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Published on: June 5, 2019
Shear stress-dependent platelet function after LDL cholesterol apheresis
Lukas E Spieker1, Frank Ruschitzka, Juan J Badimon
1Cardiology, University Hospital, CH-8091 Zürich, Switzerland. lukas.spieker@usz.ch
Insights
LDL apheresis significantly reduces platelet adhesion in patients with coronary artery disease. This lipid-lowering therapy also decreases fibrinogen and C-reactive protein levels, impacting cardiovascular health.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Lipidology
Background:
- Platelets are key in acute coronary syndrome (ACS), driving thrombus formation and atherosclerotic lesion progression.
- Arterial occlusion due to platelet thrombi is a major factor in ACS and stroke.
- Understanding platelet function is critical for managing cardiovascular disease.
Purpose of the Study:
- To assess the impact of LDL apheresis on platelet function in patients with coronary artery disease.
- To investigate how lipid lowering affects shear-stress dependent platelet adhesion.
Main Methods:
- Six patients with coronary artery disease underwent LDL apheresis.
- Blood samples were collected pre- and post-apheresis.
- Shear-stress dependent platelet adhesion was measured using whole blood in a cone-and-plate viscometer.
Main Results:
- LDL apheresis significantly reduced LDL cholesterol, HDL cholesterol, triglycerides, fibrinogen, lipoprotein (a), and CRP levels.
- Shear-stress dependent platelet adhesion was significantly reduced post-apheresis.
- Heparin administration prolonged clotting time but did not affect platelet adhesion.
Conclusions:
- A single LDL apheresis session effectively reduces shear-stress dependent platelet adhesion in coronary artery disease patients.
- LDL apheresis offers benefits beyond cholesterol reduction by lowering fibrinogen and CRP.
- These findings highlight LDL apheresis as a potential therapeutic strategy for modulating platelet activity in cardiovascular disease.
Background:
Platelets play a crucial role in the pathogenesis of acute coronary syndrome (ACS). Thrombus formation with subsequent arterial occlusion is a major determinant in ACS and stroke. Platelets also essentially contribute to the development and progression of atherosclerotic lesions. The aim of the present study was to investigate the effects lipid lowering by LDL apheresis on platelet function in patients with coronary artery disease.
Methods:
In six patients with angiographically proven coronary artery disease, venous blood samples were obtained before and after LDL cholesterol apheresis. Citrated whole blood (200 microl) was circulated in polystyrene wells at a shear rate of 1875 s(-1) for 2 min with a rotating teflon cone. Shear-stress dependent platelet adhesion was measured before and after apheresis.
Results:
After apheresis, there were significant reductions in LDL (-58%) and HDL (-17%) cholesterol, triglycerides (-43%), fibrinogen (-52%), lipoprotein (a) (-57%) and CRP (-57%) levels. LDL apheresis significantly reduced shear-stress dependent platelet adhesion. Bolus administration of heparin significantly prolonged activated clotting time, but had no significant effect on platelet adhesion or aggregates.
Conclusions:
In patients with coronary artery disease, shear-stress dependent platelet adhesion is reduced by a single LDL apheresis. In addition to its cholesterol-lowering effect, LDL apheresis reduces circulating levels of fibrinogen and C-reactive protein.
