title: [HDL level or HDL function as the primary target in preventive cardiology].
abstract: The risk for myocardial infarction can be reduced by almost 50% solely by lowering LDL cholesterol. Despite success reducing LDL and cholesterol, atherosclerosis and myocardial infarction remain significant challenges. However, mechanisms of the reverse cholesterol transport system might be used more effectively in the foreseeable future. Although the benefit of high HDL cholesterol appears to be obvious, most clinical trials aimed at increasing HDL cholesterol failed to generate convincing results. Therefore, the question arises as to whether indeed only HDL level or perhaps rather more HDL function is of considerable therapeutic relevance. If function is the crucial issue drugs such as CETP (cholesteryl ester transfer protein) activators or SR-B1 (scavenger receptor type B-1) upregulators could be beneficial. These types of drugs could improve HDL metabolism and might have beneficial effects despite the fact that they lower HDL levels. Ongoing studies on next generation CETP inhibitors and nicotinic acid will clarify this question and might help in our struggle against atherosclerosis.
authors.affiliation: Dr.-Pohl-Stiftungsprofessur für Präventive Kardiologie, Klinik für Innere Medizin - Kardiologie, UKGM Standort Marburg und Philipps-Universität Marburg, Baldingerstr., 35033, Marburg, Deutschland. juergen.schaefer@uni-marburg.de
authors.forename: J R
authors.initials: JR
authors.lastname: Schaefer
mesh_terms: D000924:Anticholesteremic Agents / Q000009:adverse effects / Q000627:therapeutic use; D050197:Atherosclerosis / Q000097:blood / Q000517:prevention & control*; D000069059:Atorvastatin; D053480:Cholesterol Ester Transfer Proteins / Q000819:agonists / Q000037:antagonists & inhibitors / Q000502:physiology; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood; D002986:Clinical Trials as Topic; D004359:Drug Therapy, Combination; D057239:Early Termination of Clinical Trials; D005260:Female; D005464:Fluorobenzenes / Q000009:adverse effects / Q000627:therapeutic use; D006538:Heptanoic Acids / Q000009:adverse effects / Q000627:therapeutic use; D006801:Humans; D008297:Male; D026901:Membrane Transport Proteins / Q000502:physiology; D009203:Myocardial Infarction / Q000097:blood / Q000401:mortality / Q000517:prevention & control*; D009525:Niacin / Q000009:adverse effects / Q000627:therapeutic use; D011743:Pyrimidines / Q000009:adverse effects / Q000627:therapeutic use; D011758:Pyrroles / Q000009:adverse effects / Q000627:therapeutic use; D011804:Quinolines / Q000009:adverse effects / Q000627:therapeutic use; D016032:Randomized Controlled Trials as Topic; D012016:Reference Values; D000068718:Rosuvastatin Calcium; D051122:Scavenger Receptors, Class B / Q000502:physiology; D013449:Sulfonamides / Q000009:adverse effects / Q000627:therapeutic use; D015996:Survival Rate; D015854:Up-Regulation / Q000502:physiology
chemical_list: D000924:Anticholesteremic Agents; C506642:CETP protein, human; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D005464:Fluorobenzenes; D006538:Heptanoic Acids; D026901:Membrane Transport Proteins; D011743:Pyrimidines; D011758:Pyrroles; D011804:Quinolines; C495124:SCARB1 protein, human; D051122:Scavenger Receptors, Class B; D013449:Sulfonamides; D009525:Niacin; C483909:torcetrapib; D000068718:Rosuvastatin Calcium; D000069059:Atorvastatin