Abstract
In the treatment of homozygous and therapy-resistant hypercholesterolemia, lipid apheresis enables not only low density lipoprotein (LDL) cholesterol to be lowered by approximately 60%, but also oxidative stress factors to be influenced and adhesion molecules reduced. This was investigated in a group of 12 patients using the heparin-induced extracorporeal LDL precipitation (H.E.L.P.) procedure.A significant lowering of LDL cholesterol and fibrinogen leads to an improvement in rheology and endothelial function, detectable and measurable within approximately 20 h by assessing minimum coronary resistance using positron emission tomography (PET) performed in 35 patients. This effect is detectable even after the first lipid apheresis session (H.E.L.P. procedure), documented in 12 patients.Lipid apheresis appears to be the most effective procedure in the treatment of elevated lipoprotein(a) [Lp(a)]. A chosen group of nine patients with selective elevated Lp(a) illustrated both the influence on endothelial dysfunction, in the shape of sharply increased minimum coronary resistance, and the reduction through lipid apheresis, indicating that Lp(a) seems to exert a similar effect on the vascular wall and vascular function as LDL cholesterol.
Highlights
Lipid apheresis appears to be the most effective procedure in the treatment of elevated lipoprotein(a) [Lp(a)]
We investigated the influence of a single H.E.L.P. apheresis session on the plasma concentration of parameters of lipid peroxidation before as well as after apheresis, as well as 1 week later, immediately prior to the apheresis treatment in 12 patients with heterozygous familial hypercholesterolemia and known CAD who were participating in the chronic weekly H.E.L.P. apheresis program at our hospital
Prior to the H.E.L.P. treatment, the following mean values were measured in the patients: total cholesterol 255 ± 52 mg/dl, low density lipoprotein (LDL) cholesterol 164 ± 44 mg/dl, HDL cholesterol 60 ± 11 mg/dl, and triglyceride 135 ± 70 mg/dl
Summary
Lipid apheresis appears to be the most effective procedure in the treatment of elevated lipoprotein(a) [Lp(a)]. A chosen group of nine patients with selective elevated Lp(a) illustrated both the influence on endothelial dysfunction, in the shape of sharply increased minimum coronary resistance, and the reduction through lipid apheresis, indicating that Lp(a) seems to exert a similar effect on the vascular wall and vascular function as LDL cholesterol. An extension of the half-life of LDL particles in the circulatory system is the result, caused by missing and/or defective LDL receptors or by impaired LDL internalization. This leads to an increased susceptibility of the LDL particles to oxidation. The consequence is a formation of minimally modified LDL and oxidized LDL (OxLDL) [5]
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