The prevalence of contrast nephropathy in patients undergoing percutaneous coronary intervention in acute coronary syndrome

Year 2018, , 34 - 39, 30.06.2018

Muhammed Karadeniz , Hüseyin Kandemir , Taner Sarak , Çağlar Alp

https://doi.org/10.32322/jhsm.410522

Cited By: 2

Abstract

Objective: Contrast nephropathy (KMN) is
defined as an acute renal injury due to intravenous contrast agents applied in
diagnostic or therapeutic interventions and is an important cause of
hospitalization due to acute renal failure. In this study, the frequency of
coronary intervention and contrast agent nephropathy was investigated in acute
coronary syndrome.

Material and Method: According
to the European Urogenital Radiology Society Guide, "An increase of 25 or
0.5 mg/dl in serum creatinine within 3 days after administration of contrast
medium without any other etiological cause". After approval of the Ethics
Committee, 336 patients who met the inclusion criteria were included in the
study. Patients younger than 18 years of age with chronic renal insufficiency,
heart failure, coronary by-pass history, serum creatinine control after the
procedure and patients without percutaneous coronary intervention were excluded
from the study.

Results: BMD was detected in 11.9% of the 336
patients included in the study. The mean age of 40 patients who developed CMN
was 73.9±10.2 / year, and the mean age of 296 patients who did not have CMN was
59.4±12.3 /year. The mean age was significantly higher in the DM group (p
<0.001). The mean body mass index (BMI) was 28.2 ± 4.7kg / m² in the
non-developing group, while the BMI average was 26.5 ± 3.3kg / m². The mean VKI
was lower in the DM group (p = 0.044). The mean SYNTAX score was 16.6 ± 8.3 in
the non-developing group, whereas the mean in the group with the improved KMN
was 22.5 ± 10.3. The SYNTAX score was higher in the KMN-developing group than
in the non-KMN group (p=0.001). There was no difference between two groups in
terms of AKS type, DM, HT and sex (p=0.713, p=0.317, p=0.055, p=0.589).

Conclusion: Strategies should be implemented to
prevent other CMD developments, provided that hydration is absolute before and
after the procedure in groups at risk for which contrast media should be given.

Keywords

Contrast nephropathy, acute coronary syndrome, percutaneous coronary intervention

Akut koroner sendromda perkütan koroner girişim yapılan hastalarda kontrast nefropati prevalansı

Abstract

Amaç: Kontrast madde
nefropatisi (KMN), tanı veya tedavi
amaçlı yapılan girişimlerde uygulanan intravenöz kontrast ajanlara bağlı olarak
gelişen akut böbrek hasarı olarak tanımlanmıştır ve akut böbrek yetersizliğine
bağlı olarak hastaneye yatışlarda önemli bir nedendir. Bu çalışmada akut
koroner sendromda koroner girişim ve kontrast madde nefropatisi sıklığı
araştırılmıştır.

Gereç ve Yöntem: Avrupa Ürogenital Radyoloji Cemiyeti Kılavuzu’na göre KMN tanımı; “başka
bir etiyolojik sebep olmaksızın, kontrast madde verilmesinden sonraki 3 gün
içinde serum kreatinin düzeyinde başl25 veya 0.5 mg/dl artış olması” olarak
kabul edilmiştir. Etik Kurul onayı sonrası dahil edilme
kriterlerine uyan 336 hasta çalışmaya alındı. 18 yaşından küçük, kronik böbrek
yetersizliği olan, kalp yetmezliği olan, koroner by-pass öyküsü olan, işlem
sonrası serum kreatinini kontrol edilemeyen hastalar ve perkütan koroner
girişim yapılmayan hastalar çalışma dışı bırakıldı.

Sonuçlar: Çalışmaya dahil edilen 336 hastanın %11,9’unda
KMN saptandı. KMN gelişen 40 hastanın yaş ortalaması 73,9±10,2/yıl, KMN
gelişmeyen 296 hastanın yaş ortalaması 59,4±12,3/yıl idi. KMN gelişen grupta
yaş ortalaması istatistiksel olarak anlamlı derecede yüksek bulundu
(p<0.001). KMN gelişmeyen hasta grubunda vücut kitle indeksi (VKİ)
ortalaması 28,2±4,7kg/m² iken, KMN gelişen grupta VKİ ortalaması 26,5±3.3kg/m²
idi. KMN gelişen grupta VKİ ortalaması daha düşük bulundu (p=0.044). KMN gelişmeyen
hasta grubunda SYNTAX skoru ortalama 16,6±8,3 iken, KMN gelişen hasta grubunda
ortalama 22,5±10,3 idi. KMN gelişen grupta SYNTAX skoru KMN gelişmeyen gruba
göre daha yüksek bulundu (p=0.001). AKS tipi, DM, HT ve cinsiyet açısından iki
grup arasında fark bulunmadı (p=0.713, p=0.317,p=0.055, p=0.589).

Sonuç: Kontrast madde verilmesi gereken risk altındaki
gruplarda işlem öncesinde ve sonrasında hidrasyon mutlak olması şartıyla diğer
KMN gelişmesini önleyici stratejiler uygulanmalıdır.

Keywords

Kontrast nefropati, akut koroner sendrom, perkütan koroner girişim

References

• 1. McCullough PA, Wolyn R, Rocher LL, Levin RN, O’Neill WW. Acute renal failure aftercoronary intervention: Incidence, risk factors, and relationship to mortality. Am J Med1997;103:368-75.2. Eisenberg RL, Bank WO, Hedgock MW. Renal failure after major angiography can be avoided with hydration. AJR 1981; 136(5): 859.61.
• 4. Detrenis, S. Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art. Nephrol Dial Transplant 2005; 20(8): 1542-50.
• 5. Morcos SK, Thomsen HS, Webb JA. Conrast-media-induced nephrotoxicity: a consensus report. Contrast Media Safety Committee, European Society of Urogenital Radiology (ESUR) Eur Radiol 1999;9:1602-13.
• 6. Spinler SA, Goldfarb S. Nephrotoxicity of contrast media after cardiac angiography:Pathogenesis, clinical course, and preventive measures, including the role of lowosmolalitycontrast media. Ann Pharmacother 1992;26:56-64.
• 7. Lepor NE, Mathur VS. Radiocontrast Nephropathy. Curr Interv Cardiol Rep 2000;2:335-341.
• 8. Asif A, Epstein M. Prevention of radiocontrast-induced nephropathy. Am JKidney Dis 2004; 44: 12-24.
• 9. Merten GJ, Burgess WP, Gray LV, Holleman JH. Prevention of contrastinducednephropathy with sodium bicarbonate: a randomized controlled trial.JAMA 2004; 291: 2328-34.
• 10. Jorgensen AL. Contrast-induced nephropathy: pathophysiology and preventive strategies. Crit Care Nurse 2013;33:37–46.
• 11. Brendan J, Barrett M, Patrick SP. Contrast-induced Nephropathy in Emergency Department Patients Receiving Abdominal Contrast-Enhanced Computed Tomography. Ann Emerg Med 2008;52:136.
• 12. Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis 2002;39:930–6.
• 13. Detrenis, S. Lights and shadows on the pathogenesis of contrast-inducednephropathy: state of the art. Nephrol Dial Transplant 2005; 20(8): 1542-50.
• 14. Heyman SN, Rosenberger C, Rosen S. Regional alterations in renalhaemodynamics and oxygenation: a role in contrast medium-inducednephropathy. Nephrol Dial Transplant 2005; 20 Suppl 1: i6.
• 15. Pflueger A. Role of adenosine in contrast media-induced acute renal failurein diabetes mellitus. Mayo Clin Proc 2000; 75(12): 1275-83.
• 16. Porter GA. Contrast-associated nephropathy. Am J Cardiol 1989; 64(9): 22E.2E.
• 17. Heyman SN, Reichman J, Brezis M. Pathophysiology of radiocontrast nephropathy: a role for medullary hypoxia. Invest Radiol 1999; 34(11): 685-91.
• 18. Deray G, Martinez F, Cacoub P, Baumelou B, Baumelou A, Jacobs C. A role of adenosine, calcium and ischemia in radiocontrast media induced intrarenal vasoconstriction. Am J Nephrol 1990; 10(4): 316-22.
• 19. Heyman SN, Clark BA, Kaiser N, Spokes K, Rosen S, Brezis M. Radiocontrast induced endothelin release in vivo and in vitro. J Am Soc Nephrol 1992; 3(1): 58-65.
• 20. Agmon Y, Dinour D, Brezis M. Disparate effects of adenosine A-1 and A-2 receptor agonists on intrarenal blood flow. Am J Physiol 1993; 265(6): F802-6.
• 21. Arend LJ, Bakris GL, Burnett JC Jr. Role of intrarenal adenosine in the renal hemodynamic response to contrast media. J Lab Clin Med 1987; 110(4): 406-11.
• 22. Bakris GL, Burnett JC Jr. A role of calcium in radiocontrast-induced reduction in renal hemodynamics. Kidney Int 1985; 27(2): 465-8.
• 23. Smith MW, Ambudkar IS, Phelps PC, Rogec AL, Trump BF. MgCl2-induced changes in cytosolic Ca2+ of cultured rabbit renal tubular cells. Biochim Biophys Acta 1987; 931(2):13042.
• 24. Brezis M, Heyman SN, Dinour D, Epstein FH, Rosen S. Role of nitric oxide in renal medullary oxygenation: studies in isolated and intact rat kidney. J Clin Invest 1991; 88(2): 390-5.
• 25. Agmon Y, Peleg H, Greenfeld Z, Rosen S, Brezis M. Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat. J Clin Invest 1994; 94(3): 1069-75.
• 26. Jabs K, Zeidel ML, Silva P. Prostaglandin E2 inhibits Na-K ATPase activity in the inner medullary collecting duct. Am J Physiol 1989; 257(3): F424-30.
• 27. Lear S, Silvia P, Kelly VE, Epstein FH. Prostaglandin inhibits oxygen consumption in rabbit medullary thick ascending limb. Am J Physiol 1990; 258(5): F1372-8.
• 28. Toprak Ö, Cirit M, Bayata S, Yesil M. Radyokontrast nefropatisi risk profilinin gözden geçirilmesi ve risk degerlendirilmesi. Anadolu Kardiyol Derg. 2004: 4; 331-335
• 29. Başarıcı İ, Belgi A. Radyokontrast ilişkili nefropati. Türk Kardiyol Dern Arş.2003;31: 781-88
• 30. Thomson HS, Morcos SK. Contrast media and the kidney: European Society of Urogenital Radiololgy (ESUR) guidelines. Br J Radiol 2003; 76:513-518.
• 31. Berns AS. Nephrotoxicity of contrast media. Kidney Int 1989; 36:730-740.
• 32. Mehran R, Aymong ED, Nikolsky E, Lasic Z. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validitation. J Am Coll Cardiol 2004;44: 1393-9.
• 33. Parfrey PS, Griffiths SM, Barrett BJ, et al. Contrast material-induced renal failure in patients with diabetes mellitus, re-nal insufficiency, or both: a prospective controlled study. N Engl J Med 1989:320: 143-149.
• 34. Thomsen HS, Morcos SK. Contrast media and the kidney. European Society of Urogenital Radiology (ESUR) guidelines. Br J Radiol 2003; 76(908):513-8.
• 35. Pannu N, Wiebe N, Tonelli M; Alberta Kidney Disease Network. Prophylaxis strategies for contrast-induced nephropathy. JAMA 2006;295:2765-79.
• 36. Ecebay A. Tip2 Diabetes Mellitus Tanısı olan ancak Belirgin Nefropatisi Olmayan Hastalarda; Kontrast Madde Nefropatisinin Görülme Sıklığı ve N-Asetilsisteinin Kontrast Madde nefropatisi Üzerindeki Etkilerinin Araştırılması, Uzmanlık Tezi, İstanbul Haseki Eğitim ve araştırma Hastanesi 5.İç Hastalıkları Kliniği, İstanbul 2007:74
• 37. Tepel M, van der Giet M, Schwarzfeld C, Laufer U. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 2000; 343: 180-4.
• 38. Kshirsagar AV, Poole C, Mottl A, Shoham D. N-acetylcysteine for the prevention of radiocontrast induced nephropathy: a meta-analysis of prospective controlled trials. J Am Soc Nephrol 2004; 15: 761-9.
• 39. Gonzales DA, Norsworthy KJ, Kern SJ, Banks S. A meta-analysis of Nacetylcysteine in contrast-induced nephrotoxicity: unsupervised clustering to resolve heterogeneity. BMC Med 2007; 14: 5-32.
• 40. Zagler A, Azadpour M, Mercado C, Hennekens CH. N-acetylcysteine and contrast-induced nephropathy: a meta-analysis of 13 randomized trials. Am Heart J 2006; 151: 140-5.
• 41. Liu R, Nair D, Ix J, Moore DH. N-acetylcysteine for the prevention of contrast-induced nephropathy. A systematic review and meta-analysis. J Gen Intern Med 2005; 20: 193-200.
• 42. Duong MH, MacKenzie TA, Malenka DJ. N-acetylcysteine prophylaxis significantly reduces the risk of radiocontrast-induced nephropathy: comprehensive meta-analysis. Catheter Cardiovasc Interv 2005; 64: 471-9.
• 43. Misra D, Leibowitz K, Gowda RM, Shapiro M. Role of N-acetylcysteine in prevention of contrast-induced nephropathy after cardiovascular procedures: a meta-analysis. Clin Cardiol 2004; 27: 607-10.
• 44. Alonso A, Lau J, Jaber BL, Weintraub A. Prevention of radiocontrast nephropathy with N-acetylcysteine in patients with chronic kidney disease: a meta-analysis of randomized, controlled trials. Am J Kidney Dis 2004; 43:1-9.
• 45. Heinrich MC, Kuhlmann MK, Grgic A, et al. Cytotoxic effects of ionic high-osmolar,nonionic monomeric, and nonionic iso-osmolardimeric iodinated contrast media on renal tubular cells in vitro. Radiology 2005;235:843–9.
• 46. Briguori C, Visconti G, Focaccio A, et al. Renal Insufficiency After Contrast Media Administration Trial II (REMEDIAL II):Renal Guard System in high-risk patients for contrast-induced acute kidney injury. Circulation 2011;124:1260–9.
• 47. Pannu N, Manns B, Lee H, et al. Systematic review of the impact of Nacetylcysteine on contrast nephropathy. Kidney Int 2004;65:1366–74.
• 48. Baker WL, Anglade MW, Baker EL, et al. Use of N-acetylcysteine to reduce post-cardiothoracic surgery complications: a meta-analysis. Eur J Cardiothorac Surg 2009;35: 521-7.
• 49. MacNeill BD, Harding SA, Bazari H, et al. Prophylaxis of contrast-induced nephropathy in patients undergoing coronary angiography. Catheter Cardiovasc Interv 2003;60:458–61.
• 50. Miner SE, Dzavik V, Nguyen-Ho P, et al. N-Acetylcysteine reduces contrast-associated nephropathy but not clinical events during long-term follow-up. Am Heart J 2004;148:690–5.
• 51. Danilo Fliser, Maurice Laville, Adrian Covic, et al. A European Renal Best Practice (ERBP) position statement on the Kidney Disease Improving Global Outcomes (KDIGO) Clinical Practice Guidelines on Acute Kidney Injury: Part 1: Definitions, conservative management and contrast-induced nephropathy. Nephrol Dial Transplant 2012;27:4263–72.
• 52. Pflueger A, Larson TS, Nath KA, King BF, Gross JM, Knox FG. Role of adenosine in contrast media-induced acute renal failure in diabetes mellitus. Mayo Clin Proc 2000; 75:1275-1283.
• 53. Coresh J, Astor BC, Greene T et al. Prevalence of chronic kidney disease and decreased kidney function in the adults US population: Third National Health and Examination Survey. Am J Kidney Dis 2003; 41: 1-12.
• 54. Levey AS, Coresh J, Balk E et al. National Kidney Foundation practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Ann Intern Med 2003; 139: 137-147.
• 55. Weinrauch LA, Healy RV, l.eland OS Jr, et al. Coronary angiography and acute renal failure in diabetic azotemic ne-phropathy. Ann Intern Med 1977;86:56-59.
• 56. Best PJ, Lennon R, Ting HH, et al. The impact of renal insufficiency on clinical outcomes in patients undergoing percutaneous interventions. J Am Coll Cardiol 2002;39:1113-1119.
• 57. Özden A. Ratlarda Deneysel Olarak Oluşturulan İyonik Kontrast Madde Kaynaklı Böbrek Hasarında Oksidatif Stresin Fonksiyonu ve Olası Oksidatif Stres Üzerine Kafeik Asit Fenetil Esterin Etkisinin Araştırılması, Uzmanlık Tezi, Süleyman Demirel Üniversitesi Tıp Fakültesi Radyodiagnostik Anabilim Dalı, Isparta 2008:79
• 58. Gleeson, TG, Bulugahapitiya S. Contrast- induced nephropathy. Am J Roentgenol 2004; 183: 1673-89.
• 59. Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196 patients: A randomized trial. The Iohexol Cooperative Study. Kidney Int 1995;47:254–61.
• 60. Mohammed NM, Mahfouz A, Achkar K, et al. Contrast-induced Nephropathy;Heart Views 2013;14:106-16.
• 61. McCullough PA, Adam A, Becker CR, et al. “Risk prediction of contrast-induced nephropathy,” The American Journal of Cardiology 2006; 98: 27–36.
• 62. Beyazal H, Kontrast Madde Nefropatisinin Önlenmesinde İzotonik Sodyum Klorür, Sodyum Bikarbonat ve İzotonik Sodyum Klorürle Birlikte Diltiazemin Etkinliğinin Karşılaştırılması, Uzmanlık Tezi, Erciyes Üniversitesi Tıp Fakültesi İç Hastalıkları Anabilim Dalı, Kayseri 2006:60
• 63. Mueller C, Buerkle G, Buettner HJ, Petersen J. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med 2002; 162: 329-36.
• 64. Rihal CS, Textor SC, Grill DE, Berger PB. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002; 105: 2259–64.
• 65. Muntner P. Exposure to radiologic contrast media and an increased risk of treated end-stage renal disease. Am J Med Sci 2003; 326(6): 353-9.
• 66. Manske CL, Sprafka JM, Strony JT, Wang Y. Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography. Am J Med 1990; 89: 615-20.
• 67. Cronin RE. Contrast-induced nephropathy: pathogenesis and prevention. Pediatr Nephrol 2009; 25(2): 191-204.
• 68. Gomes AS, Baker JD, Martin-Paredero V, Dixon SM, Takiff H, Machleder HI et al. Acute renal dysfunction after major arteriography. AJR Am J Roentgenol 1985; 145: 1249-53.
• 69. Brandes RP, Fleming I, Busse R. Endothelial aging. Cardiovasc Res 2005;66: 286-94.
• 70. Davidson C, Stacul F, McCullough PA, Tumlin J, Adam A, Lameire N et al. CIN Consensus Working Panel. Contrast medium use. Am J Cardiol 2006; 18: 42-58.
• 71. Lautin EM, Freeman NJ, Schoenfeld AH, Bakal CW, Haramati N, Friedman AC et al. Radiocontrastassociated renal dysfunction: incidence and risk factors. AJR Am J Roentgenol 1991; 157: 49-58.
• 72. Marenzi G, Lauri G, Campodonico J, Marana I. Comparison of two hemofiltration protocols for prevention of contrast-induced nephropathy in high-risk patients. Am J Med 2006; 119: 155-62.
• 73. Nough H, Eghbal F. Incidence and Main Determinants of Contrast-Induced Nephropathy following Coronary Angiography or Subsequent Balloon Angioplasty.
• 74. Sadeghi HM, Stone GW, Grines CL, Mehran R. Impact of renal insufficiency in patients undergoing primary angioplasty for acute myocardial infarction. Circulation 2003; 108: 2769–75.
• 75. Dangas G, Iakovou I, Nikolsky E, Aymong ED. Contrast-induced nephropathy after percutaneous coronary interventions in relation to chronic kidney disease and hemodynamic variables. Am J Cardiol 2005; 95: 13-9.
• 76. Davidson C, Stacul F, McCullough PA, Tumlin J, Adam A, Lameire N et al. CIN Consensus Working Panel. Contrast medium use. Am J Cardiol 2006;18: 42-58.
• 77. Freeman RV, O'Donnell M, Share D, Meengs WL. Nephropathy requiring dialysis after percutaneous coronary intervention and the critical role of an adjusted contrast dose. Am J Cardiol 2002; 90: 1068-73.
• 78. Nikolsky E, Mehran R, Turcot D, Aymong ED. Impact of chronic kidney disease on prognosis of patients with diabetes mellitus treated with percutaneous coronary intervention. Am J Cardiol 2004; 94: 300-5.
• 79. Lindholt JS. Radiocontrast induced nephropathy. Eur J Vasc Endovasc Surg 2003;25:296-304.
• 80. Andrade L, Campos SB, Seguro AC. Hypercholesterolemia aggravates radiocontrastnephrotoxicity: protective role of arginine. Kıdney Int 1998;53:1736-1742.
• 81. Liao JK. Effects of statins on 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibition beyond low-density lipoprotein cholesterol. Am J Cardiol 2005;96:24-33.
• 82. Muntner P, Coresh J, Smith JC, Eckfeldt J, Klag MJ. Plasma lipids and risk of developing renal dysfunction: the atherosclerosis risk in communities study. Kidney Int 2000;58:293-301.
• 83. Manttari M, Tiula E, Alikoski T, Manninen V. Effects of hypertension and dyslipidemia on the decline in renal function. Hypertension 1995;26:670-5.
• 84. Schaeffner ES, Kurth T, Curhan GC, Glynn RJ, Rexrode KM, Baigent C, Buring JE,Gaziano JM. Cholesterol and the risk of renal dysfunction in apparently healthy men. J Am Soc Nephrol 2003;14:2084-91.
• 85. John S, Schlaich M, Langenfeld M, Weihprecht H, Schmitz G, Weidinger G, SchmiederRE. Increased bioavailability of nitric oxide after lipid lowering therapy in hypercholesterolemic patients: A randomized, placebo-controlled, double-blind study.Circulation 1998;98:211-6.
• 86. Tamai O, Matsuoka H, Itabe H, Wada Y, Kohno K, Imaizumi T. Single LDL apharesisimproves endothelium-dependent vasodilatation in hypercholesterolemic humans.Circulation 1997;95:76-82.
• 87. Kutzing MK, Firestein BL. Altered uric acid levels and disease states. J Pharmacol Exp Ther 2008; 324: 1-7.
• 88. Chonchol M, Shlipak MG, Katz R, et al. Relationship of uric acid with progression of kidney disease. Am J Kidney Dis 2007; 50: 239-247.
• 89. Kuo CF, Luo SF, See LC, et al. Hyperuricaemia and accelerated reduction in renal function. Scand J Rheumatol 2011; 40: 116-121.
• 90. Iseki K, Ikemiya Y, Inoue T, et al. Significance of hyperuricemia as a risk factor for developing ESRD in a screened cohort. Am J Kidney Dis 2004; 44: 642-650.
• 91. Iseki K, Oshiro S, Tozawa M, et al. Significance of hyperuricemia on the early detection of renal failure in a cohort of screened subjects. Hypertens Res 2001; 24: 691-697.
• 92. Sianos G, Morel MA, Kappetein AP, et al. The SYNTAX score: an angiographic tool grading the complexity of coronary artery disease. Euro Intervention, 2005. 1: p. 219-27.93. Serruys PW, Morice MC, Kappetein AP, et al. Percutaneous coronary intervention versus coronary-artery bypass grafting for severe coronary artery disease. N Engl J Med 2009;360:961–72.94. Levy EM, Viscoli CM, Horwitz RI (1996) The effect of acute renal failure on mortality: a cohort analysis. JAMA 275:1489–1494
• 95. Kip K. The problem with composite end points in cardiovascular studies: the story of major adverse cardiac events and percutaneous coronary intervention.J Am Coll Cardiol. 2008 Feb 19;51(7):701-7.