Fisiopatología, perfil epidemiológico y manejo terapéutico en el síndrome coronario agudo

José Alberto Battilana-Dhoedt, Cristina Cáceres-de Italiano, Nancy Gómez, Osmar Antonio Centurión

Resumen


Las enfermedades cardiovasculares siguen siendo ampliamente la primera causa de muerte en el mundo actual. La cardiopatía isquémica conlleva a una importante carga de gastos de Salud Pública, por lo cual es importante conocer la prevalencia, epidemiología, fisiopatología y el manejo diagnóstico y terapéutico adecuado del síndrome coronario agudo (SCA). Los hallazgos recientes indican que los primeros pasos en la aterosclerosis son esencialmente inflamatorios. Una respuesta inflamatoria sistémica a menudo acompaña al SCA, y la documentación de su presencia ha sido ampliamente reconocida como un indicador de eventos coronarios a repetición. La medicina basada en la evidencia sugiere fuertemente la importancia de la etiología inflamatoria en el SCA. Los factores tradicionales de riesgo coronario terminan en un pasaje final común que desarrolla un proceso inflamatorio en la pared arterial. El entendimiento mejorado y la comprensión adecuada de la influencia de los procesos inflamatorios en el SCA pueden llevar no solo a una mejor utilización de la terapéutica actualmente disponible sino también al desarrollo de nuevas herramientas terapéuticas. Sin duda alguna los refinamientos constantes en las diferentes estrategias terapéuticas del SCA, sumados a la combinación del entendimiento científico en el uso adecuado de los marcadores inflamatorios, los nuevos agentes farmacológicos y las nuevas técnicas de intervención coronaria percutánea con los nuevos stents y otros dispositivos intracoronarios van a aclarar nuestras dudas y mejorar nuestro manejo diagnóstico y terapéutico del síndrome coronario agudo basado en la evidencia científica.

Palabras clave


Síndrome coronario agudo; troponina; infarto de miocardio

Texto completo:

PDF

Referencias


Libby P, Tabas I, Fredman G, Fisher E. Inflammation and its resolution as determinants of acute coronary syndromes. Circ Res 2014; 114(12):1867-79.

Ridker PM. Targeting inflammatory pathways for the treatment of cardiovascular disease. Eur Heart J 2014;35:540-43.

Morton AC, Rothman AM, Greenwood JP, Gunn J, Chase A, Clarke B, et al. The effect of interleukin-1 receptor antagonist therapy onmarkers of inflammation in non-ST elevation acute coronary syndromes: the MRC-ILA heart study. Eur Heart J 2015;36:377-84.

Libby P. Mechanisms of the acute coronary syndromes and their implications for therapy. N Engl J Med 2013; 368:2004-13.

Libby P, Tabas I, Fredman G, Fisher E. Inflammation and its resolution as determinants of acute coronary syndromes. Circ Res 2014 114(12): 1867-79.

Toss H, Lindahl B, Siegbahn A, Wallentin L. Prognostic influence of increased fibrinogen and C-reactive protein levels in unstable coronary artery disease: The FRISC study. Circulation 1997; 96(12): 4204-10.

Fang L, Moore XL, Dart AM, Wang LM. Systemic inflammatory response following acute myocardial infarction. J Geriatr Cardiol 2015; 12(3): 305-12.

Puri R, Nissen SE, Libby P, Shao M, Ballantyne CM, Barter PJ, et al. C-reactive protein, but not low-density lipoprotein cholesterol levels, associate with coronary atheroma regression and cardiovascular events after maximally

intensive statin therapy. Circulation 2013;128:2395-2403.

Centurión OA. Inflammation in acute coronary syndromes: Systemic, coronary plaque, or myocardial source? J Cardiol Cardiovasc Ther. 2015;1(1): 555551.

Kelly CR, Weisz G,Maehara A, Gary S.Mintz, Roxana Mehran , Alexandra J.Lansky,et al. Relation of C-reactive protein levels to instability of untreated vulnerable coronary plaques. Am J Cardiol 2014;114:376–83.

Centurión OA. Serum biomarkers and source of inflammation in acute coronary syndromes and percutaneous coronary interventions. Cardiovasc Revasc Med 2016;17:119-28.

Ridker PM, Luscher TF. Anti-inflammatory therapies for cardiovascular disease. Eur Heart J 2014;35:1782–91.

Hartmann P, Schober A, Weber C. Chemokines and microRNAs in atherosclerosis. Cell Mol Life Sci 2015;72:3253–66.

Usman A, Ribatti D, Sadat U, Gillard JH. From lipid retention to immune-mediated inflammation and associated angiogenesis in the pathogenesis of atherosclerosis. J Atheroscler Thromb 2015;22:739–49.

Libby P, Hansson GK. Involvement of the immune systemin human atherogenesis: Current knowledge and unanswered questions. Lab Invest 1991;64:5–15.

Valtonen VV. Infection as a risk factor for infarction and atherosclerosis. Ann Med 1991;23:539–43.

Davies MJ, Thomas AC. Plaque fissuring-the cause of acute myocardial infarction, sudden ischemic death and crescendo angina. Br Heart J 1985; 53(4): 363-73.

Heeschen C, van Den Brand MJ, Hamm CW, Simoons ML. Angiographic findings in patients with refractory unstable angina according to troponin T status. Circulation 1999; 100(4): 1509-14.

Suzuki M, Saito M, Nagai T, Saeki H, Kazatani Y. Systemic versus coronary levels of inflammation in acute coronary syndromes. Angiology 2006; 57(4): 459-63.

Baumann H, Gauldic J. The acute phase response. Immunol Today 1994; 15(2): 74-80.

Bentzon JF, Otsuka F, Virmani R, Falk E. Mechanisms of plaque formation and rupture. Circ Res 2014;114:1852–66.

Kataoka Y, Puri R, Nicholls SJ. Inflammation, plaque progression and vulnerability: evidence from intravascular ultrasound imaging. Cardiovasc Diagn Ther 2015;5(4):280–9.

Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation 1995;92:657–71.

New SE, Goettsch C, Aikawa M, Marchini JF, Shibasaki M, Yabusaki K, et al. Macrophagederived matrix vesicles: an alternative novel mechanism for microcalcification in atherosclerotic plaques. Circ Res 2013;113:72–7.

Virmani R, Kolodgie FD, Burke AP, Finn AV, Gold HK, Tulenko TN, et al. Atherosclerotic plaque progression and vulnerability to rupture: angiogenesis as a source of intraplaque hemorrhage. Arteriosc Thromb Vasc Biol 2005;25(10):2054–61.

Rogers WJ, Frederick PD, Stoehr E, Canto JG, Ornato JP, Gibson CM et al. Trends in presenting characteristics and hospital mortality among patients with ST elevation and non-ST elevation myocardial infarction in the National Registry of Myocardial Infarction from 1990 to 2006. Am Heart J. 2008;156:1026-34.

Kaartinen M, Pentilla A, Kovanen PT. Accumulation of activated mast cells in the shoulder region of human coronary atheroma, the predilection site of atheromatous rupture. Circulation 1994;90:1669–78.

Pasterkamp G, Schoneveld AH, van der Wal AC, Hijnen DJ, van Wolveren WJ, Plomp S, et al. Inflammation of the atherosclerotic cap and shoulder is common and locally observed feature in unruptured plaques of femoral and coronary arteries. Arterioscler Thromb Vasc Biol 1999;19:54-8.

Grupo de Trabajo para el manejo del síndrome coronario agudo (SCA) en pacientes sin elevación persistente del segmento ST de la Sociedad Europea de Cardiología (ESC). Guía de práctica clínica de la ESC para el manejo del

síndrome coronario agudo en pacientes sin elevación persistente del segmento ST. Rev Esp Cardiol. 2012; 65(2):173.e1-e55.

Hernandez Leiva E. Epidemiología del síndrome coronario agudo y la insuficiencia cardiaca en Latinoamérica. Rev Esp Cardiol 2011 64 (Suppl 2):34-43.

Fadine Reis E, Brunori C, López A, Ruíz Z, Cavalcante V, Santos J, et al. Asociación de factores de riesgo cardiovasculares con las diferentes presentaciones del síndrome coronario agudo. Rev Lat Enferm 2014 22(4):538-46.

Valdez Martín A, Rivas Estani E, Martínez Benítez P, Chipi Rodríguez Y, Reyes Navia G, Echevarría Sifontes L. Caracterización del síndrome coronario agudo en adultos menores de 45 años de una institución especializada en la Habana, Cuba, entre 2013 y 2014. Rev Med UIS. 2015;28(3):281-90.

Degano I, Elosua R, Marrugat J. Epidemiología de la enfermedad cardiovascular en España en los últimos 20 años (I): Epidemiología del síndrome coronario agudo en España: estimación del número de casos y la tendencia de 2005 a 2049. Rev Esp Cardiol 2013 66(6):472-81.

Cordero A, López R, Carrillo P, Frutos A, Miralles S, Gunturiz C. Cambios en el tratamiento y el pronóstico del síndrome coronario agudo con la implantación del código infarto en un hospital con unidad de hemodinámica. Rev Esp Cardiol 2016 69(8):754-59.

Guardas Eduardo S, Prieto Juan Carlos D, Sanhueza P, Dauvergne Christian M, Asenjo Rene G, Corbalán Román H. Guías 2009 de la Sociedad Chilena de Cardiología para el tratamiento del Infarto Agudo del Miocardio con supradesnivel del ST. Rev Chil Cardiol 2009; 28: 223-54.

Balcázar Rincón L, Ramírez Alcántara Y, Ramos Ortega G. Aptitud clínica en un servicio de urgencias para la atención del paciente con síndrome isquémico coronario agudo. In Atención Fam 2016 23(4):150-54.

Rivas Hurtado A, Villalobos Vega R. Evaluación de trombólisis exitosa en el infarto agudo de miocardio por criterios no invasivos de reperfusión. Rev Mex Cardiol 1997; 8(3):85-92.

Stone GW, Maehara A, Lansky AJ, de Bruyne B, Cristea E, Mintz GS et al. A prospective natural-history study of coronary atherosclerosis. N Engl J Med 2011; 364:226-35.

Eguchi K, Manabe I. Toll-like receptor, lipotoxicity, and chronic inflammation: the pathological link between obesity and

cardiometabolic disease. J Atheroscler Thromb 2014;21:629-39.

Ridker PM, CushmanM, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973-79.

van derWal AC, Becker AE, van der Loos CM, et al. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation 1994;89:36-44.

Kohli P, Cannon CP. Acute coronary syndromes in 2011: walking the tightrope between efficacy and bleeding. Nat Rev Cardiol. 2012;9:69-71.

Fuster V, Lewis A. Mechanisms leading to myocardial infarction: Insights from studies of vascular biology. Circulation. 1994;90:2126-46.

Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation 1995;92:657-71.

Taylor GJ, Humphries JO, Mellits ED, Pitt B, Schulze RA, Griffith LSC, et al. Predictors of clinical course, coronary anatomy and left ventricular function after recovery from acute myocardial infarction. Circulation 1980;62:960-70.

Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K,et al. Heart disease and stroke statistics–2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2009;119:480-86.

Ferguson JJ, Lau TK. New antiplatelet agents for acute coronary syndromes. Am Heart J. 1998;135(5 Pt 2 Su):S194-S200.

Ferguson JJ, Waly HM, Wilson JM. Fundamentals of coagulation and glycoprotein IIb/IIIa receptor inhibition. Eur Heart J 1998; 19:3-9.

Braunwald E, Maseri A, Armstrong PW, Califf RM, Gibler WB, Hamm CW, et al. Rationale and clinical evidence for the use of GP IIb/IIIa inhibitors in acute coronary syndromes. Eur Heart J 1998;19 Suppl D:D22-D30.

De Luca G, Marino P. Advances in antithrombotic therapy as adjunct to reperfusion therapies for ST-segment elevation myocardial infarction. Thromb Haemost. 2008;100:184-95.

Krishnaswamy A, Lincoff AM, Cannon CP. Bleeding complications of unfractionated heparin. Expert Opin Drug Saf. 2011; 10: 77-84.

Tavano D, Visconti G, D’Andrea D, Focaccio A, Golia B, Librera M, et al. Comparison of bivalirudin monotherapy versus unfractionated heparin plus tirofiban in patients with diabetes mellitus undergoing elective percutaneous

coronary intervention. Am J Cardiol 2009;104:1222-28.

Moliterno DJ. TENACITY Steering Committee and Investigators. A randomized two-by-two comparison of high-dose bolus tirofiban versus abciximab and unfractionated heparin versus bivalirudin during percutaneous coronary revascularization and stent placement: the tirofiban evaluation of novel dosing versus abciximab with clopidogrel and inhibition of thrombin (TENACITY) study trial. Catheter Cardiovasc Interv 2011;77:1001-9.

Tarantini G, Brener SJ, Barioli A, Gratta A, Parodi G, Rossini R, et al. Impact of baseline hemorrhagic risk on the benefit of bivalirudin versus unfractionated heparin in patients treated with coronary angioplasty: a meta-regression analysis of randomized trials. Am Heart J. 2014;167:401-412.e6.

Valgimigli M, Calabrò P, Cortese B, Frigoli E, Garducci S, Rubartelli P, et al; MATRIX investigators. Scientific foundation and possible implications for practice of the Minimizing Adverse Haemorrhagic Events by Transradial Access Site and Systemic Implementation of AngioX (MATRIX) trial. J Cardiovasc Transl Res. 2014;7:101-11.

Centurión OA. Actual role of platelet glycoprotein IIb/IIIa receptor inhibitors as adjuntive pharmacological therapy to primary angioplasty in acute myocardial infarction: In the light of recent randomized trials and observational studies with bivalirudin. Open Cardiovasc Med J 2010;4:135-45.

Centurión OA. Bivalirudin in contemporary PCI for non-ST-segment acute coronary syndromes: what is the current role of platelet glycoprotein IIb/IIIa receptor inhibitor agents? Crit Pathw Cardiol 2011;10:87-92.

Centurión OA. Current Role of Platelet Glycoprotein IIb/IIIa Inhibition in the Therapeutic Management of Acute Coronary Syndromes in the Stent Era. J Cardiol Curr Res 2016;5(5): 00175. DOI: 10.15406.

Centurión OA. Heparin versus Bivalirudin in contemporary percutaneous coronary intervention: a welcome back to an old friend unfractionated heparin. Crit Pathw Cardiol 2015;14:62-6.

Centurión OA. Heparin versus bivalirudin in acute myocardial infarction: Unfractionated heparin monotherapy elevated to primary treatment in contemporary percutaneous coronary intervention. Open Cardiovasc Med J 2016;10:122-29.

Sojitra P, Doshi M, Galloni M, Vignolini C, Vyas A, Chevli B, et al. Preclinical evaluation of a novel abluminal surface coated sirolimus eluting stent with biodegradable polymer matrix. Cardiovasc Diagn Ther 2015;5(4):254-63.

Siontis GC, Stefanini GG, Mavridis D, Siontis KC, Alfonso F, Pérez-Vizcayno MJ, et al. Percutaneous coronary interventional strategies for treatment of in-stent restenosis: a network meta-analysis. Lancet 2015;386:655-64.

Liou K, Nagaraja V, Jepson N, Ooi SY. Optimal duration of dual antiplatelet therapy following drug-eluting stents implantation: a meta-analysis of 7 randomised controlled trials. Int J Cardiol 2015;201:578–80.

Shah AS, McAllister DA, Mills R, et al. Sensitive troponin assay and the classification of myocardial infarction. Am J Med 2015;128:493-501.

Cervellin G, Mattiuzzi C, Bovo C, Lippi G. Diagnostic algorithms for acute coronary syndrome. Is one better than another? Ann Transl Med 2016;4(10):193. doi: 10.21037/atm.2016.05.16.

Sheyin O, Perez X, Louis BP, Kurian D. The optimal duration of dual antiplatelet therapy in patients receiving percutaneous coronary intervention with drug-eluting stents. Cardiology J 2016; 23(3): 307-316.


Enlaces refback

  • No hay ningún enlace refback.



Creative Commons License Todo el contenido de esta revista, excepto dónde está identificado, está bajo una Licencia Creative Commons

---------------------------------------------------------------------------------------------


Mem. Inst. Investig. Cienc. Salud