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Research Article| Volume 20, ISSUE 1, P43-47, February 1999

LDL-apheresis: questions for the future

      LDL particles constitute the predominant form of transport of cholesterol towards tissue. It is now obvious that LDL particles are one of the major causative factors in the development of coronary heart disease (CHD). Numerous studies have established the relationship between plasma LDL-cholesterol levels and coronary heart disease [

      Shepherd J et al. Prevention of coronary heart disease with pravastatin in men with hypercholestérolemia. N Engl J Med 1995;333:1301–1307

      ,

      Smith GD, Song F, Sheldon TA. Cholesterol lowering and mortality: the importance of considering initial level of risk. BMJ 1993;306:1367–1373

      ,

      Scandinavan simvastatin survival study group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the scandinavian simvastatin survival study (4S). Lancet 1994;344:1383–1389

      ]. Perhaps the most convincing evidence that these lipoproteins are causative factors in this disease is the genetic disorder, familial hypercholesterolemia. Homozygous patients develop massive LDL concentrations and frequently die within the second decade of life from complications of atherosclerosis.
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      References

      1. Shepherd J et al. Prevention of coronary heart disease with pravastatin in men with hypercholestérolemia. N Engl J Med 1995;333:1301–1307

      2. Smith GD, Song F, Sheldon TA. Cholesterol lowering and mortality: the importance of considering initial level of risk. BMJ 1993;306:1367–1373

      3. Scandinavan simvastatin survival study group. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the scandinavian simvastatin survival study (4S). Lancet 1994;344:1383–1389

      4. Aengevaeren WRM, Kroon AA, Stalenhoef AFH, Uijen GJH, van de Werf T. Low density lipoprotein apheresis improves regional myocardial perfusion in patients with hypercholesterolemia and extensive coronary heart disease. JACC 1996;28:1696–1704

      5. Dairou F, Assogba U, Bruckert E, De Gennes JL, Truffert J. Efficacité biologique des LDL aphérèses dans les hypercholestérolémies majeures. Ann Med Interne 1994;145(5):328–332

      6. Dairou F, Rottembourg G, De Gennes JL, Assogba U, Bruckert E, Jacobs C, Truffert J. Comparaison des traitements des formes sévères d'hypercholestérolémie familiale par échange plasmatique total et épuration sélective des lipoproteines de basse densité (LDLaphérèse). Presse médicale 1988;33(17):1679–1682

      7. Bosch T, Schmidt B, Blumenstein M, Gurland HJ. Lipid apheresis by hemoperfusion: in vitro efficacy and ex vivo biocompatibility of a new low-density lipoprotein adsorber compatible with human whole blood. Arti Org 1993;17:640–652

      8. Klein JM, Drobinski G, Bruckert E, Dairou F, Thomas D, De Gennes JL, Grogosgeat Y. Results of serial coronary angiography in patients with homozygous familial hypercholesterolemia. European Heart J 1988;9:1067–1073

      9. Jaudon M-C, Assogba U, Bourely B, Dairou F, Bruckert E, Delattre J. Selenium deficiency in hypercholesterolemic patients treated by LDL apheresis. Lancet 1994;343:1160

      10. Assogba U, Lepage S, Bruckert E, Bonnefont-Rousselot D, Dairou F, DE Gennes JL, Delattre J. Blood antioxidants (vitamin E and beta-carotene) in long-term low density lipoprotein apheresis. Clin Chim Acta 1995;235:147–157

      11. Persson-Moschos M, Bonnefont-Rousselot D, Assogba U, Bruckert E, Jaudon MC, Delattre J, Akesson B. Preferential depletion of selenoprotein P in hypercholesterolemic patients treated by LDL-apheresis. Clin Chim Acta 1995;204:209–212

      12. Dejager S, Bruckert E, Chapman MJ. Diminished oxidative resistance of low density lipoprotein subspecies in combined hyperlipidemia. J Lipid Res 1993;34:295–308

      13. Faucher C, Albert C, Beaufils H, Jouanneau C, Dupouet L. Remission of a refractory nephrotic syndrome after low-density lipoprotein apheresis based on dextrant sulphate adsorption. Nephrol Dial Transplant 1997;12:1037–1039