De los factores de riesgo de enfermedad arterial a la placa ateromatosa detección de la placa de alto riesgo

Autores/as

  • Ricardo Esper Universidad Nacional de Buenos Aires

Palabras clave:

Poder oxidativo, Placas de ateroma, Cascada de coagulación, Contenido o composición determinante de riesgo, Nuevos métodos diagnósticos

Resumen

La ateroesclerosis es un fenómeno patológico caracterizado por e engrosamiento y endurecimiento de las paredes arteriales debido a la acumulación de lípidos, carbohidratos, productos sanguíneos y depósitos de calcio dentro del espacio subendotelial. Los factores de riesgo de enfermedad arterial impactan en las arterias de toda la economía. Hoy es claro que la composición de la placa es el mayor determinante del riesgo de ruptura de la misma y la trombosis sobreimpuesta. Siguiendo a la ruptura, el core lipídico y su alto contenido de factor tisular, provee un poderoso substrato para la activación de la cascada de la coagulación. Se han efectuado avances significativos en la comprensión de los mecanismos que enmarcan esta enfermedad, y existe considerable evidencia que la composición de la placa es un determinante mayor para el comienzo y la severidad de los síndromes coronarios agudos. En consecuencia, la capacidad para identificar dicha composición y monitorizar su progresión. constituyen informaciones de incalculable valor respecto al desarrollo de síndromes coronarios agudos. La cineangiocoronariografía convencional falla en predecir episodios agudos, de manera que pierde el valor como de preferencia en este tema, y ha impulsado a los investigadores a desarrollar nuevos métodos, invasivos y no tnvasivos, para reconocer la placa ateroesclerótica de alto riesgo y las áreas comprometidas para intervenciones oportunas.

Descargas

Los datos de descargas todavía no están disponibles.

Biografía del autor/a

Ricardo Esper, Universidad Nacional de Buenos Aires

Profesor de Medicina Interna

Citas

Ross R, Glomset JA. The pathogenesis of the atherosclerosis. N Engl J Mcd 1976: 295: 369-377

Ross R. Atherosclerosis - an inflarnrnatory disease. N Engi J Med 1999; 340: 115-126

Giveriz MM, Sawyer DB, Colueci WS. Antioxidauts and niyoeardial contractily. Il]ununating the "dark side' of E-adrencrgic receptor activation. Circulation 2001:103:782-783

Kaski JC, García Moll X. Marcadores serológicos de inflamación y placas aterocscleróticas vulnerables. In: Esper RJ, Vilariño JO (Eds): La placa ateroescleróca vulnerable. Buenos Aires, American Marketing & Communication:2000:65-73

Tsiitiikas S. Wilzum JI— Measuring ci re u latí ng ox i cli z ecl 1 ow - cien si ty lipoprotein to evaluate coronary risk. Circulation 2001:103:1930-1932

Esper RJ, Vilariño JO. Disfurición endotelial. Temas Cardiol. Clín 1999: n° 3.1-12 Libby P Molecular bases of the acute coronar y sin cl ro ni es. C ir e u la t ion 1995:91:2844-2850

Lobby P Sinion Dl. Jnflamrnation and trombosis. The clot thickens. Circulation 2001:103:1718-1720

Falk E, Shah PK, Fustcr y. Coronary pl a tin e di sr u p 1 ion. Ci r e u la ti o u 1995;92:657-671

Badimon JJ, Osende J, Zaman A, Rauch U, Shimho D, F'uster V. Ruptura de la placa y trombosis en la enfermedad aterocselerática coronaria. En: Esper RJ, Vilariño JO (Eds(: La placa ateroesclerótica vulnerable. Buenos Aires, American Marketing & Coniutunication: 2000:1-10

Glagov S. Wcisenberg E, Zarins CK, et al. Compensatory cnlargement of human atherosclerotic coronary arteries. N Engl J Med 1987;316:1371-1375

Ambrose JA, Tannenbaum MA, Alexopoulos D, et al. Angiographic progression of coronary artery disease and the dcveloprnent of myocardlal infarction. J Am Coli Cardiol 1988; 12:56-62

Berenson GS, Srinivasan SR, Bao W, et al. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. N Engi 3 Med 1998:338:1650-1656

Napoli C. D'Armiento FE Manzini FR et al. Fatty streak formation occurs in human fetal aortas an dis grcatly enhance by maternal hypercholesterolcmia. In timal accumulation of low density lipoprotein and its oxidation precede nionocyte recruitment into early atherosclerosis lesions. J Clin lnvest 1997:100:2680-2690

Napoli C. Glass CK, Witztum JL, et al. Influence of maternal hypercholestcrolemia cluring pregnancy on progression of early atherosclerotic lesions jo chi]dhood. Fate of Early Leslons in Childrcns (F'ELIC) study. Lancet 1999:354:1234-1241

Kannel WB. Prevalence, inciclence, ami mortally of coronary heart disease. In: Fuster V, Ross R, Topo] EJ (Eds): Atherosclerosis and coronary artery disease. Philadelphla. Lippincott-Rayen; 1996:13-21

Aronow WS, Ahn C. Prevalence of coexistence of coronary artery disease, pe r i j) 1 eral arterial d i seas e, a n d artherothrombotic brain infarction ¡o men and women >62 years of age. Am 3 Cardiol 1994:74:64-65

Libby E Sukhova G, Lee Rl', Galís ZS. Citoquines regulate vascular functions related to stability of the atherosclerosis plaque. J Carcliovasc Pharmacol 1995 ; 25 :S9-S 12

Littñc WC, Downes TR, Applegate RJ. The underlinc coronary lesion in rnyocarclial infarction: implications of coronary angiography. Clin. Cardiol 1991; 14:868-874

Esper RJ. Regresión de la aterosclerosis- Rey Argent Cardiol 1997; 65:241-250

Esper RJ. The Role of Lipid-Lowering Therapy in Multiple Risk Factor Managernent. Drugs 1998: 56(suppl 1): 1-7 Ambrose JA, Winters SL, Arora RR, et al. Angiography evolution of coronary artery morphoiogy in unstable angina. J Am Coil Cardiol 1986; 7:472-478

Yokoka K, Takatsu H, Susuki T, et al. Process of progression of coronary artery lesions from mild of moderate stenosis to moderate or severe stenosis a stydy based on four serial coronary arteriograms per year. Circulation 1999: 100: 903-909

Vaseghi ME Hassan K, Siadaly S, et al. Angiographic predictors of plaque progression in mildly lo rnoderaiely diseased coronary arteries. Am J Cardiol 1999;84:96P

Inglessis 1, Palacios lE Técnicas de imágenes de placas vulnerables y síndromes isquémicos agudos en arterias coronarias. In: Esper RJ, Vilariño JO (Eds); La placa ateroesclerótica vulnerable. Buenos Aires, American Marketing & Communication; 2000: 45-54

Pandian Ng. InLravascular and intracardiac ultrasouncl imaging. An oid concept now on the road to reality. Circulation 1989; 80: 1091-1094

Yamagishi M. Terashima M. Awano K, et al. Morphology of vulnerable coronary plaque: insights fron follow-up of patients examined by intravascular ultrasound before an acute coronary syndrornes. J Am Col] Cardiol 2000: 35: 106-111

Zouridakis EG. Evaluación local de la vulnerabilidad de la placa atcroesclerosa. lo: Esper RJ, Vilariño JO (Eds): La placa ateroesclerótica vulnerable. Buenos Aires, American Marketing & Comrnunication: 2000: 40-44

Uchida Y, Nakamura E, 'i'omaru T, el al. Predictbon of acule coronary sindromes by perculancous coronary angioscopy in patients with stable angina. Am Heart 3 1995; 130: 195-203

Strumpf RK, Euser RR, Eagan J'II Angioscopy: a valuable tool in the deployment and evaluatio of intracoronary stents. Am Heart J 1993; 126: 1204-1210

Casscells W, Hathorn B, David M, et al. Thermal detection of cellular infil trates in living atherosclerotic plaques: possíhle implication for plaque rupture and thrombosis. Lancet 1996; 347: 1447-1451

Stefanadls C, Diamantopoulos L. Vlachopoulos C, et al. Thermal heterogeneity within human atherosclerotic coronary arteries detected in vivo: a new niethod of detectlon by application of a special thcrrnography catheter. Circulation 1999; 99: 1965-1971

Stefanadis C, Diamantopoulos L, Dernellis J et al. Heat production of atherosclerotic plaques and inflammation assessed by the acute phase proteins in acute coronary syndromes. J Mol Ccli Cardiol 2000: 32: 43-52

Payad ZA, Fuster V. Evaluación de la placa aterosclerótica vulnerable por resonancia magnética. In: Esper RJ, Vilariño JO (Eds): La placa aterosclerótica vulnerable. Buenos Aires, American Marketing & Conirriunication; 2000: 34-39 Hatsukami TS, Ross S, Poliossar NT. et al. Visualizatiori of flhrous cap thickness and rupture in human atherosclerotic carotid plaque in vivo with high-resolution magnetic resonance imaging. Circulation 2000; 102: 959-964

Viamonte M Jr. Woodhouse C, Agataslon A, Bugnone A, King D. Diagnóstico precoz de la aterosclerosis coronaria por toniografía computarizada ultrarrápida. In : Esper RJ, Vilariño Jo Eds): La placa aterosclerótica vulnerable. Buenos Aires, American Marketing & Communication; 2000: 25-33

El Sharnouby KA. Evaluación de la aLerosclñerosis carotídea por ultrasonido. In: Esper RJ, Vilariño Jo Eds): La placa aterosclerótica vulnerable. Buenos Aires, American Marketing & Comrnunication; 2000: 55-64

Esper RJ. Interrogando al endotelio. Rey Argeni Cardiol 2000: 68: 429-439

Vilariño JO, CacharrónJL, Suarez DH, Kura M. Machado R, Bolaño AL, Esper RJ. Evaluación de la función endotelial por eco-Doppler. Influencia de la edad, sexo y factores de riesgo. Rey Argent Cardiol 1998; 66: 523-532

Séller AM, Drexler H, Saurier B. y col. Endothelium-mediated coronary blood flow modulation in humaus: effect of age, atherosclerosis. hypercholesterolemia, and hypertension. J Clin Invest 1993; 92: 652-662

Celermajer DS, Sorensen KE, Spiegelhalter DJ, y col. Ageing is associated with endotelial dysfunction in healthy men years before the age-related decline in womwn. J Am Coil Cardiol 1994; 24:471-476

Gordon JB, Ganz F Nabel EG, y col. Atherosclerosis and endotelial function influence the coronary vasomotor response lo exercise. J Clin Invest 1989; 83: 1946-1952

Nabel Eg, Selwyn AP Ganz P Large coronary arteries in hurnans are responsive lo changing biood flow: an endothelium-dependent mechanism that fail in patients with atherosclerosis. J Am Col] Cardiol 1990: 16: 349-356

Williams JK, Adams MR, Klopfenstein HS. Estrogen modulates responses of atherosclerotic coronary arteries. Circulation 1990; 81: 1680-2687

Lieberman EH, Gerhard MD, Ucata A, y col. Estrogen improves endotheliurn-dependent, flow-mediated vasodilation in postmenopausal women. Ann Interm Mcd 1994: 121: 936-941

Creager MA, Cooke JP, Mendelsohn ME, y col. Impaired vasodilatation of forearm resistence vessels in hypercholesterolemic humans. J Cii Invest 1990; 86: 228-234

Panza JA, Cannon III RO (Eds): Endothelium, nitrid oxide, and atherosclerosis. New York, Futura Publishing Inc. 1999 CelermajerDS, Sorensen KE, Georgakopoulos D, y col: Cigarette smoking is associated with dose-related and potentially reversible impairment of cndothelium-clependent clilation in healthy youngadults.Circulation 1993; 88 (par[ 1): 2149-2155

Zeiher A, Schachinger y, Minners J. Long-term cigaretie smoking irnpairs en do t he 1 ium - dep en cien t coronary vasodilator function. Circulation 1995; 92: 1094-1100

Celermajer DS, Adams MR, Clarkson P y col. Passive smoking and impaired eridothelium-dependen( arterial dilatation in healthy young adults. N Engl J Mcd 1996; 334: 150-154

Mark AL, Correla M, Morgan DA, y col. Obesity.induccd hipertension. New concepts from the emerglng biology of obesity. Hypertension 1999; 33(part II): 537-541

Johnstone MT, Creager SJ, Scales KM, y col. Impaired endothelium-dependent vasodilaUon in patients with insulin-depencicnt diabetes mellitus. Circulation 1993; 88: 2510-2516

Snell PG, Mitchell JH. Physical inactivity. An easily modified risk factor?. Circulation 1999; 100: 2-4 Celerniajer DS, Sorensen K, Ryalls M, y col. Impaired ericlotelial function occurs in the systemic arteries of children with homozygous homocystinuria but not in Iheír heterozygous parents. 3 Am Coli Cardiol 1993; 22: 854-858

Egashira K. Hirooka Y, Kai H. Sigimachi M, y col. Rcduction lo serum cholesterol with pravastatin improves cndothclium-dependent vasomotion in patients with hyperchol este rolemia. Circulation 1994: 89: 2519-2524

Treasure CB, Klein JI- Weintraub WS, y col. Beneficial effects of cholesterol-lowering therapy on the coronary endotheliuni in patients with coronary artery disease. N Engi 3 Med 1995; 332: 481-487

Waters D. Cho1estero1 lowering. Should it continue to be the last thing we do. Circulation 1999; 99: 3215-3217

Webb D, Vallance P (Eds). Enclothelial function in hypertension. Bcrling, Springer-Verlag, 1997 Horning B, Maier V, Drexier H. Physical training improves endothelial function in patients with chronic heart failure. Circulation 1996,; 93: 210-214

Creager MA, Gallgher Sj, Girerd Xi, y col. L-Arginine improves cndotheliuni-clepcndent vasodilation in hypercholesterolemic hurnans. 3 Clin Invst 1992; 90: 1248-1253

Drexler H, Zeiher AM, Meinertz 'L y col. Correcting endothelial dysfunction in coronary niicrocirculatíon of hypercholesterolemic patients by L-arginine. Lancet 1991: 338: 1546-1550

Clarkson D, Adams MR, Powe A, y col. Oral L .arginine improves endothelium-dependent clilation jo hypercholesterolemic young adults. J Clin Invest 1996; 97: 1989-1994

Griendling KK, Alexander RW. Oxidative stress and cardiovascular disease. Circulation 1997; 96: 3264-3265

Rídke PM, Cushman M, Stampfer Mi, y col. Inflammation, aspirin and the risk of cardiovascular disease in apparently healthy men. N Engi. J Meci 1997; 336: 973-979

Ridker PM. Inflammation. infection and cardiovascular risk. How good is the clinical evidence? Circulation 1998; 96: 1671-1674

Levine GN, Frci B. Koulouris SN. y col. Ascorbic acid reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation 1996; 93: 1107-1113

Gokce N. Keaney JF Jr, Frci B, y col. Long-term ascorbic acid administration reverses endothelial vasomotor dysfunction lo patients with coronary artery disease. Circulation 1999; 99: 3234-3240

Solzbach U, Hoi-nig B, Jeserich M y col. Vitainin C improves endotelial dysfunction of epycardial coronary arteries in hypertcnsive patients. Circulation 1997; 96: 1513-1519

Ploinick GD, Corretti MC, Vogel RA. Effcct of antioxidant vitamins on the transient impair-mcnt of endothclial-deperident brachial artery vasoactivily foliowing a single high-fat meal. JAMA 1997; 278: 1682-1686 70,

Heitzcr '1', Just H, Munzel T. Antioxidant vitamin C improves endothelial dysfunction lo chronic smokers. Circulation 1996; 94: 6-9 71. Esper RJ, Machado R, Vilariño J, y col. Endothelium-dependenl response in hypercholesterolemic coronary artery disease patients under the cffects of simvastatin aoci erialapril, either separately o combined. Am heart J 2000; 140: 684-689

Esper Rj. Efectos "pleiotrópicos" de los antagonistas del calcio. Rey Argent Cardiol 2001; 69: 225-232

Esper RJ, Vilariño JO. Tratamiento de la clisfunción endotelial. In: Esper RJ, Vilariño JO (eds): La placa ateroesclerosa vulnerable. Buenos Aires, American Marketing & communication 2000: 113-128 Yatacco R, Corretti M, Garder A, y col. Endotelial Reactivity an cardiac risk factors in older patients with periferal arterial disease. Am J Cardiol 1999; 83: 754-758

Schachinger V. Britten M. Zeiher AM, y col. Impaireci epicardial coronary vasoreactivity predicts for adverse cardiovascular events during long-termo follow-up. Circulation 1999; 100 (Suppl 1): 1-54 (abslract)

Neunteufl T, Heher S. Katzenchlager R, Wolfl G. Late prognostic value 0f flow-rneclialed dilation in (he brachial artery of patients with chest pain. Am J Cardiol 2000; 86: 207-2 10

Al Suwaidi J, Hamasaki S. Higano ST y col. Long-term follow up of patients with mild coronary artery disease and endothclial dysfunction. Circulation 2000: 101:948-954

Schoeder SC, Enderle M. Ossen R, y col. lnfluencc of vessel size on (he flow mediated dilation (FMD%) of (he brachial artery. Circulation 1999; 100 (suppl 1): 1-102 (Ahslract)

Esper RJ, Vilariño JO, Cacharron JL, y col. lmpaired endotelial function in patients with rapidly stabilizecl unestable angina: assesrncnt by noninvasivc braquial artery ul lrasonographv. Clin. Cardiol 1999; 22: 699-703

Descargas

Publicado

2004-08-09

Cómo citar

1.
Esper R. De los factores de riesgo de enfermedad arterial a la placa ateromatosa detección de la placa de alto riesgo . Rev Fac Cien Med Univ Nac Cordoba [Internet]. 9 de agosto de 2004 [citado 10 de mayo de 2024];61:39-52. Disponible en: https://revistas.unc.edu.ar/index.php/med/article/view/32578

Número

Sección

Artículos Originales