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Vol. 54. Núm. 2.
Páginas 64-75 (Enero 2002)
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Vol. 54. Núm. 2.
Páginas 64-75 (Enero 2002)
DOI: 10.1016/S0003-3170(02)74728-7
Acceso a texto completo
Importancia de la hipercoagulabilidad en la cirugía de la isquemia crónica de extremidades inferiores
The importance of hypercoagulability in the surgery of chronic ischaemia of the lower limbs
Importáncia da hipercoagulabilidade na cirurgia da isquemia crónica dos membros inferiores
Visitas
...
S. Cáncer-Pérez, F. Acín-García
Autor para correspondencia
facing@meditex.es

correspondence: Hospital Universitario de Getafe. Ctra. de Toledo km 12,500. E-28901 Getafe (Madrid). Fax: +34916839748.
, A. Fernández-Heredero, L. de Benito-Fernández, A. Bueno-Bertomeu, J. Alfayate-García, J.R. March-García, A. López-Quintana de Carlos
Servicio de Angiología y Cirugía Vascular. Hospital Universitario de Getafe. Madrid, España.
Información del artículo
Summary
Introduction

A high prevalence of hypercoagulability states has been described in patients with chronic ischaemia. Objective. To determine the prevalence and importance of hypercoagulability states inpatients with chronic occlusive disorders of the lower limbs needing revascularization.

Patients and methods

A prospective study was made between October 1999 and April 2000. In 52 patients we determined: antithrombin 111, proteins C and S, anticardiolipin antibodies, plasminogen, α2-antiplasmin and resistance to activated protein C. We recorded risk factors, clinical features, surgery performed and its results and analyze their relation to hypercoagulability changes.

Results

There was antithrombin 111 deficit in 6% of patients, protein C deficit in 31%, protein Sdeficit in 2%, anticardiolipin antibodies in 10%, and resistance to activated protein C (RAPC) in 12%. In 29% of the patients one alteration was observed; in 13% more than one and in 58% no alteration was seen. Thrombosis occurred in 50% (3/6) as compared with 13% (6/46) of the patients without RAPC (p=0.05). In patients with several alterations, thrombosis occurred in 42% (3/7) compared with 13% (6/45) of the other patients (p=0.08). 33% (2/6) of the patients with RAPC had thrombosis early, compared with 2.1% (1/46) of the remainder (p=0.03). 28% (2/7) of the patients with several alterations had early thrombosis compared with 2.2% (1/45) of the remainder (p=0.04).

Conclusions

There is a high prevalence of hypercoagulability states in chronic ischaemia. These findings have therapeutic implications.

Key words:
Chronic ischaemia
Hypercoagulability
Resistance to activated protein C
Revas-cularization
Resumen
Introducción

Se ha descrito una alta prevalencia de estados de hipercoagu-labilidad en pacientes con isquemia crónica.

Objetivo

Determinar la prevalencia e importancia de estados de hipercoagulabilidad en pacientes con patología oclusiva crónica de extremidades inferiores, que precisan revascularización.

Pacientes y métodos

Estudio prospectivo octubre 1999-abril 2000. En 52 pacientes se determinó: antitrombina III, proteína C y S, anticuerpos anticardiolipina, plasminógeno, α2-antiplasminay resistencia a la proteína C activada. Se registraron factores de riesgo, clínica, cirugía realizada y resultados, y se analizó su relación con alteraciones de hipercoagulabilidad.

Resultados

El 6% presentaban déficit de antitrombina III; el 31%, déficit de proteína C; el 2%, déficit de proteína S; el 10%, anticuerpos anticardiolipina, y el 12%, resistencia a la proteína C activada (RPCA). El 29% de los pacientes presentaban una alteración; el 13%, más de una, y el 58%, ninguna. El50% (3/6) de los pacientes con RPCA se trombo-saron, frente al 13% (6/46) de los pacientes sin RPCA (p=0,05). El 42% (3/7) de los pacientes con varias alteraciones se trombosaron, frente al 13% (6/45) del resto (p=0,08). El 33% (2/6) de los pacientes con RPCA presentaron trombosis precoz, frente al 2,1% (1/46) del resto (p=0,03). El 28% (2/7) de los pacientes con varias alteraciones presentaron trombosis precoz, frente al 2,2% (1/45) del resto (p=0,04).

Conclusiones

Laprevalencia de estados de hipercoagulabilidad en isquémicos crónicos es elevada. Estos hallazgos inducen implicaciones terapéuticas.

Palabras clave:
Hipercoagulabilidad
Isquemia crónica
Resistencia a laproteína C activada
Revascularización
Palabras clave:
Hipercoagulabilidade
Isquemia crónica
Resistência á proteína C activada
Revascularização
Resumo
Introdução

Foi descrita uma alta prevalência de estados de hipercoagulabilidade em doentes com isquemia crónica.

Objectivo

Determinar a prevalência e importância dos estados de hipercoagulabilidade nos doentes com patologia oclusiva crónica dos membros inferiores, necessitando de revascularização.

Doentes e métodos

Estudo prospectivo de Outubro 1999-Abril 2000 de 52 doentes, determinou-se: antitrombina III, proteína C e S, anticorpos anticardiolipina, plasminogénio, α2-antiplasmina e resistência à proteína C activada. Registaram-se os factores de risco, sinto-matologia, cirurgia realizada e resultados, e analisou-se a relação com alterações de hi-percoagulabilidade.

Resultados

6% apresentavam défice de antitrombina III, 31% défice de proteína C, 2% défice de proteína S, 10% anticorpos anticardiolipina, e 12% resistência à proteína C activada (RPCA). 29% dos doentes apresentavam uma alte-ração, 13% mais de uma, e 58% nenhuma. 50% (3/6) dos doentes com RPCA sofreram trombose, face a 13% (6/46) dos doentes sem RPCA (p=0,05). 42% (3/7) dos doentes com várias alterações sofreram trombose, face a 13% (6/45) dos restantes (p=0,08). 33% (2/6) dos doentes com RPCA apresentaram trombose precoce, face a 2,1% (1/46) dos restantes (p=0,03). 28% (2/7) dos doentes com várias alterações apresentaram trombose precoce, face a 2,2% (1/45) dos restantes (p=0,04).

Conclusoes

Aprevalência de estados de hipercoagulabilidade nos isquémicos crónicos é elevada. Estes achados induzem implicações terapêuticas.

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Bibliografía
[1.]
D. Silver, A. Vouyouka.
The caput medusae of hypercoagulability.
J Vasc Surg., 31 (2000), pp. 396-405
[2.]
J.H. Griffin, B. Evatt, T.S. Zimmerman, A.J. Kleiss, C. Wideman.
Deficiency of protein C in congenital thrombotic disease.
J Clin Invest, 68 (1981), pp. 1370-1373
[3.]
C.F. Allaart, S.R. Poort, F.R. Rosendaal, P.H. Reitsma, R.M. Bertina, E. Briet.
Increased risk of venous thrombosis in carriers of hereditary protein C deficiency defect.
Lancet, 341 (1993), pp. 134-138
[4.]
H.P. Schawrz, M. Fischer, P. Hopmeier, M.A. Batard, J.H. Griffin.
Plasma protein S deficiency in familial thrombotic disease.
Blood, 64 (1984), pp. 1297-1300
[5.]
P.C. Comp, C.T. Esmon.
Recurrent venous thromboembolism in patients with a partial deficiency of protein S.
N Engl J Med., 311 (1984), pp. 1525-1528
[6.]
C.G. Lauer, T.J. Reid III, C.S. Wideman, B.L. Evatt, B.M. Alving.
Free protein S deficiency in a family with venous thrombosis.
J Vasc Surg., 12 (1990), pp. 541-544
[7.]
M. Makris, M. Leach, N.J. Beauchamp, M.E. Daly, P.C. Cooper, K.K. Hampton, et al.
Genetic analysis, phenotypic diagnosis, and risk of venous thrombosis in families with inherited deficiencies of protein S.
Blood, 95 (2000), pp. 1935-1941
[8.]
A.I. Schafer.
The hypercoagulable states.
Ann Intern Med., 102 (1985), pp. 814-828
[9.]
A. Chervu, G.P. Clagett.
Bleeding & clotting disorders.
Current Diagnosis & Treatment in Vascular Surgery, pp. 55-79
[10.]
J. Eldrup-Jorgensen, D.P. Flanigan, L. Brace, A.P. Sawchuk, S.G. Mulder, C.P. Anderson, et al.
Hypercoagulable states and lower limb ischemia in young adults.
J Vasc Surg., 9 (1989), pp. 334-341
[11.]
M.C. Donalson, D.S. Weinberg, M. Belkin, A.D. Whitte-more, J.A. Mannick.
Screening for hypercoagulable states in vascular surgical practice: a preliminary study.
J Vasc Surg., 11 (1990), pp. 825-831
[12.]
J.D. Eason, J.L. Mills, W.C. Beckett.
Hypercoagulable states in arterial thromboembolism.
Surg Gynecol Obstet, 174 (1992), pp. 211-215
[13.]
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 ischaemia.
Br J Surg., 81 (1994), pp. 811-814
[14.]
S.A. Ray, M.R. Rowley, D.H. Bevan, R.S. Taylor, J.A. Dormandy.
Hypercoagulable abnormalities and postoperative failure of arterial reconstruction.
Eur J Vasc Endovasc Surg., 13 (1997), pp. 363-370
[15.]
R.B. Rutherford, J.D. Baker, C. Ernst, K.W. Johnston, J.M. Porter, S. Ahn, D.N. Jones.
Recommended standards for reports dealing with lower extremity ischemia: revised version.
J Vasc Surg., 26 (1997), pp. 517-538
[16.]
R.M. Bertina.
Factor V Leiden and other coagulation factor mutations affecting thrombotic risk.
Clin Chem, 43 (1997), pp. 1678-1683
[17.]
J.B. Towne, V.M. Bernhard, C. Hussey, J.C. Garancis.
Antithrombin deficiency: a cause of unexplained thrombosis in vascular surgery.
Surgery, 89 (1981), pp. 735-742
[18.]
S. Nitecki, B. Brenner, A. Hoffman, N. Lanir, A. Schramek, S. Torem.
Lower limb ischaemia in primary antiphospholipid syndrome.
Eur J Vasc Surg., 7 (1993), pp. 414-419
[19.]
C.K. Shortell, K. Ouriel, R.M. Green, J.J. Condemi, J.A. DeWeese.
Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis.
J Vasc Surg., 15 (1992), pp. 158-166
[20.]
R.W. Lee, L.M. Taylor, G.J. Landry, S.H. Goodnight, G.L. Moneta, J.M. Edwards, et al.
Prospective comparison of infrainguinal bypass grafting in patients with and without antiphospholipid antibodies.
J Vasc Surg., 24 (1996), pp. 524-533
[21.]
B. Dahlbäck, M. Carlsson, P.J. Svensson.
Familial thrombophilia due to a previously unrecognised mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C.
Proc Natl Acad Sci U S A, 90 (1993), pp. 1004-1008
[22.]
R.M. Bertina, B.P. Koeleman, T. Koster, F.R. Rosendaal, R.J. Driven, H. de Ronde, et al.
Mutation in blood coagulation factor V associated with resistance to activated protein C.
Nature, 369 (1994), pp. 64-67
[23.]
T. Koster, F.R. Rosendaal, H. de Ronde, E. Briét, J.P. Vandenbroucke, R.M. Bertina.
Venous thrombosis due to poor anticoagulant response to activated protein C: Leiden Thrombophilia Study.
Lancet, 342 (1993), pp. 1503-1506
[24.]
P.J. Svensson, B. Dahlbäck.
Resistance to activated protein C as a basis for venous thrombosis.
N Engl J Med., 330 (1994), pp. 517-522
[25.]
J. Sánchez, J. Román, M.J. de la Torre, F. Velasco, A. Torres.
Low prevalence of the factor V Leiden among patients with ischemic stroke.
Haemostasis, 27 (1997), pp. 9-15
[26.]
F. Demarmels Biasiutti, C. Merlo, M. Furlan, I. Sulzer, B.R. Binder, B. Lammle.
No association of APC resistance with myocardial infarction.
Blood Coagul Fibrinolysis, 6 (1995), pp. 456-459
[27.]
F.R. Rosendaal, T. Koster, J.P. Vandenbroucke, P.H. Reitsma.
High risk of thrombosis in patients homozygous for factor V Leiden (activated protein C resistance).
Blood, 85 (1995), pp. 1504-1508
[28.]
N.J. Beauchamp, M.E. Daly, K.K. Hampton, P.C. Cooper, F.E. Preston, I.R. Peake.
High prevalence of a mutation in the factor V gene within the U.K.
population: relationship to activated protein C resistance and familial thrombosis. Br J Haematol, 88 (1994), pp. 219-222
[29.]
P.M. Ridker, C.H. Hennekens, K. Lindpaintner, M.J. Stampfer, P.R. Eisenberg, J.P. Miletich.
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., 332 (1995), pp. 912-917
[30.]
D.C. Rees, M. Cox, J.B. Clegg.
World distribution of factor V Leiden.
Lancet, 346 (1995), pp. 1133-1134
[31.]
M.A. Laffan.
Activated protein C resistance and myocardial infarction.
Heart, 80 (1998), pp. 319-321
[32.]
B. Zóller, P.J. Svensson, X. He, B. Dalhback.
Identification of the same factor V gene mutation in 47 out of 50 thrombosis-prone families with inherited resistance to activated protein C.
J Clin Invest, 94 (1994), pp. 2521-2524
[33.]
H. de Ronde, R.M. Bertina.
Laboratory diagnosis of APC-resistance: a critical evaluation of the test and development of diagnostic criteria.
Thromb Haemost, 72 (1994), pp. 880-886
[34.]
B. Dahlbäck.
Factor V gene mutation causing inherited resistance to activated protein C as a base for venous thromboembolism.
J Intern Med., 237 (1995), pp. 221-227
[35.]
E.S.K. Sampram, B. Lindblad, B. Dahlbäck.
Activated protein C resistance in patients with peripheral vascular disease.
J Vasc Surg., 28 (1998), pp. 624-629
[36.]
M. Fisher, J.A. Fernández, S.F. Ameriso, D. Xie, A. Gruber, A. Paganini-Hill, J.H. Griffin.
Activated protein C resistance in ischemic stroke not due to factor V arginine 506 glutamine mutation.
Stroke, 27 (1996), pp. 1163-1166
[37.]
J.H. Griffin, B. Evatt, C. Wideman, J.A. Fernández.
Anticoagulant protein C pathway defective in majority of thrombophilic patients.
Blood, 82 (1993), pp. 1989-1993
[38.]
K. Ouriel, R.M. Green, J.A. DeWeese, C. Cimino.
Activated protein C resistance: prevalence and implications in peripheral vascular disease.
J Vasc Surg., 23 (1996), pp. 46-52
[39.]
P.W.S. Foley, C.D. Irvine, G.R. Standen, C. Morse, F.T. Smith, C. McGrath, et al.
Activated protein C resistance, factor V Leiden and peripheral vascular disease.
Cardiovasc Surg., 5 (1997), pp. 157-160
[40.]
M.C. Donalson, M. Belkin, A.D. Whittemore, J.A. Mannick, J.A. Longtine, D.M. Dorfman.
Impact of activated protein C resistance on general vascular surgical patients.
J Vasc Surg., 25 (1997), pp. 1054-1060
[41.]
S. Kiechl, A. Muigg, P. Santer, M. Mitterer, G. Egger, M. Oberhollenzer, et al.
Poor response to activated protein C as a prominent risk predictor of advanced atherosclerosis and arterial disease.
Circulation, 99 (1999), pp. 614-619
[42.]
T.K. Makris, P.G. Krespi, A.N. Hatzizacharias, A.E. Gialeraki, G. Anastasiadis, F.K. Triposkiadis, et al.
Resistance to activated protein C and FV leiden mutation in patients with a history of acute myocardial infarction or primary hypertension.
Am J Hypertens, 13 (2000), pp. 61-65
[43.]
J. Emmerich, M. Alhenc-Gelas, M. Aiach, J.N. Fiessinger.
Resistance to activated protein C: role in venous and arterial thrombosis.
Biomed Pharmacother, 50 (1996), pp. 254-260
[44.]
M. Cushman, F.R. Rosendaal, B.M. Psaty, E.F. Cook, J. Valliere, L.H. Kuller, et al.
Factor V Leiden is not a risk factor for arterial vascular disease in the elderly: results from the Cardiovascular Health Study.
Thromb Haemost, 79 (1998), pp. 912-915
[45.]
C.D. Bushnell, L.B. Goldstein.
Diagnostic testing from coagulopathies in patients with ischemic stroke.
Stroke, 31 (2000), pp. 3067-3078
[46.]
J. Mansourati, A. da Costa, S. Munier, B. Mercier, B. Tardy, C. Ferec, et al.
Prevalence of factor V Leiden in patients with myocardial infarction and normal coronary angiography.
Thromb Haemost, 83 (2000), pp. 822-825
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