelation in coronary artery disease between lipids and hemostasis, in which platelets, high density lipoprotein, and lipoproteins rich in triglycerides and cholesterol esters may play a role.

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