Download PDF
Semin Vasc Med 2004; 4(2): 197-202
DOI: 10.1055/s-2004-835378
Copyright © 2004 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001 USA.

Mechanistic Insights and Clinical Relevance of the Interaction between Acute Coronary Syndromes and Lipid Metabolism

Luis C.L Correia1 , Marcel Th.B Twickler2 , Andrei C. Sposito1
  • 1Heart Institute (InCor), Zerbini Foundation, Brasília, Brazil
  • 2Department of Endocrinology and Metabolic Diseases, Catholic University Nijmegen/Radboud University, Nijmegen, The Netherlands
Further Information

Publication History

Publication Date:
11 October 2004 (online)

    Permissions and Reprints

As part of the acute phase reaction, lipid metabolism is significantly altered in patients with unstable coronary syndromes. The clinical relevance and the mechanisms underlying this phenomenon are discussed in this article. Cholesterol reduction takes place in the first hours of an acute coronary event; thus, plasma levels determined at this point should be interpreted with caution. This reduction may be just a consequence of the inflammatory response, or it may be also related to an increase in cellular uptake of cholesterol for tissue repair and hormonal synthesis. A synergistic effect between this predisposition to cholesterol reduction and statin therapy appears to exist during acute coronary syndromes. Triglyceride changes are variable during acute coronary syndromes, and recent data indicate that the pattern of triglyceride variation is a potential risk marker in those patients, possibly because it reflects neurohumoral changes related to the acute phase.

KEYWORDS

Acute coronary syndromes - lipoproteins - cholesterol - triglycerides

REFERENCES

  • 1 Murray C JL, Lopes A D. Global comparative assessments in the health sector. World Health Organization Geneva, Switzerland; 1994
    Google Scholar
  • 2 Gotto Jr A M. Triglyceride: the forgotten risk factor.  Circulation. 1998;  97(11) 1027-1028
    PubMedGoogle Scholar
  • 3 Ahnve S, Angelin B, Edhag O, Berglund L. Early determination of serum lipids and apolipoproteins in acute myocardial infarction: possibility for immediate intervention.  J Intern Med. 1989;  226(5) 297-301
    PubMedGoogle Scholar
  • 4 Brugada R, Wenger N K, Jacobson T A, Clark W S, Cotsonis G, Iglesias A. Changes in plasma cholesterol levels after hospitalization for acute coronary events.  Cardiology. 1996;  87(3) 194-199
    PubMedGoogle Scholar
  • 5 Fyfe T, Baxter R H, Cochran K M, Booth E M. Plasma-lipid changes after myocardial infarction.  Lancet. 1971;  2(7732) 997-1001
    PubMedGoogle Scholar
  • 6 Wattanasuwan N, Khan I A, Gowda R M, Vasavada B C, Sacchi T J. Effect of acute myocardial infarction on cholesterol ratios.  Chest. 2001;  120(4) 1196-1199
    CrossrefPubMedGoogle Scholar
  • 7 Rosenson R S. Myocardial injury: the acute phase response and lipoprotein metabolism.  J Am Coll Cardiol. 1993;  22(3) 933-940
    PubMedGoogle Scholar
  • 8 Pfohl M, Schreiber I, Liebich H M, Haring H U, Hoffmeister H M. Upregulation of cholesterol synthesis after acute myocardial infarction-is cholesterol a positive acute phase reactant?.  Atherosclerosis. 1999;  142(2) 389-393
    CrossrefPubMedGoogle Scholar
  • 9 Gore J M, Goldberg R J, Matsumoto A S, Castelli W P, McNamara P M, Dalen J E. Validity of serum total cholesterol level obtained within 24 hours of acute myocardial infarction.  Am J Cardiol. 1984;  54(7) 722-725
    PubMedGoogle Scholar
  • 10 Ballantyne F C, Melville D A, McKenna J P, Morrison B A, Ballantyne D. Response of plasma lipoproteins and acute phase proteins to myocardial infarction.  Clin Chim Acta. 1979;  99(1) 85-92
    CrossrefPubMedGoogle Scholar
  • 11 Ritland S, Enger S C. Changes in the lipoprotein pattern during two years following myocardial infarction.  Acta Med Scand. 1972;  191(5) 447-450
    PubMedGoogle Scholar
  • 12 Birchwood B. Serum lipids and lipoprotein following acute myocardial infarction in women.  Nutr Metab. 1972;  14(1) 38-47
    PubMedGoogle Scholar
  • 13 Ryder R E, Hayes T M, Mulligan I P, Kingswood J C, Williams S, Owens D R. How soon after myocardial infarction should plasma lipid values be assessed?.  Br Med J (Clin Res Ed). 1984;  289(6459) 1651-1653
    PubMedGoogle Scholar
  • 14 Kawano M, Namai K, Yaginuma T, Kawakami M, Kanazawa Y. Earlier decrease in plasma lipids than increase in C-reactive protein during very acute phase of myocardial infarction.  Atherosclerosis. 2001;  156(2) 477-478
    CrossrefPubMedGoogle Scholar
  • 15 Chatelain P, Latour J G, Tran D, de Lorgeril M, Dupras G, Bourassa M. Neutrophil accumulation in experimental myocardial infarcts: relation with extent of injury and effect of reperfusion.  Circulation. 1987;  75(5) 1083-1090
    PubMedGoogle Scholar
  • 16 Bell D, Jackson M, Millar A M, Nicoll J J, Connell M, Muir A L. The acute inflammatory response to myocardial infarction: imaging with indium-111 labelled autologous neutrophils.  Br Heart J. 1987;  57(1) 23-27
    PubMedGoogle Scholar
  • 17 Ettinger W H, Varma V K, Sorci-Thomas M et al.. Cytokines decrease apolipoprotein accumulation in medium from Hep G2 cells.  Arterioscler Thromb. 1994;  14(1) 8-13
    PubMedGoogle Scholar
  • 18 Sammalkorpi K T, Valtonen V V, Maury C P. Lipoproteins and acute phase response during acute infection. Interrelationships between C-reactive protein and serum amyloid-A protein and lipoproteins.  Ann Med. 1990;  22(6) 397-401
    PubMedGoogle Scholar
  • 19 de Beer F C, Soutar A K, Baltz M L, Trayner I M, Feinstein A, Pepys M B. Low density lipoprotein and very low density lipoprotein are selectively bound by aggregated C-reactive protein.  J Exp Med. 1982;  156(1) 230-242
    CrossrefPubMedGoogle Scholar
  • 20 Slunga L, Johnson O, Dahlen G H, Eriksson S. Lipoprotein(a) and acute-phase proteins in acute myocardial infarction.  Scand J Clin Lab Invest. 1992;  52(2) 95-101
    PubMedGoogle Scholar
  • 21 Fresco C, Maggioni A P, Signorini S et al.. Variations in lipoprotein levels after myocardial infarction and unstable angina: the LATIN trial.  Ital Heart J. 2002;  3(10) 587-592
    PubMedGoogle Scholar
  • 22 Correia L C, Sposito A C, Passos L C et al.. Short-term effect of atorvastatin (80 mg) on plasma lipids of patients with unstable angina pectoris or non-Q-wave acute myocardial infarction.  Am J Cardiol. 2002;  90(2) 162-164
    CrossrefPubMedGoogle Scholar
  • 23 Correia L C, Magalhaes L P, Santana O et al.. Effect of atorvastatin (80 mg) on recurrent ischemia in unstable angina pectoris or non-ST-elevation acute myocardial infarction.  Am J Cardiol. 2003;  91(11) 1355-1357
    CrossrefPubMedGoogle Scholar
  • 24 Correia L C, Sposito A C, Lima J C et al.. Anti-inflammatory effect of atorvastatin (80 mg) in unstable angina pectoris and non-Q-wave acute myocardial infarction.  Am J Cardiol. 2003;  92(3) 298-301
    CrossrefPubMedGoogle Scholar
  • 25 Krauss R M, Grunfeld C, Doerrler W T, Feingold K R. Tumor necrosis factor acutely increases plasma levels of very low density lipoproteins of normal size and composition.  Endocrinology. 1990;  127(3) 1016-1021
    PubMedGoogle Scholar
  • 26 Feingold K R, Grunfeld C. Tumor necrosis factor-alpha stimulates hepatic lipogenesis in the rat in vivo.  J Clin Invest. 1987;  80(1) 184-190
    PubMedGoogle Scholar
  • 27 Querfeld U, Ong J M, Prehn J et al.. Effects of cytokines on the production of lipoprotein lipase in cultured human macrophages.  J Lipid Res. 1990;  31(8) 1379-1386
    PubMedGoogle Scholar
  • 28 Kern P A. Recombinant human tumor necrosis factor does not inhibit lipoprotein lipase in primary cultures of isolated human adipocytes.  J Lipid Res. 1988;  29(7) 909-914
    PubMedGoogle Scholar
  • 29 Friedman G, Barak V, Chajek-Shaul T et al.. Recombinant human interleukin-1 suppresses lipoprotein lipase activity, but not expression of lipoprotein lipase mRNA in mesenchymal rat heart cell cultures.  Biochim Biophys Acta. 1991;  1089(1) 83-87
    PubMedGoogle Scholar
  • 30 Gerritsen J, TenVoorde B J, Dekker J M et al.. Measures of cardiovascular autonomic nervous function: agreement, reproducibility, and reference values in middle age and elderly subjects.  Diabetologia. 2003;  46(3) 330-338
    PubMedGoogle Scholar
  • 31 Klingenspor M, Ebbinghaus C, Hulshorst G et al.. Multiple regulatory steps are involved in the control of lipoprotein lipase activity in brown adipose tissue.  J Lipid Res. 1996;  37(8) 1685-1695
    PubMedGoogle Scholar
  • 32 Pecquery R, Leneveu M C, Giudicelli Y. In vivo desensitization of the beta, but not the alpha 2-adrenoreceptor-coupled-adenylate cyclase system in hamster white adipocytes after administration of epinephrine.  Endocrinology. 1984;  114(5) 1576-1583
    PubMedGoogle Scholar
  • 33 Lefebvre P, Luyckx A, Bacq Z M. Effects of denervation on the metabolism and the response to glucagon of white adipose tissue of rats.  Horm Metab Res. 1973;  5(4) 245-250
    PubMedGoogle Scholar
  • 34 Omland T, Aarsland T, Aakvaag A, Lie R T, Dickstein K. Prognostic value of plasma atrial natriuretic factor, norepinephrine and epinephrine in acute myocardial infarction.  Am J Cardiol. 1993;  72(3) 255-259
    CrossrefPubMedGoogle Scholar

 Dr.
Andrei C SpósitoM.D. Ph.D. 

Director, Department of Cardiology, Instituto do Coração (InCor-DF)-Fundação Zerbini

Estrada do Contorno do Bosque-Cruzeiro Novo, Brasília

DF, Brazil, 70685.700