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
- 2
Gotto Jr A M.
Triglyceride: the forgotten risk factor.
Circulation.
1998;
97(11)
1027-1028
- 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
- 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
- 5
Fyfe T, Baxter R H, Cochran K M, Booth E M.
Plasma-lipid changes after myocardial infarction.
Lancet.
1971;
2(7732)
997-1001
- 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
- 7
Rosenson R S.
Myocardial injury: the acute phase response and lipoprotein metabolism.
J Am Coll Cardiol.
1993;
22(3)
933-940
- 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
- 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
- 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
- 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
- 12
Birchwood B.
Serum lipids and lipoprotein following acute myocardial infarction in women.
Nutr Metab.
1972;
14(1)
38-47
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
- 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
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