Herz

, Volume 24, Issue 1, pp 13–25 | Cite as

Labordiagnostik in der präventiven Kardiologie

  • Muhidien Soufi
  • Bernd Noll
  • Matthias Herzum
  • Bernd Simon
  • Armin Steinmetz
  • Bernhard Maisch
  • Jürgen R. Schaefer
Article
  • 33 Downloads

Zusammenfassung

In den letzten Jahren wurden zahlreiche kardiovaskuläre Risikofaktoren identifiziert. Ihre Bestimmung optimiert die Risikoabschätzung, die jedoch nach wie vor eine „Schätzung” bleibt. Die sichere Vorhersage eines drohenden kardiovaskulären Ereignisses ist derzeit noch immer nicht möglich. Entsprechend sorgfältig muß der Einsatz einer aufwendigen Labordiagnostik geplant und auf den Einzelfall bezogen eingesetzt werden.

Häufig reicht es für die notwendigen therapeutischen Entscheidungen aus, das Gesamtcholesterin, die Triglyzeride, das HDL-sowie LDL-Cholesterin und das Lp(a) zu bestimmen. Eine weiterführende Diagnostik sollte bei schwereren Dyslipidämien, familiär gehäuft auftretender koronarer Herzkrankheit und bei Patienten mit einer koronaren Herzkrankheit ohne offenkundige Stoffwechselstörungen durchgeführt werden. Neben den Laborparametern sind Faktoren wie die genetische Belastung und Familienanamnese sowie die klinischen Daten (vorbekannte koronare Herzkrankheit oder arterielle Verschlußkrankheit, arterielle Hypertonie, Diabetes mellitus, Raucher) für eine Risikostratefizierung von großer Bedeutung.

Die alleinige Betrachtung der Laborparameter wird in der Regel keine suffiziente Beratung und Therapie der Betroffenen ermöglichen. Mittlerweile stehen „Expertensysteme” bereit, die eine Risikoabschätzung unter Eingabe der Laborparameter (LDL-Cholesterin, HDL-Cholesterin, Triglyzeride) sowie relevanter klinischer Angaben (Blutdruck, familiäre Belastung, Anamnese etc.) erlauben. Der Zugriff zu diesem System ist unter der Adresse „http://www.chd-taskforce.com” im Internet möglich.

Schüsselwörter

Labordiagnostik Präventive Kardiologie Lipoproteine Risikofaktoren 

Laboratory procedures in preventive cardiology

Abstract

In recent years a large number of coronary artery disease risk factors were discovered. The knowledge of these factors improves the estimate of the coronary artery disease (CAD) risk — however it still remains to be only an “estimate”. A perfect prediction of an upcoming CAD event is not possible, despite all high score laboratory technology. Therefore the use of specialized laboratory procedures should be applied carefully.

Knowing the blood levels of cholesterol, triglycerides, HDL-and LDL-cholesterol and Lp(a) can be sufficient for many therapeutical decisions. Severe dyslipidemia, familial CAD and CAD without any obvious reasons demand a more specialized work-up, however, risk stratification factors such as family history, clinical history (CAD, hypertension, diabetes mellitus, smoker) and genetics are crucial, apart from the above mentioned laboratory values.

Purely on the basis of the lipidologic baseline concentrations we can’t give well based recommendations for the treatment of individual patients. Currently there are expert systems available which allow a risk estimate once important laboratory values (LDL cholesterol, HDL cholesterol, Triglycerides) as well as clinical data (blood pressure, family history, clinical history) are available. This system can be accessed by internet under „http://www.chd-taskforce.com”.

Key Words

Laboratory procedures Preventive Cardiology Lipoproteins Risk factors 
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Literatur

  1. 1.
    Ahrens EHJ, Hirsch J, Oette K, et al. Carbohydrate-induced and fat-induced lipemia. Trans Assoc Am Phys 1961;74:134–46.PubMedGoogle Scholar
  2. 2.
    Alaupovic P. Apolipoproteins and lipoproteins. Atherosclerosis 1971;13:141–6.PubMedCrossRefGoogle Scholar
  3. 3.
    Amouyel P, Brousseau T, Fruchart JC, et al. Apolipoprotein Eepsilon 4 allele and Alzheimer’s disease [letter]. Lancet 1993;342:1309.PubMedGoogle Scholar
  4. 4.
    Assmann G, Schmitz G, Menzel HJ, et al. Apolipoprotein E polymorphism and hyperlipidemia. Clin Chem 1984;30:641–3.PubMedGoogle Scholar
  5. 5.
    Assmann G, Funke H, Jabs HU. Analytical procedures for the detection and characterization of apolipoprotein E mutants. Am Heart J 1987;113:598–603.PubMedCrossRefGoogle Scholar
  6. 6.
    Aufenanger J, Weber U, Haux P, et al. A specific method for direct determination of lipoprotein cholesterol in electrophoretical patterns. Clin Chim Acta 1988;177:197–208.PubMedCrossRefGoogle Scholar
  7. 7.
    Aufenanger J. Lipiddiagnostik im Routinelabor. Labor-Medizin 1989;12:386–95.Google Scholar
  8. 8.
    Bachorik PS. Collection of blood samples for lipoprotein analysis. Clin Chem 1982;28:1375–8.PubMedGoogle Scholar
  9. 9.
    Bernard S, Moulin P, Lagrost L, et al. Association between plasma HDL-cholesterol concentration and Taq1B CETP gene polymorphism in non-insulin-dependent diabetes mellitus. J Lipid Res 1998;39:59–65PubMedGoogle Scholar
  10. 10.
    Blasi F, Denti F, Erba M, et al. Detection of Chlamydia pneumoniae but not Helicobacter pylori in atherosclerotic plaques of aortic aneurysms. J Clin Microbiol 1996;34:2766–9.PubMedGoogle Scholar
  11. 11.
    Brink PA, Steyn LT, Coetzee GA, et al. Familial hypercholesterolemia in South African Afrikaners. Pvu II and StuI DNA polymorphisms in the LDL-receptor gene consistent with a predominating founder gene effect. Hum Genet 1987;77:32–5.PubMedCrossRefGoogle Scholar
  12. 12.
    Cremer P, Seidel D, Wieland H. Quantitative Lipoproteinelektrophorese: Ihre routinemäßige Anwendung im Vergleich mit anderen Verfahren zur differenzierten Untersuchung des Fettstoffwechsels. Lab Med 1985;9:39–51.Google Scholar
  13. 13.
    Duchateau P, Rader D, Duverger N, et al. Tangier disease: isolation and characterization of LpA-I, LpA-II, LpA-I: A-II and LpA-IV particles from plasma. Biochim Biophys Acta 1993;1182:30–6.PubMedGoogle Scholar
  14. 14.
    Fredrickson DS, Lees RS. A system for phenotyping hyperlipo-proteinemia. Circulation 1965;31:321–7.PubMedGoogle Scholar
  15. 15.
    Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of low density lipoprotein cholesterol without use of the preparative ultracentrifuge. Clin Chem 1972;18:499–502.PubMedGoogle Scholar
  16. 16.
    Fruchart JC, Ailhaud G, Bard JM. Heterogeneity of high density lipoprotein particles. Circulation 1993;87:III22–7.PubMedGoogle Scholar
  17. 17.
    Fumeron F, Betoulle D, Luc G, et al. Alcohol intake modulates the effect of a polymorphism of the cholesteryl ester transfer protein gene on plasma high density lipoprotein and the risk of myocardial infarction. J Clin Invest 1995;96:1664–71.PubMedCrossRefGoogle Scholar
  18. 18.
    Gebührenordnung für Ärzte (GOÄ). Mit Gebührenverzeichnis für ärztliche Leistungen (Stand 01.01.1996). Köln: Deutscher Ärzteverlag, Oktober 1997 (Nachdruck).Google Scholar
  19. 19.
    Gerdes C, Fisher RM, Nicaud V, et al. Lipoprotein lipase variants D9N and N291S are associated with increased plasma triglyzeride and lower high-density lipoprotein cholesterol concentrations: studies in the fasting and postprandial states: the European Atherosclerosis Research Studies. Circulation 1997; 96:733–40.PubMedGoogle Scholar
  20. 20.
    Gofman JW, Lindgreen FT, Elliot H. Ultracentrifugal studies of lipoproteins of human serum. J Biol Chem 1949;179:973–8.PubMedGoogle Scholar
  21. 21.
    Hackler R, Schaefer JR, Motzny S, et al. Rapid determination of apolipoprotein E phenotypes from whole plasma by automated isoelectric focusing using PhastSystem and immunofixation. J Lipid Res 1994;35:153–8.PubMedGoogle Scholar
  22. 22.
    Hagen RD, Upton SJV, Avakian EV, et al. Increase in serum lipid and lipoprotein levels with movement from the supine to standing position in adult men and women. Prev Med 1986;15:85–8.Google Scholar
  23. 23.
    Hixson JE, Vernier DT. Restriction isotyping of human apolipoprotein E by gene amplification and cleavage with HhaI. J Lipid Res 1990;31:545–8.PubMedGoogle Scholar
  24. 24.
    Hoffer MJ, Bredie SJ, Boomsma DI, et al. The lipoprotein lipase (Asn291→Ser) mutation is associated with elevatedlipid levels in families with familial combined hyperlipidaemia. Atherosclerosis 1996;119:159–67.PubMedCrossRefGoogle Scholar
  25. 25.
    Horvath C, El Rassi Z. Polytopic chromatography of proteins. Chromatogr Forum 1986;10:49–56.Google Scholar
  26. 26.
    Kinoshita M, Okazaki M, Kato H, et al. Analysis of apolipoproteins in high density lipoproteins by high performance liquid chromatography. J Biochem 1984;95:1111–8.PubMedGoogle Scholar
  27. 27.
    Kuivenhoven JA, de Knijff P, Boer Jm, et al. Heterogeneity at the CETP gene locus. Influence on plasma CETP concentrations and HDL cholesterol levels. Arterioscler Thromb Vasc Biol 1997;17:560–8.PubMedGoogle Scholar
  28. 28.
    Kuivenhoven JA, Jukema JW, Zwinderman AH, et al. The role of a common variant of the cholesteryl ester transfer protein gene in the progression of coronary atherosclerosis. The Regression Growth Evaluation Statin Study Group. N Engl J Med 1998;338:86–93.PubMedCrossRefGoogle Scholar
  29. 29.
    Lolin YI, Sanderson JE, Cheng SK, et al. Hyperhomocysteinaemia and premature coronary artery disease in the Chinese. Heart 1996;76:117–22.PubMedCrossRefGoogle Scholar
  30. 30.
    Mailly F, Tugrul Y, Reymer PW, et al. A common variant in the gene for lipoprotein lipase (Asp9→Asn). Functional implications and prevalence in normal and hyperlipidemic subjects. Arterioscler Thromb Vasc Biol 1995;15:468–78.PubMedGoogle Scholar
  31. 31.
    Malinow MR, Ducimetiere P, Luc G, et al. Plasma homocyst(e)ine levels and graded risk for myocardial infarction: findings in two populations at contrasting risk for coronary heart disease. Atherosclerosis 1996;126:27–34.PubMedCrossRefGoogle Scholar
  32. 32.
    Montalescot G. Homocysteine: the new player in the field of coronary risk. Heart 1996;76:101–2.PubMedCrossRefGoogle Scholar
  33. 33.
    Motti C, Funke H, Rust S, et al. Using mutagenic polymerase chain reaction primers to detect carriers of familial defective apolipoprotein B-100. Clin Chem 1991;7:1762–6.Google Scholar
  34. 34.
    Muhlestein JB, Anderson JL, Hammond EH, et al. Infection with Chlamydia pneumoniae accelerates the development of atherosclerosis and treatment with azithromycin prevents it in a rabbit model. Circulation 1998;97:633–6.PubMedGoogle Scholar
  35. 35.
    Noble RP. Electrophoretic separation of plasma lipoproteins in agarose gel. J Lipid Res 1968;9:693–700.PubMedGoogle Scholar
  36. 36.
    Page ICH, Moinuddin M. The effect of venous occlusion on serum cholesterol and total protein concentration—a warning. Circulation 1962;25:561–2.Google Scholar
  37. 37.
    Pullinger CR, Hennessy LK, Chatterton JE, et al. Familial ligand-defective apolipoprotein B. Identification of a new mutation that decreases LDL receptor binding affinity. J Clin Invest 1995;95: 1225–34.PubMedCrossRefGoogle Scholar
  38. 38.
    Rader DJ, Castro G, Zech LA, et al. In vivo metabolism of apolipoprotein A-I on high density lipoprotein particles LpA-I and LpA-I, A-II. J Lipid Res 1991;32:1849–59.PubMedGoogle Scholar
  39. 39.
    Riesen WF. Lipiddiagnostik im Speziallaboratorium. Labor-Medizin 1989;12:396–403.Google Scholar
  40. 40.
    Saikku P, Leinonen M, Mattila K, et al. Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet 1988;2:983–6.PubMedCrossRefGoogle Scholar
  41. 41.
    Schaefer JR, Hackler R, Brand S, et al. Apolipoprotein AI, AII, and AIV isoforms in plasma determined by automated isoelectric focusing with PhastSystem and immunofixation. Clin Chem 1995;41:76–81.PubMedGoogle Scholar
  42. 42.
    Scott J. Testing for Alzheimer’s. Nature 1985;366:502.CrossRefGoogle Scholar
  43. 43.
    Scott J. Apolipoprotein E and Alzheimer’s disease. Lancet 1993;342:696.PubMedCrossRefGoogle Scholar
  44. 44.
    Soutar AK, Knight BL, Patel D. Identification of a point mutation in growth factor repeat C of the low density lipoprotein-receptor gene in a patient with homozygous familial hypercholesterolemia that affects ligand binding and intracellular movement of receptors. Proc Natl Acad Sci USA 1989;86:4166–70.PubMedCrossRefGoogle Scholar
  45. 45.
    Utermann G, Menzel HJ, Kraft HG, et al. Lp(a) glycoprotein phenotypes. Inheritance and relation to Lp(a)-lipoprotein concentrations in plasma. J Clin Invest 1987;80:458–65.PubMedCrossRefGoogle Scholar
  46. 46.
    Utermann G, Hees M, Steinmetz A. Polymorphism of apolipoprotein E and occurrence of dysbetalipoproteinaemia in man. Nature 1977;269:604–7.PubMedCrossRefGoogle Scholar
  47. 47.
    Young SG, Pullinger CR, Zysow BR, et al. Four new mutations in the apolipoprotein B gene causing hypobetalipoproteinemia, including two different frameshift mutations that yield truncated apolipoprotein B protein of identical length. J Lipid Res 1993;34:501–7.PubMedGoogle Scholar

Copyright information

© Urban & Vogel 1999

Authors and Affiliations

  • Muhidien Soufi
    • 1
  • Bernd Noll
    • 1
  • Matthias Herzum
    • 1
  • Bernd Simon
    • 1
  • Armin Steinmetz
    • 2
  • Bernhard Maisch
    • 1
  • Jürgen R. Schaefer
    • 1
  1. 1.Zentrum für Innere Medizin, Klinik für Innere Medizin und KardiologiePhilipps-Universität MarburgMarburg
  2. 2.Abteilung für Innere MedizinSt. Nikolaus-Stiftshospital GmbHAndernach

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