Short-term Prognostic Value of Lipid Measurements in Patients with Angina pectoris

Ignasi Bolibar; Arnold von Eckardstein; Gerd Assmann; Simon Thompson; The ECAT Angina Pectoris Study Group

doi:10.1055/s-0037-1614155

Thrombosis and Haemostasis, Inhaltsverzeichnis

Thromb Haemost 2000; 84(06): 955-960
DOI: 10.1055/s-0037-1614155

Review Article

Schattauer GmbH

Short-term Prognostic Value of Lipid Measurements in Patients with Angina pectoris

Ignasi Bolibar

¹Servei d’Epidemiología Clinica y Salud Pública, Barcelona, Spain

,

Arnold von Eckardstein

²Institut für Klinische Chemie und Laboratoriumsmedizin and Institut für Arterioskleroseforschung, Münster, Germany

,

Gerd Assmann

²Institut für Klinische Chemie und Laboratoriumsmedizin and Institut für Arterioskleroseforschung, Münster, Germany

,

Simon Thompson

³Department of Medical Statistics and Evaluation, Imperial College School of Medicine, Hammersmith Hospital, London, UK

,

The ECAT Angina Pectoris Study Group

› Institutsangaben

Abstract

Summary

We studied the role of various markers of lipid metabolism, hemostasis and inflammation in a two year follow-up of 3000 patients with angina pectoris, during which time 106 patients experienced myocardial infarction or sudden coronary death. Low levels of high density lipoprotein (HDL) cholesterol and of apolipoprotein (apo) A-I were most strongly associated with increased coronary risk. The relative risk per standard deviation increase was 0.68 for HDL cholesterol (95% confidence interval 0.55 to 0.84) and 0.66 for apoA-I (0.54 to 0.81). These associations were independent of other coronary risk factors, other lipid measurements, hemostatic factors, and C-reactive protein (CRP). The associations of total and LDL cholesterol, triglycerides, apoB, and lipoprotein(a) with coronary events were not independent of HDL cholesterol or hemostatic factors. We conclude that HDL cholesterol or apoA-I, hemostatic risk factors, and CRP are important prognostic markers of coronary events in secondary prevention.

Keywords

HDL cholesterol - apolipoprotein A-I - hemostatic factors - C-reactive protein - acute phase markers

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References
1 Task Force Report. Prevention of coronary heart disease in clinical practice: Recommendations of the second joint task force of European and Other Societies on coronary prevention. Atherosclerosis 1998; 140: 199-270.
2 International task force for prevention of coronary heart disease. Coronary heart disease: Reducing the risk The scientific background to primary and secondary prevention of coronary heart disease. A worldwide view. Nutr Metab Cardiovasc Dis 1998; 08: 205-71.
3 Gordon D, Rifkind BM. Current concepts: high density lipoproteins – the clinical implications of recent studies. N Engl J Med 1989; 321: 1311-5.
4 Rader D, Hoeg JM, Brewer Jr HB. Quantification of plasma apolipoproteins in the primary and secondary prevention of coronary artery disease. Ann Intern Med 1994; 120: 1012-25.
5 Stein JH, Rosenson RS. Lipoprotein Lp(a) excess and coronary heart disease. Arch Intern Med 1997; 157: 1170-6.
6 Hokanson JE, Austin MA. Plasma triglyceride level is a risk factor for cardiovascular disease independent of high-density lipoprotein cholesterol level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk 1996; 03: 213-9.
7 Bolibar I, Thompson S, von Eckardstein A, Sandkamp M, Assmann G. on behalf of the ECAT Angina Pectoris Study Group. Dose, response relationships of serum lipid measurements with the extent of coronary stenosis: strong, independent, and comprehensive. Arterioscler Thromb Vasc Biol 1995; 15: 1035-42.
8 Detrano R, Hsiai T, Wang S. et al. Prognostic value of coronary calcification and angiographic stenoses in patients undergoing coronary angiography. J Am Coll Cardiol 1996; 27: 285-90.
9 Byrne CD. Triglyceride-rich lipoproteins: are links with atherosclerosis mediated by a procoagulant and proinflammatory phenotype?. Atherosclerosis 1999; 145: 1-15.
10 Hamsten A, Karpe F, Bavenholm P, Silveira A. Interactions amongst insulin, lipoproteins, and hemostatic function relevant to coronary heart disease. J Int Med 1994; 236 (suppl.) 75-88.
11 Sammalkorpi KT, Valtonen VV, Maury CP. Lipoproteins and acute phase response during acute infection Interrelationships between C-reactive protein and serum amyloid-A protein and lipoproteins. Ann Med 1990; 22: 397-401.
12 Ridker PM. Evaluating novel cardiovascular risk factors: can we better predict heart attacks?. Ann Intern Med 1999; 130: 933-7.
13 Thompson SG, Kienast J, Pyke SDM, Haverkate F, van de Loo JCW. for the European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group. Hemostatic Factors and the risk of myocardial infarction or sudden death in patients with angina pectoris. N Engl J Med 1995; 332: 635-41.
14 Haverkate F, Thompson SG, Pyke SDM, Gallimore JR, Pepys MB. for the European Concerted Action on Thrombosis and Disabilities Angina Pectoris Study Group Production of C, reactive protein and risk of coronary events in stable and unstable angina. Lancet 1997; 349: 462-7.
15 ECAT Angina Pectoris Study Group. ECAT Angina Pectoris Study: baseline associations of hemostatic factors with extent of coronary arteriosclerosis and other coronary risk factors in 3000 patients with angina pectoris undergoing coronary angiography. Eur Heart J 1993; 14: 8-17.
16 DeLong DM, DeLong ER, Wood PD, Lippel K, Rifkind B. A comparison of methods for the estimation of plasma low and very low density lipoprotein cholesterol: the lipid research clinics prevalence study. JAMA 1986; 256: 2372-7.
17 CASS principal investigators and their associates. Myocardial infarction and mortality in the Coronary Artery Surgery Study (CASS) randomised trial. N Engl J Med 1984; 310: 750-8.
18 Greenland S. Quantitative methods in the review of epidemiologic literature. Epidemiol Rev 1987; 09: 1-30.
19 Miller M, Seidler A, Moalemi A, Pearson TA. Normal triglyceride levels and coronary artery disease events: The Baltimore Coronary Observational Study. J Am Coll Cardiol 1998; 31: 1252-7.
20 Sacks FM, Moye LA, Davis BR. et al. Relationship between plasma LDL concentrations during treatment with pravastatin and recurrent coronary events in the cholesterol and recurrent events trial. Circulation 1998; 97: 1446-52.
21 Gotto Jr AM, Whitney E, Stein EA. et al. Relation between baseline and on treatment parameters and first acute major coronary events in the Air Force/Texas Coronary Atheroscelrosis Prevention Study (AFCAPS/Tex-CAPS). Circulation 2000; 101: 477-84.
22 Rubins HB, Robins SJ, Collins D. et al. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high, density lipoprotein cholesterol. N Engl J Med 1999; 341: 410-8.
23 Manninen V, Tenkanen L, Koskinen P. et al. Joint effects of serum triglycerides and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study Implications for treatment. Circulation 1992; 85: 37-45.
24 Ruotolo G, Ericsson CG, Tettamanti C. et al. Treatment effects on serum lipoprotein lipids, apolipoproteins and low density lipoprotein particle size and relationships of lipoprotein variables to progression of coronary artery disease in the Bezafibrate Coronary Atherosclerosis Intervention Trial (BECAIT). J Am Coll Cardiol 1998; 32: 1648-56.
25 Ballantyne CM, Herd JA. Ferlic et al. Influence of low HDL on progression of coronary artery disease and response to fluvastatin therapy. Circulation 1999; 99: 736-43.
26 Després JP, Marette A. Relation of components of insulin resistance syndrome to coronary risk. Curr Opin Lipid 1994; 05: 274-82.
27 Laakso M. Insulin resistance and coronary heart disease. Curr Opin Lipidol 1996; 07: 217-26.
28 Ridker PM, Glynn RJ, Hennekens CH. C-reactive protein adds to the predicitive value of total and HDL cholesterol cholesterol in determining risk of first myocardial infarction. Circulation 1998; 97: 2007-11.
29 Lamarche B, Moorjani S, Lupien PJ. et al. Apolipoprotein A, I and B levels and the risk of ischaemic heart disease during a five year follow-up of men in the Quebec Cardiovascular Study. Circulation 1996; 94: 273-8.
30 Gould AL, Rossouw JE, Santanello NC, Heyse J, Furberg CD. Cholesterol reduction yields clinical benefit Impact of statin trials. Circulation 1998; 97: 946-52.
31 Sacks FM, Pfeffer MA, Moye LA. et al. for the Cholesterol and Recurrent Events Trial Investigators The effect of pravastatin on coronary events after myocardial infaction in patients with average cholesterol levels. N Engl J Med 1996; 335: 1001-9.
32 Tonkin A, Aylward P, Colquhoun D. et al. Prevention of cardiovascular events and death with pravastatin in patients with coronary heart disease and a broad range of initial cholesterol levels. N Engl Med 1998; 339: 1349-57.
33 Sgoutas DS, Turen T. Effect of freezing and thawing on the immunoassay of Lipoprotein(a). Clin Chem 1992; 38: 1873-7.