NEFROPATIA INDUCIDA POR EL CONTRASTE EN PACIENTES SOMETIDOS A ANGIOPLASTIA PRIMARIA POR INFARTO AGUDO DE MIOCARDIO

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La angioplastia primaria es la mejor estrategia para la reperfusión miocárdica en el infarto agudo de miocardio con elevación del segmento ST. Sin embargo, se asocia con riesgo elevado de nefropatía por contraste, una complicación renal que se acompaña de un marcado incremento en el riesgo de morbimortalidad. En este marco, deben llevarse a cabo estrategias farmacológicas de protección renal.
marenzi9.jpg Autor:
Giancarlo Marenzi
Columnista Experto de SIIC
Artículos publicados por Giancarlo Marenzi
Recepción del artículo
16 de Noviembre, 2006
Aprobación
12 de Diciembre, 2006
Primera edición
28 de Mayo, 2007
Segunda edición, ampliada y corregida
7 de Junio, 2021

Resumen
La nefropatía inducida por el contraste (NIC), definida como un incremento absoluto (> 0.5 mg/dl) o relativo (> 25%) en la creatinina sérica que tiene lugar 48-72 horas luego de la administración de medios de contraste, es una complicación frecuente de las intervenciones coronarias percutáneas (ICP) y está asociada con riesgo de morbimortalidad elevado. Los pacientes con infarto agudo de miocardio con elevación del segmento ST (IMEST) tratados con ICP primarias constituyen una población con alto riesgo de NIC debido a su inestabilidad hemodinámica, a la necesidad de administrar importantes volúmenes de contraste y a la ausencia de una profilaxis efectiva. La NIC puede afectar al 20% de estos pacientes y se asocia con un curso clínico intrahospitalario más complicado, hospitalización prolongada y marcado incremento en la tasa de mortalidad. La edad > 75 años, la localización anterior del infarto, un prolongado tiempo de reperfusión, un volumen de contraste > 300 ml y el uso de balón de contrapulsación se asocian en forma independiente con la NIC. Por consiguiente, es necesario probar e implementar estrategias preventivas para la protección renal durante las intervenciones coronarias primarias, particularmente en pacientes de alto riesgo. Recientemente, se demostró que la N-acetilcisteína, administrada en bolo intravenoso antes de la ICP primaria y luego por vía oral durante dos días, puede reducir -en forma dependiente de la dosis- la incidencia de NIC y mejorar la evolución clínica de los pacientes con IMEST tratados con ICP primaria.

Palabras clave
infarto agudo de miocardio, nefropatía inducida por contraste, insuficiencia renal, angioplastia primaria


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Abstract
Contrast-induced nephropathy (CIN), defined as an absolute (> 0.5 mg/dl) or a relative (> 25%) increase in serum creatinine occurring 48-72 hours after contrast medium administration, is a frequent complication of percutaneous coronary interventions (PCI), and is associated with an increased morbidity and mortality risk. Patients with ST-segment elevation acute myocardial infarction (STEMI) treated with primary PCI represent a population at high risk for CIN due to hemodynamic instability, need for high contrast volume, and lack of effective prophylaxis. CIN has been reported to occur in almost 20% of these patients and to be associated with complicated in-hospital clinical course, prolonged hospitalization, and markedly increased mortality rate. Age > 75 years, anterior infarct location, prolonged time-to-reperfusion, contrast agent volume > 300 ml, and use of an intra-aortic balloon pump have been found to be independently associated with CIN. Therefore, preventive strategies for kidney protection during primary PCI need to be developed and tested, particularly in high-risk patients. Recently, N-acetylcysteine, given as an intravenous bolus before primary PCI and followed by oral administration for the following two days, has been shown to reduce the incidence of CIN and improve clinical outcomes of STEMI patients treated with primary PCI, with a dose-dependent effect.

Key words
acute myocardial infarction, contrast-induced nephropathy, renal insufficiency, primary angioplasty


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Clasificación en siicsalud
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Especialidades
Principal: Nefrología y Medio Interno
Relacionadas: Diagnóstico por Imágenes, Farmacología, Medicina Farmacéutica, Medicina Interna



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Enviar correspondencia a:
Giancarlo Marenzi, Centro Cardiologico Monzino, I.R.C.C.S, Institute of Cardiology, University of Milan, 20138, Via Parea 4, Milán, Italia
Bibliografía del artículo
1. Maitino AJ, Levin DC, Parker L, et al. Nationwide trends in rates of utilization of noninvasive diagnostic imaging among the Medicare population between 1993 and 1999. Radiology 227:113-117, 2003.
2. Barrett BJ, Parfrey PS. Preventing nephropathy induced by contrast medium. N Engl J Med 354:379-86, 2006.
3. Morcos SK. Prevention of contrast media nephrotoxicity - the story so far. Clinical Radiology 59:381-389, 2004.
4. Marenzi G, Marana I, Lauri G, et al. The prevention of radiocontrast-agent-induced nephropathy by hemofiltration. N Engl J Med 349:1331-1338, 2003.
5. Gruber L. Clinical features and prognostic implications of contrast-induced nephropathy. In: Contrast-induced nephropathy, Bartorelli AL & Marenzi G, editors, Taylor & Francis 35-45, 2006.
6. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 105:2259-64, 2002.
7. Bartholomew BA, Harjai KJ, Dukkipati S, et al. Impact of nephropathy after percutaneous coronary intervention and a method for risk stratification. Am J Cardiol 93:1515-19, 2004.
8. Gruber L, Mehran R, Dangas G, et al. Acute renal failure requiring dialysis after percutaneous coronary interventions. Catheter Cardiovasc Interv 52:409-16, 2001.
9. McCullough PA, Wolyn R, Rocher LL, et al. Acute renal failure after coronary intervention: incidence, risk factors and relationship to mortality. Am J Med 103:368-75, 1997.
10. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention. J Am Coll Cardiol 44;1393-9, 2004.
11. Keeley EC, Boura JA, Grines CL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet 361:13-20, 2003.
12. Stone GW, Grines CL, Cox DA, et al. Comparison of angioplasty with stenting, with or without abcximab, in acute myocardial infarction. N Engl J Med 346:957-66, 2002.
13. Grines CL, Cox DA, Stone GW. Coronary angioplasty with or without stent implantation for acute myocardial infarction. Stent Primary Angioplasty in Myocardial Infarction Study Group. New Engl J Med 341:1949-56, 1999.
14. Beattie JN, Soman SS, Sandber KR, et al. Determinants of mortality after myocardial infarction in patients with advanced renal dysfunction. Am J Kidney Dis 37:1191-1200, 2001.
15. Sadeghi HM, Stone GW, Grines CL, et al. Impact of renal insufficiency in patients undergoing primary angioplasty for acute myocardial infarction. Circulation 108:2769-2775, 2003.
16. Marenzi G, Lauri G, Assanelli E, et al. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction. J Am Coll Cardiol 44:1780-17855, 2004.
17. Dragu R, Behar S, Sandach A, et al. Should primary percutaneous coronary intervention be the preferred method of reperfusion therapy for patients with renal failure and ST-elevation acute myocardial infarction? Am J Cardiol 97:1142-45, 2006.
18. Goldberg A, Hammerman H, Petchreski S, et al. Inhospital and 1-year mortality of patients who develop worsening renal function following acute ST-elevation myocardial infarction. Am Heart J 150:330-337, 2005.
19. Gibson CM, Pinto DS, Murphy SA et al. Association of creatinine and creatinine clearance on presentation in acute myocardial infarction with subsequent mortality. J Am Coll Cardiol 42:1535-1543, 2003.
20. Tepel M, Van Del Giet M, Schwarzfeld NR et al. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 343:180-184, 2000.
21. Briguori C, Manganelli F, Scarpato P, et al. Acetylcysteine and contrast agent-associated nephrotoxicity. J Am Coll Cardiol 40:298-303, 2002.
22. Marenzi G, Assanelli E, Bartorelli AL. Management of acute coronary syndromes in patients with renal insufficiency. Current Cardiology Review 2:11-16, 2006.
23. Drager LF, Andrade L, Barros de Toledo JF, et al. Renal effects of N-acetylcysteine in patients at risk for contrast nephropathy: decrease in oxidant stress-mediated renal tubular injury. Nephrol Dial Transplant 7:1803-7, 2004.
24. Lopez BL, Snyder JW, Birenbaum DS, Ma XI. N-acetylcysteine enhances endothelium-dependent vasorelaxation in the isolated rat mesenteric artery. Ann Emerg Med 32:405-410, 1998.
25. Baker CSR, Wragg A, Kumar S, et al. A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study. J Am Coll Cardiol 41:2114-2118, 2003.
26. Webb JG, Pate GE, Humpries KH, et al. A randomized controlled trial of intravenous N-acetylcysteine for the prevention of contrast-induced nephropathy after cardiac catheterization: lack of effect. Am Heart J 148:422-9, 2004.
27. Arstall MA, Yang J, Stafford I, Betts WH, Horowitz JD. N-acetylcysteine in combination with nitroglycerin and streptokinase for the treatment of evolving acute myocardial infarction: safety and biochemical effects. Circulation 92:2855-62, 1995.
28. Sochman J, Kole J, Vrana M, Fabian J. Cardioprotective effects of N-acetylcysteine: the reduction in the extent of infarction and occurrence of reperfusion arrhythmias in the dog. Int J Cardiol 28:191-6, 1990.
29. Sochman J, Vrbska J, Musilova B, Rocek M. Infarct size limitation: acute N-acetylcysteine (ISLAND trial): preliminary analysis and report after the first 30 patients. Clin Cardiol 19:94-100, 1996.
30. Marenzi G, Assanelli E, Marana I, et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med 354:2773-82, 2006.
31. Dhalla NS, Golfman L, Taked S, Takeda A, Nagano M. Evidence for the role of oxidative stress in acute ischemic heart disease: a brief report. Can J Cardiol 15:587-93, 1999.
32. Grech ED, Dodd NJF, Jackson MJ, Morrison WL, Faragher EB, Ramsdale DR. Evidence for free radical generation after primary percutaneous transluminal coronary angioplasty recanalization in acute myocardial infarction. Am J Cardiol 77:122-7, 1996.
33. Anfossi G, Russo I, Massucco P, Mattiello L, Cavalot F, Trovati M. N-acetyl-L-cysteine exerts direct anti-aggregating effect on human platelets. Eur J Clin Invest 31:452-461, 2001.

 
 
 
 
 
 
 
 
 
 
 
 
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