Información del artículo
A pesar de que existe una serie de factores de riesgo considerados como mayores y que explican más del 80% de la incidencia de la enfermedad cardiovascular (ECV), hay una importante proporción de la población en la que no se dispone de marcadores claros que permitan adoptar una intervención eficiente. Un nuevo enfoque de la arteriosclerosis sitúa a la inflamación crónica como uno de los factores que favorece el desarrollo de la ECV y, en consecuencia, los marcadores de inflamación han atraído la atención de multiples investigadores; entre ellos la concentración de la proteína C reactiva medida por métodos de alta sensibilidad (hs-PCR), ha proporcionado un cuerpo de evidencia suficiente como para que se recomiende su uso en los casos en que el pronóstico en función de los factores de riesgo mayores no está suficientemente bien definido. Incluso se está empezando a recomendar la redefinición del nivel de riesgo cardiovascular en los individuos en que se detecta una elevación mantenida de las concentraciones de esta proteína. Además de la PCR, existen otros marcadores de inflamación que quizás aporten nueva información en un futuro próximo, entre los que destacan la IL-18 y la fosfolipasa A2 unida a lipoproteínas (Lp-PLA2), si bien los métodos de que se dispone para su medición en la actualidad no pueden considerarse como de utilidad para la práctica clínica.
Palabras clave:
Enfermedad cardiovascular
Inflamación
Proteína C reactiva
IL-18
Lp-PLA2
Although there is a series of risk factors which are considered major risk factors and explain more than 80% of the incidence of cardiovascular disease (CVD), there is a substantial proportion of the population without clear markers that would allow effective intervention strategies. A new focus in arteriosclerosis views chronic inflammation as one of the factors encouraging the development of CVD and consequently markers of inflammation have attracted the attention of multiple researchers; among these markers, C-reactive protein concentration measured by high sensitivity methods (hs-CRP) has provided a body of evidence that is sufficient to recommend its use in patients without a sufficiently well defined prognosis according to major risk factors. Redefinition of the level of cardiovascular risk is even beginning to be recommended in individuals with persistent elevation of CRP concentrations. In addition to CRP there are other markers of inflammation that may provide new information in the near future. Notable among these are interleukin (IL)-18 and phospholipase A2 together with lipoproteins (Lp-PLA2), although the methods currently available for their measurement cannot be considered useful in clinical practice
Key words:
Cardiovascular disease
Inflammation
C reactive protein
IL-18
Lp-PLA2
El Texto completo está disponible en PDF
Bibliografía
[1.]
J.T. Willerson, P.M. Ridker.
Inflammation as a cardiovascular risk facto.
Circulation, 109 (2004), pp. II2-II10
[2.]
Executive Summary of The Third Report of The National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol In Adults (Adult Treatment Panel III). JAMA. 2001.285:2486-97.
[3.]
S. Yusuf, S. Hawken, S. Ounpuu, T. Dans, A. Avezum, F. Lanas, on behalf of the INTERHEART Study Investigators, et al.
Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study.
Lancet, 364 (2004), pp. 937-952
[4.]
U.N. Khot, M.B. Khot, C.T. Bajzer, S.K. Sapp, E.M. Ohman, S.J. Brener, et al.
Prevalence of conventional risk factors in patients with coronary heart disease.
JAMA, 290 (2003), pp. 898-904
[5.]
P. Greenland, M.D. Knoll, J. Stamler, J.D. Neaton, A.R. Dyer, D.B. Garside, et al.
Major risk factors as antecedents of fatal and nonfatal coronary heart disease events.
JAMA, 290 (2003), pp. 891-897
[6.]
P.M. Ridker, N.J. Brown, D.E. Vaughan, D.G. Harrison, J.L. Mehta.
Established and Emerging Plasma Biomarkers in the Prediction of First Atherothrombotic Events.
Circulation, 109 (2004), pp. IV6-IV19
[7.]
P. Libby, P.M. Ridker, A. Maseri.
Inflammation and atherosclerosis.
Circulation, 105 (2002), pp. 1135-1143
[8.]
S.M. Prescott, T.M. McIntyre, G.A. Zimmerman, D.M. Stafforini.
Molecular events in acute inflammation.
Arterioscler Thromb Vasc Biol, 22 (2002), pp. 727-733
[9.]
R. Ross.
Atherosclerosis: an inflammatory disease.
N Engl J Med, 340 (1999), pp. 115-126
[10.]
P.K. Shah.
Plaque disruption and thrombosis: potential role of inflammation and infection.
Cardiol Clin, 17 (1999), pp. 271-281
[11.]
P.M. Ridker.
Clinical application of C-reactive protein for cardiovascular disease detection and prevention.
Circulation, 107 (2003), pp. 363-369
[13.]
W.J. Jabs, E. Theissing, M. Nitschke, J.F. Bechtel, M. Duchrow, S. Mohamed, et al.
Local generation of C-reactive protein in diseased coronary artery venous bypass grafts and normal vascular tissue.
Circulation, 108 (2003), pp. 1428-1431
[14.]
P. Calabro, J.T. Willerson, E.T. Yeh.
Inflammatory cytokines stimulated C-reactive protein production by human coronary artery smooth muscle cells.
Circulation, 108 (2003), pp. 1930-1932
[15.]
P.E. Szmitko, C.H. Wang, R.D. Weisel, J.R. De Almeida, T.J. Anderson, S. Verma.
New markers of inflammation and endothelial cell activation: Part I.
Circulation, 108 (2003), pp. 1917-1923
[16.]
J.L. Torres, P.M. Ridker.
Clinical use of high-sensitivity C-reactive protein for the prediction of adverse cardiovascular events.
Curr Opin Cardiol, 18 (2003), pp. 471-478
[17.]
J.A. Tice, W. Browner, R.P. Tracy, S.R. Cummings.
The relation of Creactive protein levels to total and cardiovascular mortality in older U.S. women.
Am J Med, 114 (2003), pp. 199-205
[18.]
T.A. Pearson, G.A. Mensah, R.W. Alexander, J.L. Anderson, R.O. Cannon 3rd, M. Criqui, Centers for Disease Control and Prevention; American Heart Association, et al.
Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for health care professionals from the Centers for Disease Control and Prevention and the American Heart Association.
Circulation, 107 (2003), pp. 499-511
[19.]
P. Sakkinen, R.D. Abbott, J.D. Curb, B.L. Rodríguez, K. Yano, R.P. Tracy.
C-reactive protein and myocardial infarction.
J Clin Epidemiol, 55 (2002), pp. 445-451
[20.]
A.P. Burke, R.P. Tracy, F. Kolodgie, G.T. Malcom, A. Zieske, R. Kutys, et al.
Elevated C-reactive protein values and atherosclerosis in sudden coronary death: association with different pathologies.
Circulation, 105 (2002), pp. 2019-2023
[21.]
C.M. Albert, J. Ma, N. Rifai, M.J. Stampfer, P.M. Ridker.
Prospective study of C-reactive protein, homocysteine, and plasma lipid levels as predictors of sudden cardiac death.
Circulation, 105 (2002), pp. 2595-2599
[22.]
P.M. Ridker, N. Rifai, M.A. Pfeffer, F.M. Sacks, L.A. Moye, S. Goldman, et al.
Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels.
Circulation, 98 (1998), pp. 839-844
[23.]
P.M. Ridker, M. Cushman, M.J. Stampfer, R.P. Tracy, C.H. Hennekens.
Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men.
N Engl J Med, 336 (1997), pp. 973-979
[24.]
A.D. Pradhan, J.E. Manson, J.E. Rossouw, D.S. Siscovick, C.P. Mouton, N. Rifai, et al.
Inflammatory biomarkers, hormone replacement therapy, and incident coronary heart disease. Prospective analysis from the Women's Health Initiative Observational Study.
JAMA, 288 (2002), pp. 980-987
[25.]
P.M. Ridker, N. Rifai, M. Clearfield, J.R. Downs, S.E. Weis, J.S. Miles, Air Force/Texas Coronary Atherosclerosis Prevention Study Investigators, et al.
Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events.
N Engl J Med, 344 (2001), pp. 1959-1965
[26.]
M. Cushman, A.M. Arnold, B.M. Psaty, T.A. Manolio, L.H. Kuller, G.L. Burke, et al.
C-reactive protein and the 10-year incidence of coronary heart disease in older men and women The Cardiovascular Health Study.
Circulation, 112 (2005), pp. 25-31
[27.]
G. Liuzzo, L.M. Biasucci, J.R. Gallimore, R.L. Grillo, A.G. Rebuzzi, M.B. Pepys, et al.
The prognostic value of C-reactive protein and serum amyloid A protein in severe unstable angina.
N Engl J Med, 331 (1994), pp. 417-424
[28.]
E.R. Ferreiros, C.P. Boissonnet, R. Pizarro, P.F. Merletti, G. Corrado, A. Cagide, et al.
Independent prognostic value of C-reactive protein in unstable angina.
Circulation, 100 (1999), pp. 1958-1963
[29.]
L. Oltrona, D. Ardissino, P.A. Merlini, A. Spinola, F. Chiodo, A. Pezzano.
C-reactive protein elevation and early outcome in patients with unstable angina pectoris.
Am J Cardiol, 80 (1997), pp. 1002-1006
[30.]
D.A. Morrow, N. Rifai, E.M. Altman, D.L. Weiner, C.H. McCabe, C.P. Cannon, et al.
C-reactive protein is a potent predictor of mortality independently of and in combination with troponin T in acute coronary syndromes: a TIMI 11A substudy. Thrombolysis in Myocardial Infarction.
J Am Coll Cardiol, 31 (1998), pp. 1460-1465
[31.]
H. Benamer, P.G. Steg, J. Benessiano, E. Vicaut, C.J. Gaultier, A. Boccara, et al.
Comparison of the prognostic value of C-reactive protein and troponin I in patients with unstable angina pectoris.
Am J Cardiol, 82 (1998), pp. 845-850
[32.]
C. Müller, H.J. Buettner, J.M. Hodgson, S. Marsch, A.P. Perruchoud, H. Roskamm, et al.
Inflammation and long-term mortality after non-ST elevation acute coronary syndrome treated with a very early invasive strategy in 1042 consecutive patients.
Circulation, 105 (2002), pp. 1412-1415
[33.]
B.D. Horne, J.B. Muhlestein, J.F. Carlquist, T.L. Bair, T.E. Madsen, N.I. Hart, et al.
Statin therapy, lipid levels, C-reactive protein and the survival of patients with angiographically severe coronary artery disease.
J Am Coll Cardiol, 36 (2000), pp. 1774-1780
[34.]
L.M. Biasucci, G. Liuzzo, R.L. Grillo, G. Caligiuri, A.G. Rebuzzi, A. Buffon, et al.
Elevated levels of C-reactive protein at discharge in patients with unstable angina predict recurrent instability.
Circulation, 99 (1999), pp. 855-860
[35.]
H. Toss, B. Lindhal, A. Siegbahn, L. Wallentin.
Prognostic influence of increased fibrinogen and C-reactive protein levels in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease.
Circulation, 96 (1997), pp. 4204-4210
[36.]
B. Lindhal, H. Toss, A. Siegbahn, P. Venge, L. Wallentin.
Markers of myocardial damage and inflammation in relation to long-term mortality in unstable coronary artery disease. FRISC Study Group. Fragmin during Instability in Coronary Artery Disease.
N Engl J Med, 343 (2000), pp. 1139-1147
[37.]
A.G. Rebuzzi, G. Quaranta, G. Liuzzo, G. Caligiuri, G.A. Lanza, J.R. Gallimore, et al.
Incremental prognostic value of serum levels of troponin T and C-reactive protein on admission in patients with unstable angina pectoris.
Am J Cardiol, 82 (1998), pp. 715-719
[38.]
J.S. Zebrack, J.B. Muhlestein, B.D. Horne, J.L. Anderson, Intermountain Heart Collaboration Study Group.
C-reactive protein and angiographic coronary artery disease: independent and additive predictors of risk in subjects with angina.
J Am Coll Cardiol, 39 (2002), pp. 632-637
[39.]
J.S. Zebrack, J.L. Anderson, S. Beddhu, B.D. Horne, T.L. Bair, A. Cheung, Intermountain Heart Collaboration Study Group, et al.
Do associations with C-rective protein and extent of coronary artery disease account for the increased cardiovascular risk of renal insufficiency?.
J Am Coll Cardiol, 42 (2003), pp. 57-63
[40.]
O. Bazzino, E.R. Ferreiros, R. Pizarro, G. Corrado.
C-reactive protein and the stress tests for risk stratification of patients recovering from unstable angina pectoris.
Am J Cardiol, 87 (2001), pp. 1235-1239
[41.]
C. Heeschen, C.W. Hamm, J. Bruemmer, M.L. Simoons, Predictive value of C-reactive protein and troponin T in patients with unstable angina: a comparative analysis. CAPTURE Investigators.
Chimeric c7E3 Anti-Platelet Therapy in Unstable angina REfractory to standard treatment trial.
J Am Coll Cardiol, 35 (2000), pp. 1535-1542
[42.]
A. Buffon, G. Liuzzo, L.M. Biasucci, P. Pasqualetti, V. Ramazzotti, A.G. Rebuzzi, et al.
Preprocedural serum levels of C-reactive protein predict early complications and late restenosis after coronary angioplasty.
J Am Coll Cardiol, 34 (1999), pp. 1512-1521
[43.]
D.P. Chew, D.L. Bhatt, M.A. Robbins, M.S. Penn, J.P. Schneider, M.S. Lauer, et al.
Incremental prognostic value of elevated baseline C-reactive protein among established markers of risk in percutaneous coronary intervention.
Circulation, 104 (2001), pp. 992-997
[44.]
F. Versaci, A. Gaspardone, F. Tomai, F. Crea, L. Chiariello, P.A. Gioffre.
Predictive value of C-reactive protein in patients with unstable angina pectoris undergoing coronary artery stent implantation.
Am J Cardiol, 85 (2000), pp. 92-95
[45.]
D.H. Walter, S. Fichtlscherer, M. Sellwig, W. Auch-Schwelk, V. Schachinger, A.M. Zeiher.
Preprocedural C-reactive protein levels and cardiovascular events after coronary stent implantation.
J Am Coll Cardiol, 37 (2001), pp. 839-846
[46.]
G. Patti, G. Di Sciascio, A. D’Ambrosio, G. Dicuonzo, A. Abbate, A. Sobrina.
Prognostic value of interleukin-1 receptor antagonist in patients undergoing percutaneous coronary intervention.
Am J Cardiol, 89 (2002), pp. 372-376
[47.]
M.H. Kaplan, J.E. Volanakis.
Interaction of C-reactive protein complexes with the complement system. I. Consumption of human complement associated with the reaction of C-reactive protein with pneumococcal C-polysaccharide and with the choline phosphatides, lecithin and sphingomyelin.
J Immunol, 112 (1974), pp. 2135-2147
[48.]
J. Siegel, R. Rent, H. Gewurz.
Interactions of C-reactive protein with the complement system. I. Protamine-induced consumption of complement in acute phase sera.
J Exp Med, 140 (1974), pp. 631-647
[49.]
S. Bhakdi, M. Torzewski, K. Paprotka, S. Schmitt, H. Barsoom, P. Suriyaphol, et al.
Possible protective role for C-reactive protein in atherogenesis: complement activation by modified lipoproteins halts before detrimental terminal sequence.
Circulation, 109 (2004), pp. 870-876
[50.]
W.K. Lagrand, H.W.M. Niessen, G.-J. Wolbink, L.H. Jaspars, C.A. Visser, F.W.A. Verheugt, et al.
C-reactive protein colocalizes with complement in human hearts during acute myocardial infarction.
Circulation, 95 (1997), pp. 97-103
[51.]
M. Pepys.
CRP or not CRP? That is the question.
Arterioscler Thromb Vasc Biol, 25 (2005), pp. 1091-1094
[52.]
K.E. Taylor, J.C. Giddings, C.W. Van den Berg.
C-reactive protein-induced in vitro endothelial cell activation is an artefact caused by azide and lipopolysaccharide.
Arterioscler Thromb Vasc Biol, 25 (2005), pp. 1225-1230
[53.]
M. Griselli, J. Herbert, W.L. Hutchinson, K.M. Taylor, M. Sohail, T. Krausz, et al.
C-reactive protein and complement are important mediators of tissue damage in acute myocardial infarction.
J Exp Med, 190 (1999), pp. 1733-1739
[54.]
B.R. Clapp, G.M. Hirschfield, C. Storry, J.R. Gallimore, R.P. Stidwill, M. Singer, et al.
Inflammation and endothelial function: direct vascular effects of human C-reactive protein on nitric oxide bioavailability.
Circulation, 111 (2005), pp. 1530-1536
[55.]
G.M. Hirschfield, M.D. Smith, S.V. Ley, S. Kolstoe, D. Thompson, S.P. Wood, et al.
Therapeutic inhibition of C-reactive protein-novel drugs, novel mechanisms [abstract].
Clin Sci, 104 (2003), pp. 65-66
[56.]
R. Paoletti, A.M. Gotto, D.P. Hajjar.
Inflammation in Atherosclerosis and Implications for Therapy.
Circulation, 109 (2004), pp. III20-III22
[57.]
J.A. Gómez-Gerique, E. Ros, J. Olivan, J.M. Mostaza, M. Vilardell, X. Pinto, ATOMIX Investigators, et al.
Effect of atorvastatin and bezafibrate on plasma levels of C-reactive protein in combined (mixed) hyperlipidemia.
Atherosclerosis, 162 (2002), pp. 245-251
[58.]
P.M. Ridker, N.J. Brown, D.E. Vaughan, D.G. Harrison, J.L. Mehta.
Established and Emerging Plasma Biomarkers in the Prediction of First Atherothrombotic Events.
Circulation, 109 (2004), pp. IV6-IV19
[59.]
A.J. Taylor, S.M. Kent, P.J. Flaherty, L.C. Coyle, T.T. Markwood, M.N. Vernalis, ARBITER: Arterial biology for the investigation of the treatment effects of reducing cholesterol.
A randomized trial comparing the effects of atorvastatin and pravastatin on carotid intima medial thickness.
Circulation, 106 (2002), pp. 1055-1060
[60.]
M.A. Albert, E. Danielson, N. Rifai, P.M. Ridker.
Effect of statin therapy on C-reactive protein levels: the Pravastatin Inflammation/CRP Evaluation (PRINCE). A randomized trial and cohort study.
JAMA, 286 (2001), pp. 64-70
[61.]
J.L. Anderson, J.F. Carlquist.
Cytokines, Interleukin-18, and the Genetic Determinants of Vascular Inflammation.
Circulation, 112 (2005), pp. 620-623
[62.]
K. Nakanishi, T. Yoshimoto, H. Tsutsui, H. Okamura.
Interleukin-18 is a unique cytokine tha stimulates both Th1 and Th2 responses depending on its cytokine milieu.
Cytokine Growth Factor Rev, 12 (2001), pp. 53-72
[63.]
C. Tenger, A. Sundborger, J. Jawien, X. Zhou.
IL-18 accelerates atherosclerosis accompanied by elevation of IFN-gamma and CXCL16 expression independently of T cells.
Arterioscler Thromb Vasc Biol, 25 (2005), pp. 791-796
[64.]
Z. Mallat, A. Corbaz, A. Scoazec, P. Graber, S. Alouani, B. Esposito, et al.
Interleukin-18/interleukin-18 binding protein signaling modulates atherosclerotic lesion development and stability.
Circ Res, 89 (2001), pp. e41-e45
[65.]
Z. Mallat, P. Henry, R. Fressonnet, S. Alouani, A. Scoazec, P. Beaufils, et al.
Increased plasma concentrations of interleukin-18 in acute coronary syndromes.
Heart, 88 (2002), pp. 467-469
[66.]
Z. Mallat, A. Corbaz, A. Scoazec, S. Besnard, G. Leseche, Y. Chvatchko, et al.
Expression of interleukin-18 in human atherosclerotic plaques and relation to plaque instability.
Circulation, 104 (2001), pp. 1598-1603
[67.]
S. Blankenberg, T. Tiret, C. Bickel, D. Peetz, F. Cambien, J. Meyer, for the AtheroGene Investigators, et al.
Interleukin 18 is a strong predictor of cardiovascular death in stable and unstable angina.
Circulation, 106 (2002), pp. 24-30
[68.]
S. Blankenberg, G. Luc, P. Ducimetiere, D. Arveiler, J. Ferrieres, P. Amouyel, PRIME Study Group, et al.
Interleukin-18 and the risk of coronary heart disease in European men: the Prospective Epidemiological Study of Myocardial Infarction (PRIME).
Circulation, 108 (2003), pp. 2453-2459
[69.]
E. Lindmark, E. Diderholm, L. Wallentin, A. Siegbahn.
Relationship between interleukin 6 and mortality in patients with unstable coronary artery disease: effects of an early invasive or noninvasive strategy.
JAMA, 286 (2001), pp. 2107-2113
[70.]
P.M. Ridker, N. Rifai, M.J. Stampfer, C.H. Hennekens.
Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men.
Circulation, 101 (2000), pp. 1767-1772
[71.]
L.M. Biasucci, G. Liuzzo, G. Fantuzzi, G. Caligiuri, A.G. Rebuzzi, F. Ginnetti, et al.
Increasing levels of interleukin (IL)-1Ra and IL-6 during the first 2 days of hospitalization in unstable angina are associated with increased risk of in-hospital coronary events.
Circulation, 99 (1999), pp. 2079-2084
[72.]
G.L. Myers, N. Rifai, R.P. Tracy, W.l. Roberts, R.W. Alexander, L.M. Biasucci, et al.
CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease Application to clinical and Public Health Practice Report From the Laboratory Science Discussion Group.
Circulation, 110 (2004), pp. e545-e549
[73.]
P. Fraunberger, M. Pfeiffer, P. Cremer, E. Holler, D. Nagel, I. Dehart, et al.
Validation of an automated enzyme immunoassay for Interleukin-6 for routine clinical use.
Clin Chem Lab Med, 36 (1998), pp. 797-801
[74.]
F. Berthier, C. Lambert, C. Genin, J. Bienvenu.
Evaluation of an automated immunoassay method for cytokine measurement using the Immulite Immunoassay system.
Clin Chem Lab Med, 37 (1999), pp. 593-599
[75.]
U. Pradhakar, E. Eirikis, H.M. Davis.
Simultaneous quantification of proinflammatory cytokines in human plasma using the LabMAP assay.
J Immunol Methods, 260 (2002), pp. 207-218
[76.]
L. Flower, R.H. Ahuja, S.E. Humphries, V. Mohamed-Ali.
Effects of sample handling on the stability of interleukin 6, tumour necrosis factor-alpha and leptin.
Cytokine, 12 (2000), pp. 1712-1716
[77.]
L. Wilhelmsen, K. Svardsudd, K. Korsan-Bengtsen, B. Larsson, L. Welin, G. Tibblin.
Fibrinogen as a risk factor for stroke and myocardial infarction.
N Engl J Med, 311 (1984), pp. 501-505
[78.]
W.B. Kannel, P.A. Wolf, W.P. Castelli, R.B. D’Agostino.
Fibrinogen and risk of cardiovascular disease. The Framingham Study.
JAMA, 258 (1987), pp. 1183-1186
[79.]
J. Ma, C.H. Hennekens, P.M. Ridker, M.J. Stampfer.
A prospective study of fibrinogen and risk of myocardial infarction in the Physicians’ Health Study.
J Am Coll Cardiol, 33 (1999), pp. 1347-1352
[80.]
J. Danesh, R. Collins, P. Appleby, R. Peto.
Association of fibrinogen, C-reactive protein, albumin, or leukocyte count with coronary heart disease: meta-analyses of prospective studies.
JAMA, 279 (1998), pp. 1477-1482
[81.]
P.M. Ridker, M.J. Stampfer, N. Rifai.
Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease.
JAMA, 285 (2001), pp. 2481-2485
[82.]
The BIP Study Group.
Secondary prevention by raising HDL cholesterol and reducing triglycerides in patients with coronary artery disease: the Bezafibrate Infarction Prevention (BIP) study.
Circulation, 102 (2000), pp. 21-27
[83.]
P.M. Ridker, C.H. Hennekens, B. Roitman-Johnson, M.J. Stampfer, J. Allen.
Plasma concentration of soluble intercellular adhesion molecule 1 and risks of future myocardial infarction in apparently healthy men.
Lancet, 351 (1998), pp. 88-92
[84.]
P.M. Ridker, J.E. Buring, N. Rifai.
Soluble P-selectin and the risk of future cardiovascular events.
Circulation, 103 (2001), pp. 491-495
[85.]
I. Malik, J. Danesh, P. Whincup, V. Bhatia, O. Papacosta, M. Walker, et al.
Soluble adhesion molecules and prediction of coronary heart disease: a prospective study and meta-analysis.
Lancet, 358 (2001), pp. 971-976
[86.]
U. Schonbeck, N. Varo, P. Libby, J. Buring, P.M. Ridker.
Soluble CD40L and cardiovascular risk in women.
Circulation, 104 (2001), pp. 2266-2268
[87.]
C. Heeschen, S. Dimmeler, C.W. Hamm, M.J. Van den Brand, E. Boersma, A.M. Zeiher, CAPTURE Study Investigators, et al.
Soluble CD40 ligand in acute coronary syndromes.
N Engl J Med, 348 (2003), pp. 1104-1111
[88.]
C.J. Packard, D.S. O’Reilly, M.J. Caslake, A.D. McMahon, I. Ford, J. Cooney, et al.
Lipoprotein-associated phospholipase A2 as an independent predictor of coronary heart disease. West of Scotland Coronary Prevention Study Group.
N Engl J Med, 343 (2000), pp. 1148-1155
[89.]
C.M. Ballantyne, R.C. Hoogeveen, H. Bang, J. Coresh, A.R. Folsom, G. Heiss, et al.
Lipoprotein-Associated Phospholipase A2, High-Sensitivity C-Reactive Protein, and Risk for Incident Coronary Heart Disease in Middle-Aged Men and Women in the Atherosclerosis Risk in Communities (ARIC) Study.
Circulation, 109 (2004), pp. 837-842
[90.]
W. Koenig, N. Khuseyinova, H. Löwel, G. Trischler, C. Meisinger.
Lipoprotein-Associated Phospholipase A2 Adds to Risk Prediction of Incident Coronary Events by C-Reactive Protein in Apparently Healthy Middle-Aged Men From the General Population: Results From the 14-Year Follow-Up of a Large Cohort From Southern Germany.
Circulation, 110 (2004), pp. 1903-1908
[91.]
E.S. Brilakis, J.P. McConnell, R.J. Lennon, A.A. Elesber, J.G. Meyer, P.B. Perger.
Association of lipoprotein-associated phospholipase A2 levels with coronary artery disease risk factors, angiographic coronary artery disease, and major adverse events at follow-up.
European Heart Journal, 26 (2005), pp. 137-144
[92.]
M.J. Caslake, C.J. Packard.
Lipoprotein-associated phospholipase A2 platelet activating factor acetylhydrolase and cardiovascular disease.
Curr Opin Lipidol, 14 (2003), pp. 347-352
[93.]
A. Zalewski, C.H. Macphee.
Role of lipoprotein-associated phospholipase A2, in atherosclerosis.
Arterioscler Thromb Vasc Biol, 25 (2005), pp. 923-931
[94.]
S.M. Grundy, J.I. Cleeman, C.N. Merz, H.B. Brewer Jr, L.T. Clark, D.B. Hunninghake, Coordinating Committee of the National Cholesterol Education Program, et al.
Implications of recent clinical trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines.
J Am Coll Cardiol, 44 (2004), pp. 720-732
Copyright © 2006. Sociedad Española de Arteriosclerosis y Elsevier España S.L.