Cirugía y Cirujanos

Contents by Year, Volume and Issue

Table of Contents

General Information

Instructions for Authors

Message to Editor

Editorial Board

>Journals >Cirugía y Cirujanos >Year 2010, Issue 1

Isordia-Salas I, Mendoza-Valdez AL, Almeida-Gutiérrez E, Borrayo-Sánchez G
Factores genéticos del sistema hemostático en pacientes jóvenes con infarto agudo del miocardio
Cir Cir 2010; 78 (1)

Language: Español
References: 40
Page: 93-97
PDF: 228.23 Kb.

Texto completo


Coronary artery disease (CAD) is the first cause of death worldwide and represents a public health issue in our country. Acute myocardial infarction (AMI) represents the main thrombotic complication of CAD. Approximately 9% of the new events of MI occur in patients ‹45 years of age. AMI is produced by development of a thrombus at the site of an atherosclerotic plaque that initiates abrupt arterial occlusion, with ischemia and cell death. AMI results from the interaction of gene-environment factors. There are several modifiable factors such as hypertension, diabetes, smoking, obesity, and hypercholesterolemia associated with AMI. However, in a large number of patients with AMI, modifiable risk factors are not present. In the last decade, several genetic variants (polymorphisms) have been identified associated with AMI in genes related to coagulation proteins, fibrinolytic system, platelet receptors, homocysteine metabolism, endothelial dysfunction, abnormal blood flow and oxidative stress. Identifying the genes associated with CAD will allow us to develop more efficacious treatment strategies and will also help to identify at-risk subjects, thereby enabling the introduction of early preventive measures. Thus, many research efforts continue to address the identification of acquired and inherited risk factors of this complex disease.

Key words: Myocardial infarction, atherothrombotic disease, polymorphism, genetic markers.


  1. American Heart Association. Heart disease and stroke statistics 2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2009;119:e21-e181.

  2. Instituto Nacional de Estadística, Geografía e Informática. Datos demográficos de mortalidad. Disponible en http://www.inegi.org.mx/est/contenidos/espanol/rutinas/ept.asp?t=mpob107&s=est&c=14742.

  3. Libby P, Theroux P. Pathophysiology of coronary artery disease. Circulation 2005;111:3481-3488.

  4. Aikawa M, Libby P. The vulnerable atherosclerotic plaque: pathogenesis and therapeutic approach. Cardiovascular Pathol 2004;13:125-138.

  5. Yamada Y, Ichihara S, Nishida T. Molecular genetics of myocardial infarction. Genomic Med 2008;2:7-22.

  6. Voetsch B, Loscalzo J. Genetic determinants of arterial thrombosis. Arterioscler Thromb Vasc Biol 2004;24:216-229.

  7. Rissanen AM, Nikkila EA. Coronary artery disease and its risk factors in families of young men with angina pectoris and in controls. Br Heart J 1997;39:875-883.

  8. Jorde LB, Williams RR. Relation between family history of coronary artery disease and coronary risk variables. Am J Cardiol 1988;62:708-713.

  9. Sorensen TI, Nielsen GG, Andersen PK, Teasdale TW. Genetic and environmental influences on premature death in adult adoptees. N Engl J Med 1988;318:727-732.

  10. Meade TW, Mellows S, Brozovic M, Miller GJ, Chakrabarti RR, North WR, et al. Haemostatic function and ischaemic heart disease: principal results of the Northwick Park Heart Study. Lancet 1986;2:533-537.

  11. Heinrich J, Balleisen L, Schulte H, Assmann G, van de Loo J. Fibrinogen and factor VII in the prediction of coronary risk: results from the PROCAM study in healthy men. Arterioscler Thromb 1994;14:54-59.

  12. Folsom AR. Haemostatic risk factors for atherothrombotic disease: an epidemiologic view. Thromb Haemost 2001;86:366-373.

  13. Behague I, Poirier O, Nicaud V, Evans A, Arveiler D, Luc G, et al. Beta fibrinogen gene polymorphisms are associated with plasma fibrinogen and coronary artery disease in patients with myocardial infarction: The ECTIM Study. Etude Cas-temoins sur I’Infarctus du Myocarde. Circulation 1996;93:440-449.

  14. Siegerink B, Rosendaal FR, Algra A. Genetic variation in fibrinogen: its relationship to fibrinogen levels and the risk of myocardial infarction and ischemic stroke. J Thromb Haemost 2009;7:385-390.

  15. Green F, Kelleher C, Wilkes H, Temple A, Meade T, Humphries S. A common genetic polymorphism associated with lower coagulation factor VII levels in healthy individuals. Arterioscler Thromb 1991;11:540-546.

  16. Iacoviello L, Di Castelnuovo A, De Knijff P, D’Orazio A, Amore C, Arboretti R, et al. Polymorphism in the coagulation factor VII gene and the risk of myocardial infarction. N Engl J Med 1998;338:79-85.

  17. Corral J, González-Conejero R, Lozano ML, Rivera J, Vicente V. Genetic polymorphisms of factor VII are not associated with arterial thrombosis. Blood Coagul Fibrinolysis 1998;9:267-272.

  18. Ekström M, Silveira A, Bennermo M, Eriksson P, Tornvall P. Coagulation factor VII and inflammatory markers in patients with coronary heart disease. Blood Coagul Fibrinolysis 2007;18:473-477.

  19. Dahlback B. Resistance to activated protein C caused by the factor V R506Q mutation is common risk factor for venous thrombosis. Thromb Haemost 1997;78:483-488.

  20. Rosendaal FR, Siscovick DS, Schwartz SM, Beverly RK, Psaty BM, Longstreth WT Jr, et al. Factor V Leiden (resistance to activated protein C), increases the risk of myocardial infarction in young women. Blood 1997;89:2817-2821.

  21. Ridker PM, Hennekens CH, Lindpaintner K, Stampfer MJ, Eisenberg PR, Miletich JP. Mutation in the gene coding for coagulation factor V and the risk of myocardial infarction, stroke, and venous thrombosis in apparently healthy men. N Engl J Med 1995;332:912-917.

  22. Settin A, Dowaidar M, El-Baz R, Abd-Al-Samad A, El-Sayed I, Nasr M. Frequency of factor V Leiden mutation in Egyptian cases with myocardial infarction. Hematology 2008;13:170-174.

  23. Doggen CJ, Cats VM, Bertina RM, Rosendaal FR. Interaction of coagulation defects and cardiovascular risk factors: increased risk of myocardial infarction associated with factor V Leiden or prothrombin 20210A. Circulation 1998;97:1037-1041.

  24. Croft SA, Daly ME, Steeds RP, Channer KS, Samani NJ, Hampton KK. The prothrombin 20210A allele and its association with myocardial infarction. Thromb Haemost 1999;81:861-864.

  25. Rosendaal FR, Siscovick DS, Schwartz SM, Psaty BM, Raghunathan TE, Vos HL. A common prothrombin variant (20210 G to A) increases the risk of myocardial infarction in young women. Blood 1997;90:1747-1750.

  26. Newman PJ, Derbes RS, Aster RH. The human platelet alloantigens, PIA1 and PIA2, are associated with a leucine 33/proline33 amino acid polymorphism in membrane glycoprotein IIIa, and are distinguishable by DNA typing. J Clin Invest 1989;83:1778-1781.

  27. Weiss EJ, Bray PF, Tayback M, Schulman SP, Kickler TS, Becker LC, et al. A polymorphism of a platelet glycoprotein receptor as an inherited risk factor for coronary thrombosis. N Engl J Med 1996;334:1090-1194.

  28. Carter AM, Catto AJ, Bamford JM, Grant PJ. Platelet GP IIIa PIA and GP Ib variable number tandem repeat polymorphism and markers of platelet activation in acute stroke. Arterioscler Thromb Vasc Biol 1998;18:1124-1131.

  29. Mikkelsson J, Perola M, Laippala P, Savolainen V, Pajarinen J, Lalu K, et al. Glycoprotein IIIa PI (A) polymorphism associates with progression of coronary artery disease and with myocardial infarction in an autopsy series of middle-aged men who died suddenly. Arterioscler Thromb Vasc Biol 1999;19:2573-2578.

  30. Wiman B. Plasminogen activator inhibitor 1 (PAi-1) in plasma: its role in thrombotic disease. Thromb Haemost 1995;74:71-76.

  31. Isordia-Salas I, Leaños-Miranda A, Sainz IM, Reyes-Maldonado, Borrayo-Sánchez G. Association of the plasminogen activator inhibitor-1 gene 4G/5G polymorphism with ST elevation acute myocardial infarction in young patients. Rev Esp Cardiol 2009;62:365-362.

  32. Mangoni AA, Jackson SH. Homocysteine and cardiovascular disease: current evidence and future prospects. Am J Med 2002;112:556-565.

  33. Alam MA, Husain SA, Narang R, Chauhan SS, Kabra M, Vasisht S. Association of polymorphism in the thermolabile 5,10-methylenetetrahydrofolate reductase gene and hyperhomocysteinemia with coronary artery disease. Mol Cell Biochem 2008;310:111-117.

  34. Yilmaz H, Isbir S, Agachan B, Ergen A, Farsak B, Isbir T. C677T Mutation of methylenetetrahydrofolate reductase gene and serum homocysteine levels in Turkish patients with coronary artery disease. Cell Biochem Funct 2006;24:87-90.

  35. Loscalzo J, Welch G. Nitric oxide and its role in the cardiovascular system. Prog Cardiovasc Dis 1995;38:87-104.

  36. Yoshimura M, Yasue H, Nakayama M, Shimasaki Y, Sumida H, Sugiyama S, et al. A missense Glu298Asp variant in the endothelial nitric oxide synthase gene is associated with coronary spasm in the Japanese. Hum Genet 1998;103:65-69.

  37. Tamemoto H, Ishikawa SE, Kawakami M. Association of the Glu-298Asp polymorphism of the eNOS gene with ischemic heart disease in Japanese diabetic subjects. Diabetes Res Clin Pract 2008;80:275-279.

  38. Cam SF, Sekuri C, Tengiz I, Ercan E, Sagcan A, Akin M, et al. The G894T polymorphism on endothelial nitric oxide synthase gene is associated with premature coronary artery disease in a Turkish population. Thromb Res 2005;116:287-292.

  39. Vasilakou M, Votteas V, Kasparian C, Pantazopoulos N, Dedoussis G, Deltas C, et al. Lack of association between endothelial nitric oxide synthase gene polymorphisms and risk of premature coronary artery disease in the Greek population. Acta Cardiol 2008;63:609-614.

  40. Granath B, Taylor RR, van Bockxmeer FM, Mamotte CD. Lack of evidence for association between endothelial nitric oxide synthase gene polymorphism and coronary artery disease in the Australian Caucasian population. J Cardiovasc Risk 2001;8:235-241.

>Journals >Cirugía y Cirujanos >Year 2010, Issue 1

· Journal Index 
· Links 

Copyright 2019