LA FUNCION DE LOS DADORES DE OXIDO NITRICO EN LA PREVENCION DE LA REESTENOSIS LUEGO DE LA INTERVENCION CORONARIA PERCUTANEA





LA FUNCION DE LOS DADORES DE OXIDO NITRICO EN LA PREVENCION DE LA REESTENOSIS LUEGO DE LA INTERVENCION CORONARIA PERCUTANEA

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Actualización acerca de la función del óxido nítrico y de los dadores de óxido nítrico con respecto a la evolución luego de la angioplastia transluminal coronaria y en relación con la incidencia de reestenosis coronaria.
wohrle9.jpg Autor:
Jochen Wöhrle
Columnista Experto de SIIC

Institución:
Department of Internal Medicine II, University of Ulm


Artículos publicados por Jochen Wöhrle
Coautor
Thorsten Nusser, MD* 
University of Ulm*
Recepción del artículo
5 de Septiembre, 2005
Aprobación
8 de Septiembre, 2005
Primera edición
27 de Abril, 2006
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La aparición de reestenosis es la principal limitación de las intervenciones coronarias percutáneas que reducen el éxito a largo plazo. El proceso de reestenosis es un mecanismo multifactorial que incluye el tono vascular, la hemostasis, el metabolismo lipídico, las células, el crecimiento celular, la migración celular, las reacciones inflamatorias y las interacciones con las plaquetas. Los dadores de óxido nítrico (ON) influyen sobre esos mecanismos y claramente demostraron propiedades antirreestenóticas en varios experimentos con animales. En estudios clínicos, la administración oral de compuestos liberadores de ON que no inducen el fenómeno de tolerancia, como la molsidomina, no redujo la frecuencia de reestenosis luego de la angioplastia coronaria. La falta de eficacia se debe a las concentraciones plasmáticas sistémicas alcanzables de ON, las cuales claramente estuvieron por debajo de los niveles efectivos en pruebas con animales. Algunas preparaciones recientes, como nuevas drogas liberadoras de ON en mayores concentraciones, la liberación local de ON por stents coronarios recubiertos o la combinación con sustancias de efectividad probada como el paclitaxel parecen ser muy prometedores.

Palabras clave
óxido nítrico, reestenosis, angioplastia coronaria, stent, Molsidomina, molsidomina


Artículo completo

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Extensión:  +/-8.49 páginas impresas en papel A4
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Abstract
The occurrence of restenosis is the main limitation of percutanoues coronary interventions limiting the long-term success. The restenotic process is a multifactorial mechanism including vascular tone, hemostasis, lipid metabolism, cells, cell growth, cell migration, inflammatory reactions and interactions with platelets. Nitric oxide donors influence these mechanisms and have clearly shown antirestenotic properties in several animal experiments. In clinical studies, the oral administration of NO-releasing compounds such as molsidomine not inducing the tolerance phenomenon did not reduce the restenosis rate after coronary angioplasty. The lack of efficacy was based on the systemic achievable plasma concentrations of NO, which were clearly below the levels being effective in animal tests. Recent developments, such as new drugs releasing NO in higher concentrations, local NO delivery by coated coronary stents or the combination with proven effective restenotic substances like paclitaxel seem to be very promising.

Key words
Molsidomine, nitric oxide, restenosis, coronary angioplasty, stent


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Clasificación en siicsalud
Artículos originales > Expertos del Mundo >
página   www.siicsalud.com/des/expertocompleto.php/

Especialidades
Principal: Cardiología
Relacionadas: Bioquímica, Cirugía, Farmacología, Medicina Interna



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Bibliografía del artículo
  1. Gruentzig AR, Sennig A, Siegenthaler WE. Nonoperative dilation of coronary-artery stenosis: percutaneous transluminal coronary angioplasty. N Engl J Med 1979; 301:61-68.
  2. Serruys PW, de Jaegere P, Kiemeneij F, et al. A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994; 331:489-495.
  3. Mintz GS, Popma JJ, Hong MK et al. Intravascular ultrasound to discern device-specific effects and mechanisms of restenosis. Am J Cardiol 1996; 78:18-22.
  4. Ferns GA, Avades TY. The mechanisms of coronary restenosis: insights from experimental models. Int J Exp Pathol 2000; 81:63-88.
  5. Gibbons GH, Dzau VJ. The emerging concept of vascular remodeling. N Engl J Med 1994; 330:1431-1438.
  6. Yutani C, Imakita M, Ishibashi UH, et al. Coronary atherosclerosis and interventions: pathological sequences and restenosis. Pathol Int 1999; 49:273-290.
  7. Stone GW, Ellis SG, Cannon L et al. A polymer-based, paclitaxel-eluting stent in patients with coronary artery disease. N Engl J Med 2004; 350:221-31.
  8. Schofer J, Schluter M, Gershlick AH et al. Sirolimus eluting stents for treatment of patients with long atherosclerotic lesions in small coronary arteries: double-blind, randomised, controlled trial (E-SIRIUS). Lancet 2003; 362:1093-9.
  9. Schampaert E, Cohen EA, Schluter M et al. The Canadian study of the sirolimus-eluting stent in the treatment of patients with long de novo lesions in small native coronary arteries (C-SIRIUS). J Am Coll Cardiol 2004; 43:1110-5.
  10. Höher M, Wöhrle J, Wohlfrom M et al. Intracoronary beta-irradiation with a rhenium-188-filled balloon catheter: a randomized triel in patients with de novo and restenotic lesions. Circulation 2003; 107:3022-7.
  11. Stone GW et al. Results of the TAXUS-V trial. Presentation at the ACC 2005
  12. Serruys PW, Luijten HE, Beatt KJ et al. Incidence of restenosis after successful coronary angioplasty: a time-related phenomenon. A quantitative angiographic study in 342 consecutive patients at 1, 2, 3, and 4 months. Circulation 1988; 77:361-71.
  13. Corcos T, David PR, Val PG, et al. Failure of diltiazem to prevent restenosis after percutaneous transluminal coronary angioplasty. Am Heart J 1985; 109:926-931.
  14. Franklin SM, Faxon DP. Pharmacologic prevention of restenosis after coronary angioplasty: review of the randomized clinical trials. Coron Artery Dis 1993; 4:232-242.
  15. Schwartz L, Bourassa MG, Lesperance J, et al. Aspirin and dipyridamole in the prevention of restenosis after percutaneous transluminal coronary angioplasty. N Engl J Med 1988; 318:1714-1719.
  16. Schwartz L, Lesperance J, Bourassa MG, et al. The role of antiplatelet agents in modifying the extent of restenosis following percutaneous transluminal coronary angioplasty. Am Heart J 1990; 119:232-236.
  17. Thornton MA, Gruentzig AR, Hollman J, et al. Coumadin and aspirin in prevention of recurrence after transluminal coronary angioplasty: a randomized study. Circulation 1984; 69:721-727.
  18. Topol EJ, Califf RM, Weisman HF, et al. Randomised trial of coronary intervention with antibody against platelet IIb/IIIa integrin for reduction of clinical restenosis: results at six months. The EPIC Investigators. Lancet 1994; 343:881-886.
  19. Cannon CP, McCabe CH, Wilcox RG et al. Oral glycoprotein IIb/IIIa inhibition with orbofiban in patients with unstable coronary syndromes (OPUS-TIMI 16) trial. Circulation 2000; 102:149-56.
  20. Verstraete M. Synthetic inhibitors of platelet glycoprotein IIb/IIIa in clinical development. Circulation 2000; 101:E76-E80.
  21. Goodnight SH. Aspirin therapy for cardiovascular disease. Curr Opin Hematol 1996; 3:355-60.
  22. Herman AG, Moncada S. Therapeutic potential of nitric oxide donors in the prevention and treatment of atherosclerosis. Eur Heart J 2005; doi:10.1093/eurheartj/ehi333 [Epub ahead of print].
  23. Reden J. Molsidomine. Blood Vessels 1990; 27:282-294.
  24. Schächinger V, Zeiher AM. NO in der Therapie der Angina pectoris: Nitrate oder Molsidomin. Internist 1997; 38:438-447.
  25. Assender JW, Southgate KM, Newby AC. Does nitric oxide inhibit smooth muscle proliferation J Cardiovasc Pharmacol 1991; 17 (Suppl. 3):S104-S107.
  26. Lahteenmaki T, Sievi E, Vapaatalo H. Inhibitory effects of mesoionic 3-aryl substituted oxatriazole-5-imine derivatives on vascular smooth muscle cell mitogenesis and proliferation in vitro. Br J Pharmacol 1998; 125:402-8.
  27. Groves PH, Banning AP, Penny WJ, et al. The effects of exogenous nitric oxide on smooth muscle cell proliferation following porcine carotid angioplasty. Cardiovasc Res 1995; 30:87-96.
  28. Belhassen L, Carville C, Pelle G et al. Molsidomine improves flow-dependent vasodilation in brachial arteries of patients with coronary artery disease. J Cardiovasc Pharmacol 2000; 35:560-3.
  29. Basista M, Grodzinska L, Swies J. The influence of molsidomine and its active metabolite SIN-1 on fibrinolysis and platelet aggregation. Thromb Haemost 1985; 54:746-9.
  30. Darius H, Grodzinska L, Hafner G, et al. Effect of molsidomine on fibrinolytic activity: a double-blind, randomized study. Z Kardiol 1991; 80 (Suppl. 5):47-50.
  31. Cooke JP. The endothelium: a new target for therapy. Vasc Med 2000; 5:49-53.
  32. Drummer C, Valta SU, Karrenbrock B, et al. Comparison of anti-platelet properties of molsidomine, isosorbide-5-mononitrate and placebo in healthy volunteers. Eur Heart J 1991; 12:541-9.
  33. Keh D, Gerlach M, Kurer I, et al. The effects of nitric oxide (NO) on platelet membrane receptor expression during activation with human alpha-thrombin. Blood Coagul Fibrinolysis 1996; 7:615-24.
  34. Katsumi H, Nishikawa M, Ma SF, et al. Physiochemical, tissue distribution, and vasodilation characteristics of nitrosated serum albumin: dilivery of nitric oxide in vivo. J Pharm Sci 2004; 93:2343-2352.
  35. Kirsten R, Nelson K, Kirsten D, et al. Clinical pharmacokinetics of vasodilators. Part II. Clin Pharmacokinet 1998; 35:9-36.
  36. Lablanche JM, Grollier G, Lusson JR, et al. Effect of the direct nitric oxide donors linsidomine and molsidomine on angiographic restenosis after coronary balloon angioplasty. The ACCORD Study. Angioplastie Coronaire Corvasal Diltiazem. Circulation 1997; 95:83-89.
  37. Wöhrle J, Höher M, Nusser T, et al. No Effect of highly dosed nitric oxide donor molsidomine on the angiographic restenosis rate after percutaneous coronary angioplasty. A randomized, placebo-controlled, double-blind trial. Can J Cardiol 2003; 19:495-500.
  38. Karrenbrock B, Heim JM, Gerzer R. Effect of molsidomine on ex vivo platelet aggregation and plasma guanosine 3':5'-cyclic monophosphate levels in healthy volunteers. Klin Wochenschr 1990; 68:213-7.
  39. McFadden EP, Stabile E, Regar E, e al. Late thrombosis in drug-eluting coronary stents after discontinuation of antiplatelet therapy. Lancet 2004; 364:1466-7.
  40. Silber S, Albertsson P, Avilés FF et al. Guidelines for percutaneous coronary interventions: the task force for percutaneous coronary interventions of the European Society of Cardiology. Eur Heart J 2005; 26:804-847.
  41. Wallace JL, Miller MJ. Nitric oxide in mucosal defense: a little goes a long way. Gastroenterology 2000;119:512-20.
  42. Hawkey CJ. Nonsteroidal anti-inflammatory drug gastropathy. Gastroenterology 2000; 119:521-35.
  43. Elliott SN, McKnight W, Cirino G, et al. A nitric oxide-releasing nonsteroidal anti-inflammatory drug accelerates gastric ulcer healing in rats. Gastroenterology 1995;109:524-30.
  44. Barrachina MD, Calatayud S, Canet A, et al. Transdermal nitroglycerin prevents nonsteroidal anti-inflammatory drug gastropathy. Eur J Pharmacol 1995; 281:R3-R4.
  45. Lanas A, Bajador E, Serrano P, et al. Nitrovasodilators, low-dose aspirin, other nonsteroidal antiinflammatory drugs, and the risk of upper gastrointestinal bleeding. N Engl J Med 2000; 343:834-39.
  46. Vilahur G, Segales E, Salas E, et al. Effects of a novel platelet nitric oxide donor (LA816), aspirin, clopidogrel, and combined therapy in inhibiting flow- and lesion-dependent thrombosis in the porcine ex vivo model. Circulation. 2004; 110:1686-93.
  47. Do YS, Kao EY, Ganaha F, et al. In-stent restenosis limitation with stent-based controlled-release nitric oxide: initial results in rabbits. Radiology. 2004; 230:377-82.
  48. Hou D, Narciso H, Kamdar K, et al. Stent-based nitric oxide delivery reducing neointimal proliferation in a porcine carotid overstretch injury model. Cardiovasc Intervent Radiol. 2005; 28:60-5.

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