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Vol. 54. Núm. 3.
Páginas 145-161 (Enero 2002)
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Vol. 54. Núm. 3.
Páginas 145-161 (Enero 2002)
DOI: 10.1016/S0003-3170(02)74740-8
Acceso a texto completo
Factores de riesgo y factores pronósticos en la arteriosclerosis precoz de extremidades inferiores
Risk factors and factors in the prognosis of early arteriosclerosis of the lower limbs
Factores de risco e factores de prognóstico naarteriosclerose precoce dosmembrosinferiores
Visitas
...
E. Puras-Mallagray
Autor para correspondencia
epuras@fhalcorcon.es

correspondence: Departamento de Cirugía. Unidad de Cirugía Vascular. Hospital Fundación Alcorcón. Budapest, 1. E-28922Alcorcón, Madrid.
, S. Luján-Huertas, M. Gutiérrez-Baz, S. Cááncer-Pérez
Unidad de Cirugía Vascular. Hospital Fundación Alcorcón. Madrid, España.
Información del artículo
Summary
Objective

To present an up-to-date review of the classical and recently described risk factors associated with early arterial disease in peripheral vascular territory, and describe the imaging techniques which permit evaluation of the stage of development of the arteriosclerotic plaque.

Development

The treatment of a patient with peripheral arterial disease should be considered in the context of the natural history of the disorder and especially with regard to the knowledge and control of risk factors and markers which may predict clinical deterioration of the condition. Arteriosclerosis starts at a very early stage of life and should be considered to be a chronic inflammatory disorder. As well as the classical factors involved in this disorder, such as hypercholesterolaemia, smoking and diabetes, there is also insulin resistance and the more recently discovered factors such as hyperhomocysteinaemia, global load of infection, procoagulant factors and the as yet unknown genetic markers. We are starting to discover how the disease develops with the help of imaging techniques such as ultrasound, computerized tomography using a beam of electrons and magnetic resonance, which allows us to detect potentially vulnerable plaques.

Conclusions

The concept of arteriosclerosis has changed considerably in recent years. Early development of this chronic inflammatory condition is linked to many factors which are still to be discovered and controlled. The analytical determinations and diagnostic techniques available to us will permit better control ofthis condition.

Key words:
Arteriosclerosis
Global load of infection
Homocysteine
Inflammation
Insulin resistance
Riskfactors
Resumen
Objetivo

Presentar una revisión actualizada de los factores de riesgo clásicos y emergentes asociados a enfermedad arterial precoz en el territorio vascular periférico, y describir las técnicas de imagen que permiten valorar el estadio evolutivo de la placa arteriosclerótica.

Desarrollo

El manejo de un paciente con enfermedad arterial periférica ha de plantearse en el contexto de la historia natural de la enfermedad y, en particular, en el conocimiento y control de los factores de riesgo y marcadores que puedan predecir el deterioro clínico de la misma. La arteriosclerosis se inicia en épocas muy tempranas de la viday debe considerarse como una enfermedad inflamatoria crónica. A los clásicos factores que influyen en esta patología, como la hipercolesterolemia, el tabaco, la diabetes o el más reciente síndrome de resistencia a la insulina, hay que añadir otros más modernos, como la hiper-homocisteinemia, la carga infecciosa global, los factores procoagulantes y los todavía poco conocidos marcadores genéticos. La enfermedad presenta unas características evolutivas que empiezan a descubrirse gracias a técnicas de imagen, como los ultrasonidos, la tomografía computadorizadapor haz de electrones y la resonancia magnética, que permiten conocer qué placas pueden considerarse vulnerables.

Conclusiones

El concepto de arteriosclerosis ha variado sustancialmente en los últimos años. El desarrollo precoz de esta entidad inflamatoria crónica se liga a una multiplicidad de factores que deben conocerse y controlarse. Las determinaciones analíticas y las técnicas de diagnóstico al alcance permitirán un mejor control de esta entidad.

Palabras clave:
Arteriosclerosis
Carga infeccios a global
Factores de riesgo
Homocisteína
Inflamación
Resistencia a la insulina
Resumo
Objectivo

Apresentar uma revisão actualizada dos factores de risco clássicos e emergentes associados á doenca arterial precoce no território vascular periférico, e des-crever as técnicas de imagem que permitem avaliar o estádio evolutivo daplaca arteriosclerótica.

Desenvolvimento

O tratamento de um doente com doença arterial periférica deve ser considerada no contexto da história natural da doença e, em particular, no conhe-cimento e controlo dos factores de risco e marcadores que podem predizer a deterio-ração clínica da doença. A arteriosclerose inicia-se em épocas muito precoces da vida e deve considerar-se uma doença inflamató-ria crónica. Entre os clássicos factores que influem nestapatologia, como a hipercolesterolemia, o tabaco, a diabetes e a mais recente síndroma de resistência à insulina, é necessário incluir outros mais modernos, como a hiperhomocisteinemia, a carga infecciosa global, os factores pró-coagulantes, e os ainda desconhecidos marcadores genéticos. A doença apresenta algumas características evolutivas que começamos a descobrir graças às técnicas de imagem, como os ultra-sons, a tomografia computorizada por feixe de electrões e a ressonância magnética, que permitem conhecer as placas que se podem considerar vulneráveis.

Conclusões

O conceito de arteriosclerose tem variado substancialmente nos últimos anos. O desenvolvimento precoce desta entidade inflamatória crónica está ligado a uma multiplicidade de factores que se devem conhecer e controlar. As determinaçõoes analíticas e as técnicas de diagnóstico ao nosso alcance permitirão um melhor controlo desta entidade.

Palavras clave:
Arteriosclerose
Carga infecciosa global
Factores de risco
Homocisteina
Inflamação
Resistência à insulina
El Texto completo está disponible en PDF
Bibliografía
[1.]
K. Ouriel.
Peripheral arterial disease.
Lancet, 358 (2001), pp. 1257-1264
[2.]
H.E. Stoffers, P.E. Rinkens, A.D. Kester, V. Kaiser, J.A. Knottnerus.
The prevalence of asymptomatic and unrecognized peripheral vascular disease.
Int J Epidemiol, 25 (1996), pp. 282-290
[3.]
H.E. Stoffers, V. Kaiser, J.A. Knottrenus.
Prevalence in general practice.
Epidemiology in peripheral vascular disease, pp. 109-115
[4.]
I. Garcia-Fernández, J.M. Llaneza, M.J. Ramos, E. Coto, F. Vaquero, L. Camblor, et al.
Variación genética y enfermedad aterosclerótica periférica: estudio preliminar.
Angiologia, 53 (2001), pp. 310-320
[5.]
C. Napoli, F.P. D'Armiento, F.P. Mancini, A. Postiglione, J.L. Witztum, G. Palumbo, et al.
Fatty streak formation occurs in human fetal aortas and is greatly enhanced by maternal hypercolesterolemia: intimal accumulation of low density lipoprotein and its oxidation precede monocyte recruitment into early atherosclerotic lesions.
J Clin Invest, 100 (1997), pp. 2680-2690
[6.]
H.C. Stary, A.B. Chandler, S. Glagov, J.R. Guyton, W.J. Insull, M.E. Rosenfeld, et al.
A definition of initial, fatty streak, and intermediate lesions of atherosclerosis: a report from the Committe on vascular lesions of the Council on Arteriosclerosis, American Heart Association.
Circulation, 89 (1994), pp. 2462-2478
[7.]
R. Ross.
Atherosclerosis: an inflamatory disease.
N Engl J Med., 340 (1999), pp. 115-126
[8.]
M. Navab, J.A. Berliner, A.D. Watson, S.Y. Hama, M.C. Territo, A.J. Lusis, et al.
The Yin and Yang of oxidation in the development of the fatty streak: a review based on the 1994 George Lyman Duff memorial lecture.
Arterioscler Thromb Vasc Biol, 16 (1996), pp. 831-842
[9.]
D.W. Morel, J.R. Hessler, G.M. Chisholm.
Low density lipoprotein cytotoxicity induced by free radical peroxidation of lipid.
J Lipid Res, 24 (1983), pp. 1070-1076
[10.]
K.K. Griendling, R.W. Alexander.
Oxidative stress and cardiovascular disease.
Circulation, 96 (1997), pp. 3264-3265
[11.]
J. Han, D.P. Hajjar, M. Febbraio, A.C. Nicholson.
Native and modified low density lipoproteins increase the functional expression of the macrophage class B scavenger receptor, CD36.
J Biol Chem, 272 (1997), pp. 21654-21659
[12.]
M.N. Diaz, B. Frei, J.A. Vita, J.F. Keaney Jr..
Antioxidants and atherosclerotic heart disease.
N Engl J Med., 337 (1997), pp. 408-416
[13.]
W.B. Kannel.
Risk factors for atherosclerotic cardiovascular outcomes in different arterial territories.
J Cardiovasc Risk, 1 (1994), pp. 333-339
[14.]
T.R. Pedersen, J. Kjekshus, K. Pyorala, A.G. Olsson, T.J. Cook, T.A. Musliner, et al.
Effect of simvastatin on ischaemic signs and symptoms in the Scandinavian simvastatin survival study (4S).
Am J Cardiol, 81 (1998), pp. 333-335
[15.]
M.H. Criqui, D. Browner, A. Fronek, M.R. Klauber, S.S. Coughlin, E. Barrett-Connor, et al.
Peripheral arterial disease in large vessels is epidemiologically distinct from small vessel disease: an analysis of risk factors.
Am J Epidemiol, 129 (1989), pp. 1110-1119
[16.]
M.H. Criqui, J.O. Denenberg, R.D. Langer, A. Fronek.
The epidemiology of peripheral arterial disease: importance of identifying the population at risk.
Vasc Med., 2 (1997), pp. 221-226
[17.]
J. Dormandy, L. Heeck, S. Vig.
Predictors of early disease in the lower limbs.
Sem Vasc Surg., 12 (1999), pp. 109-117
[18.]
S.W.K. Cheng, A.C.W. Ting, J. Wong.
Lipoprotein A and its relatioship to risk factors and severity of atherosclerotic peripheral vascular disease.
Eur J Vasc Endovasc Surg., 14 (1997), pp. 17-23
[19.]
G.H. Gibbons, R.E. Pratt, V.J. Dzau.
Vascular smooth muscle cell hypertrophy vs hyperplasia: autocrine transforming growth factor-beta 1 expression determines growth response to angiotensin II.
J Clin Invest, 90 (1992), pp. 456-461
[20.]
P.M. Vanhoutte, C.M. Boulanger.
Endorhelium-dependent responses in hypertension.
Hypertens Res, 18 (1995), pp. 87-98
[21.]
J.M. Murabito, R.B. D'Agostino, H. Silvershatz, W.F. Wilson.
Intermittent claudication: a risk profile from the Framingham Heart Study.
Circulation, 96 (1997), pp. 44-49
[22.]
G.R. Fowkes, E. Housley, R.A. Riemersma, C.A. Macintyre, E.H. Cawood, R.J. Prescott, et al.
Smoking, lipids.
Glucose intolerance and blood pressure as risk factors for peripheral arteriosclerosis compared with ischaemic heart disease in the Edinburg Artery Study. Am J Epidemiol, 135 (1992), pp. 331-340
[23.]
J.P. Strong, G.T. Malcom, C.A. McMahan, R.E. Tracy, W.P. Newman III, E.E. Herderick, et al.
Prevalence and extent of atherosclerosis in adolescents and young adults.
JAMA, 281 (1999), pp. 727-735
[24.]
R.W. Wissler, J.P. Strong.
Risk factors and progression of atherosclerosis in youth.
Am J Pathol, 153 (1998), pp. 1023-1033
[25.]
W. Erb.
Klinische Beitráge zur Pathologie des Intermittierenden Hinkens.
Munch Med Wochenschr, 2 (1911), pp. 2487
[26.]
W.B. Kannel, D. Shurtleff.
The Framingham study: cigarettes and the development of intermitent claudication.
Geriatrics, 28 (1973), pp. 61-68
[27.]
A.J. MacKaay, P.J. Becks, A.H.M. Dur, M. Bischoff, J. Scholma, R.J. Heine, et al.
The distribution of peripheral vascular disease in dutch caucasian population: comparison of type II diabetics and non-diabetic subjects.
Eur J Vasc Endovasc Surg., 9 (1995), pp. 170-175
[28.]
L. Capron, J. Jarnet, S. Kazandjian, E. Housset.
Growth promoting effects of diabetes and insulin on arteries.
Diabetes, 35 (1986), pp. 973-978
[29.]
G.M. Reaven.
Roel of insulin resistence in human disease: Banting Lecture 1988.
Diabetes, 37 (1998), pp. 1595-1607
[30.]
N.M. Kaplan.
The deadly quartet: upper body obesity, glucose intolerance, hypertriglyceridemia and hypertension.
Arch Intern Med., 149 (1989), pp. 1514-1520
[31.]
A. Misra.
Risk factors for atherosclerosis in young individuals.
J Cardiovasc Risk, 7 (2000), pp. 215-229
[32.]
W. Bao, S.R. Srinivasan, G.S. Berenson.
Persistent elevation of plasma insulin levels is associated with increased cardiovascular risk in children and young adults: the Bogalusa Heart Study.
Circulation, 93 (1996), pp. 54-59
[33.]
S.R. Srinivasan, W. Bao, W.A. Wattigney, G.S. Berenson.
Adolescent overweight is associated with adult overweight and related multiple cardiovascular risk factors: the Bogalusa Heart study.
Methabolism, 45 (1996), pp. 235-240
[34.]
X. Jiang, S.R. Srinivasan, L.S. Webber, W.A. Wattigney, G.S. Berenson.
Association of fasting insulin level with serum lipid and lipoprotein levels in children, adolescents and young adults: The Bogalusa Heart Study.
Arch Intern Med., 155 (1995), pp. 190-196
[35.]
D.L. Rainwater, A.G. Comuzzie, J.L. Vandeberg, M.C. Mahaney, J. Blangero.
Serum leptin levels are independently correlated with two measures of HDL.
Atherosclerosis, 132 (1997), pp. 237-243
[36.]
S. Arslanian, C. Supresongsin, S.C. Kalhan, A.L. Drash, R. Brna, J.E. Janosky.
Plasma leptin in children: relationship to puberty, gender, body composition, insulin sensitivity and energy expenditure.
Methabolism, 47 (1998), pp. 309-312
[37.]
M.R. Nehler, L.M. Taylor Jr., J.M. Porter.
Homocysteinemia as a risk factor for atherosclerosis: a review.
Cardivasc Surg., 6 (1997), pp. 59-67
[38.]
O. Nygärd, J.E. Nordrehaug, H. Refsum, M. Ueland, M. Farstad, S.E. Vollset.
Plasma homocysteine levels and mortality in patients with coronary artery disease.
N Engl J Med., 337 (1997), pp. 230-236
[39.]
L.A. Harker, R. Ross, S.J. Slichter, C.R. Scott.
Homocystine-induced arteriosclerosis: the role of endothelial cell injury and platelet response in its genesis.
J Clin Invest, 58 (1976), pp. 731-741
[40.]
K.A. Hajjar.
Homocysteine-induced modulation of tissue plasminogen activator binding to its endothelial cell membrane receptor.
J Clin Invest, 91 (1993), pp. 2873-2879
[41.]
A. Majors, L.A. Ehrhart, E.H. Pezacka.
Homocysteine as a risk factor for vascular disease: enhaced collagen production and accumulation by smooth muscle cells.
Arterioscler Thromb Vasc Biol, 17 (1997), pp. 2074-2081
[42.]
G.R. Upchurch Jr., G.N. Welch, A.J. Fabian, A. Pigazzi, J.F. Keaney Jr., J. Loscalzo.
Homocysteine decreases bioavailable nitric oxide by a mechanism involving glutathione peroxidase.
J Biol Chem, 272 (1997), pp. 17012-17017
[43.]
I.C. Currie, J.S. Wilson, J. Scott, A. Day, D. Stansbie, R.N. Baird, et al.
Homocysysteine: an independent risk factor for the failure of vascular intervention.
Br J Surg., 83 (1996), pp. 1238-1241
[44.]
R. Clarke, L. Daly, K. Robinson, E. Naughten, S. Cahalane, B. Fowler, et al.
Hyperhomocystinaemia: an independent risk factor for vascular disease.
N Engl J Med., 324 (1991), pp. 1149-1155
[45.]
M. Van den Berg, C.D. Stehouwer, E. Bierdrager, J.A. Rauwerda.
Plasma homocisteine and severity of atherosclerosis in young patients with lower limbs atherosclerotic disease.
Arterioscler Thromb Vasc Biol, 16 (1996), pp. 165-171
[46.]
M. Van-den-Berg, G.H. Boers, D.G. Franken, H.J. Blom, G.J. Vam Kamp, C. Jacobs, et al.
Hyperhomocysteinaemia and endothelial dysfunction in young patients with peripheral arterial occlusive disease.
Eur J Clin Invest, 25 (1995), pp. 176-181
[47.]
M. Kawashiri, K. Kajinami, A. Nohara, K. Yagi, A. Inazu, J. Koizumi, et al.
Plasma homocisteine level and development of coronary artery disease.
Coron Artery Dis, 10 (1999), pp. 443-447
[48.]
P.J. Levy, C.A. Hornung, J.L. Haynes, D.S. Rush.
Lower extremity ischemia in adults younger than forty years of age: a community-wide survey of premature atherosclerotic arterial disease.
J Vasc Surg., 19 (1994), pp. 873-881
[49.]
S.A. Ray, M.R. Rowley, A. Loh, S.A. Talbot, D.H. Bevan, R.S. Taylor, et al.
Hypercoagulable states in patients with leg ischemia.
Br J Surg., 81 (1994), pp. 811-814
[50.]
D. Silver, A. Vouyouka.
The caput medusae of hypercoagulability.
J Vasc Surg., 31 (2000), pp. 396-405
[51.]
L. Bara, V. Nicaud, L. Tiret, F. Cambien, M. Samama.
Expression of a paternal history of premature myocardial infartion on fibrinogen, factor VIIC and PAI-1 in European offspring-the EARS study.
Thromb Haemost, 71 (1994), pp. 434-440
[52.]
A. Khalil, D. Kumar, M. Venatesan.
Platelet aggregation and lipid profile in offsprings of young ischemics.
Indian Pediatr, 34 (1997), pp. 16-19
[53.]
D. Zitoun, L. Bara, A. Basdevant, M. Samama.
Levels of factor VIIc associated with decreased tissue factor pathway inhibitor and increased plasminogen activator inhibitor-1 in dislipidemias.
Arterioscler Thromb Vasc Biol, 16 (1996), pp. 77-81
[54.]
C. Guijarro, J. Tuñón, C. Bustos, M.A. Hernández-Presa, M. Ortego, J. Egido.
La formación de la placa arteriosclerosa: un proceso inflamatorio y fibroproliferativo.
Clin Invest Arteriosclerosis, 9 (1997), pp. 3-14
[55.]
P.M. Ridker.
High sensitivity C reactive protein: potencial adjunt for global risk assessment in the primary prevention cardiovascular disease.
Circulation, 103 (2001), pp. 1813-1818
[56.]
C. Guijarro.
High-Sensitivity C-reactive protein: potencial adjunt for global risk assessment in the primary prevention of cardiovascular disease.
Circulation, 104 (2001), pp. 127
[57.]
C.C. Kuo, J.T. Grayston, L.A. Campbell, Y.A. Goo, R.W. Wissler, E.P. Benditt.
Chlamydia pneumoniae in coronary arteries of young adults (1534 years old).
Proc Natl Acad Sci U S A, 92 (1995), pp. 6911-6914
[58.]
F.J. Nieto.
Infections and atherosclerosis: new clues from an old hypothesis?.
Am J Epidemiol, 148 (1998), pp. 937-948
[59.]
J. Zhu, F.J. Nieto, B.D. Horne, J.L. Anderson, J.B. Muhlestein, S.E. Epstein.
Prospective studyof pathogen burben and risk of miocardial infarction or death.
Circulation, 103 (2001), pp. 45-51
[60.]
C. Espinola-Klein, H.J. Rupprecht, S. Blankenberg, C. Bickel, H. Kopp, G. Rippin, et al.
Impact of infectious burden on extent and long term prognosis of atherosclerosis.
Circulation, 103 (2002), pp. 15-21
[61.]
J. Gutiérrez-Fernández, J. Linares-Palomino, F. Fernández-Sánchez, M. Guerrero-Fernández, E.C. López, E. Ros-Díe, et al.
Presencia de anticuerpos anti-Chlamydia pneumoniae en procesos vasculares periféricos y neurológicos.
Rev Neurol, 32 (2001), pp. 501-505
[62.]
D.A. De Luis, I. García-Arata, J. Haurie, L. de Rafael, J. González, A. Becerra, et al.
Estudio de la prevalencia de Helicobacter pylori y Chlamydia pneumoniae en placas de ateroma de pacientes diabéticos y no diabéticos con arteriosclerosis.
Clin Invest Arterioscler, 13 (2001), pp. 103-107
[63.]
C.N. Hales, D.J. Barker, P.M. Clark, L.J. Cox, C. Fall, C. Osmond, et al.
Fetal and infant growth and impared glucose tolerance at age 64.
Br Med J, 303 (1991), pp. 1019-1022
[64.]
E. Vestbo, E.M. Damsgaard, A. Froland, C.E. Mogensen.
Birth weight and cardiovascular risk factors in a epidemiological study.
Diabetología, 39 (1996), pp. 1598-1602
[65.]
C.M. Law, G.S. Gordon, A.W. Shiell, D.J. Barker, C.N. Hales.
Thiness at birth and glucose tolerance in seven-year-old children.
Diabet Med., 12 (1995), pp. 24-29
[66.]
J. Goodfellow, M.F. Bellamy, S.T. Gorman, M. Brownlee, M.W. Ramsey, M.J. Lewis, et al.
Endothelial function is impared in fit young adults of low birth weigth.
Cardiovasc Res, 40 (1998), pp. 600-606
[67.]
I. Saito, M. Nishino, H. Kawabe, H. Wainai, C. Hasegawa, T. Saruta, et al.
Leisure time physical activity and insulin resistance in young obese students with hypertension.
Am J Hypertens, 5 (1992), pp. 915-918
[68.]
S. Taimela, T. Lehtimaki, K.V. Poorkka, L. Rasanen, J.S. Viikari.
The effect of physical activity on serum total and low density lipoprotein cholesterol concentrations varies with apolipopro-tein E phenotype in male children and young adults: The Cardiovascular Risk in Young Finns Study.
Metabolism, 45 (1996), pp. 779-803
[69.]
O.T. Raitakari, K.V. Porkka, L. Rasanen, J.S. Viikari.
Relations of life-style with lipids, blood pressure and insulin in adolescents and young adults.
The Cardiovascular Risk in Young Finns Study. Atherosclerosis, 111 (1994), pp. 237-246
[70.]
D.J. Galton, R.K. Mattu, J. Cavanna.
Polymorphisms of the lipoprotein lipase gene and premature atherosclerosis.
J Intern Med., 736 (1994), pp. 63-68
[71.]
L. Tiret, P. de Knijff, H.J. Menzel, C. Ehnholm, V. Nicaud, L.M. Havekes.
ApoE polymorphism and predisposition to coronary heart disease in youths of different European populations.
Th EARS Study. European Atherosclerosis Research Study. Arterioscler Thromb, 14 (1994), pp. 1617-1624
[72.]
H.S. Hescht.
Lipid disorders and plaque imaging.
Am J Cardiol, 88 (2001), pp. 56-58
[73.]
P. Raggi, T.Q. Callister, B. Cooil, Z.X. He, J.J. Mahmariam.
Identification of patients at increased risk of first unheralded acute myocardial infartion by electron-beam computed tomography.
Circulation, 101 (2000), pp. 850-855
[74.]
M.L. Wood, F.W. Wehrli.
Principles of magnetic resonanace imaginng, 3, Mosby, (1999),
[75.]
O.T. Raitakari.
Imaging of subclincal atherosclerosis in children and young adults.
Ann Med., 31 (1999), pp. 33-40
[76.]
R.A. Vogel.
Measurement of endothelial function by braquial artery flow-mediated vasodilation.
Am J Cardiol, 88 (2001), pp. 31-34
[77.]
D.S. Celermajer, K.E. Sorensen, V.M. Gooch, D.J. Spiegelhalter, O.J. Miller, I.D. Sullivan, et al.
Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis.
Lancet, 340 (1992), pp. 1111-1115
[78.]
D.S. Celermajer, K.E. Sorensen, C. Bull, J. Robinson, J.E. Deanfield.
Endothelium-dependent dilation in the systemic arteries of asymtomatic subjects relates to coronary risk factors and their interaction.
J Am Coll Cardiol, 24 (1994), pp. 1468-1474
[79.]
J.M. McLenachan, J.K. Williams, R.D. Fish, P. Ganz, A.P. Selwyn.
Loss of flow-mediated endothelium-dependent dilation occurs early in the development of atherosclerosis.
Circulation, 84 (1991), pp. 1273-1278
[80.]
B.R. Chambers, J.W. Norris.
Outcome in patients with asymptomatic neck bruits.
N Engl J Med., 315 (1986), pp. 860-865
[81.]
G.L. Burke, G.W. Evans, W.A. Riley, A.R. Sharret, G. Howard, R.W. Barnes, et al.
Arterial wall thickness is associated with prevalent cardiovascular disease in middle-aged adults: The Atherosclerosis Risk in communities (ARIC) Study.
Stroke, 26 (1995), pp. 386-391
[82.]
D.H. O'Leary, J.F. Polak, R.A. Kronmal, S.J. Kittner, M.G. Bond, S.K. Wolfson, et al.
Distribution and correlates of sonographically detected carotid artery disease in the Cardiovascular Health Study.
Stroke, 23 (1992), pp. 1752-1760
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