Protein C-reaktif trong bệnh van động mạch chủ
Tóm tắt
Bệnh Van Động Mạch Chủ bao gồm một loạt các mức độ rối loạn từ dày lá van nhẹ mà không ngăn cản dòng chảy, "xơ cứng động mạch chủ", đến hẹp động mạch chủ bị vôi hóa nặng. Đây là một quá trình tiến triển chậm rãi của sự thay đổi van tương tự như xơ vữa động mạch do các yếu tố nguy cơ tim mạch, sự lắng đọng lipoprotein, viêm mãn tính, và hiện tượng vôi hóa. Các dấu hiệu viêm toàn thân, như CRP ở thành mạch và huyết thanh, tương tự như những gì thấy ở xơ vữa động mạch, hiện diện ở bệnh nhân bị hẹp van động mạch chủ thoái hóa và có thể là biểu hiện của một bệnh chung, hữu ích trong việc theo dõi sự tiến triển của tình trạng hẹp van.
Từ khóa
#Bệnh van động mạch chủ #protein C-reaktif #hẹp động mạch chủ #viêm mãn tính #xơ vữa động mạch.Tài liệu tham khảo
Mazzone A, Epistolato MC, De Caterina R, Storti S, Vittorini S, Sbrana S, Gianetti J, Bevilacqua S, Glauber M, Biagini A, Tanganelli P: Neoangiogenesis, T-lymphocyte infiltration, and heat shock protein-60 are biological hallmarks of an immunomediated inflammatory process in end-stage calcified aortic valve stenosis. J Am Coll Cardiol. 2004, 43: 1670-6.
Rajamannan NM, Gersh B, Bonow RO: Calcific aortic stenosis: from bench to the bedside – emerging clinical and cellular concepts. Heart. 2003, 89: 801-5.
Freeman RV, Otto CM: Spectrum of calcific aortic valve disease: pathogenesis, disease progression, and treatment strategies. Circulation. 2005, 111: 3316-26.
O'Brien KD, Reichenbackh DD, Marcovina SM, et al.: Apolipoprotein B, (a), and E accumulate in the morphologically early lesion of degenerative valvular aortic stenosis. Arterioscler Thromb. 1996, 16: 523-532.
Myers GL, Rifai N, Tracy RP, Roberts WL, Alexander RW, Biasucci LM, Catravas JD, Cole TG, Cooper GR, Khan BV, Kimberly MM, Stein EA, Taubert KA, Warnick GR, Waymack PP, : CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: report from the laboratory science discussion group. Circulation. 2004, 110: e545-9.
Galante A, Pietroiusti A, Vellini M, Piccolo P, Possati G, De Bonis M, Grillo RL, Fontana C, Favalli C: C-reactive protein is increased in patients with degenerative aortic valvular stenosis. J Am Coll Cardiol. 2001, 38: 1078-82.
Gunduz H, Akdemir R, Binak E, Tamer A, Keser N, Uyan C: Can serum lipid and CRP levels predict the "severity" of aortic valve stenosis?. Acta Cardiol. 2003, 58: 321-6.
Sanchez PL, Santos JL, Kaski JC, Cruz I, Arribas A, Villacorta E, Cascon M, Palacios I, Martín-Luengo C: Am J Cardiol. ,
Gerber IL, Stewart RA, Hammett CJ, Legget ME, Oxenham H, West TM, French JK, White HD: Effect of aortic valve replacement on c-reactive protein in nonrheumatic aortic stenosis. Am J Cardiol. 2003, 92: 1129-32.
Warrier B, Mallipeddi R, Karla PK, Lee CH: The functional role of C-reactive protein in aortic wall calcification. Cardiology. 2005, 104: 57-64.
Kajbaf S, Veinot JP, Ha A, Zimmerman D: Comparison of surgically removed cardiac valves of patients with ESRD with those of the general population. Am J Kidney Dis. 2005, 46: 86-93.
Movilli E, Feliciani A, Camerini C, Brunori G, Zubani R, Scolari F, Parrinello G, Cancarini GC: A high calcium-phosphate product is associated with high C-reactive protein concentrations in hemodialysis patients. Nephron Clin Pract. 2005, 101: c161-7.
Torun D, Sezer S, Baltali M, Adam FU, Erdem A, Ozdemir FN, Haberal M: Association of cardiac valve calcification and inflammation in patients on hemodialysis. Ren Fail. 2005, 27: 221-6.
Skowasch D, Schrempf S, Preusse CJ, Likungu JA, Welz A, Luderitz B, Bauriedel G: Tissue-resident C-reactive protein within degenerative aortic valves: correlation with serum CRP levels and modification by statins. Heart. 2005 Sep 13, ,
Lagrand WK, Visser CA, Hermens WT, Niessen HW, Verheugt FW, Wolbink GJ, Hack CE: C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon?. Circulation. 1999, 100: 96-102.
Venugopal SK, Devaraj S, Yuhanna I, Shaul P, Jialal I: Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation. 2002, 106: 1439-1441.
Venugopal SK, Devaraj S, Jialal I: C-reactive protein decreases prostacyclin release from human aortic endothelial cells. Circulation. 2003, 108: 1676-1678.
Palta S, Pai AM, Gill KS, Pai RG: New insights into the progression of aortic stenosis: implications for secondary prevention. Circulation. 2000, 101: 2497-2502.
Otto CM, Burwash IG, Legget ME, Munt BI, Fujioka M, Healy NL, Kraft CD, Miyake-Hull CY, Schwaegler RG: A prospective study of asymptomatic valvular aortic stenosis: Clinical, echocardiographic, and exercise predictors of outcome. Circulation. 1997, 95: 2262-2270.
Chandra HR, Goldstein JA, Choudhary N, O'Neill CS, George PB, Gangasani SR, Cronin L, Marcovitz PA, Hauser AM, O'Neill WW: Adverse outcome in aortic sclerosis is associated with coronary artery disease and inflammation. J Am Coll Cardiol. 2004, 43: 169-75.
Rajamannan NM, Subramaniam M, Springett M, Sebo TC, Niekrasz M, McConnell JP, Singh RJ, Stone NJ, Bonow RO, Spelsberg TC: Atorvastatin inhibits hypercholesterolemia-induced cellular proliferation and bone matrix production in the rabbit aortic valve. Circulation. 2002, 105: 2660-5.
Rajamannan NM, Subramaniam M, Stock SR, Stone NJ, Springett M, Ignatiev KI, McConnell JP, Singh RJ, Bonow RO, Spelsberg TC: Atorvastatin inhibits calcification and enhances nitric oxide synthase production in the hypercholesterolaemic aortic valve. Heart. 2005, 91: 806-10.
Rajamannan NM, Subramaniam M, Caira F, Stock SR, Spelsberg TC: Atorvastatin inhibits hypercholesterolemia-induced calcification in the aortic valves via the Lrp5 receptor pathway. Circulation. 2005, 112: I229-34.
Aronow WS, Ahn C, Kronzon I, Goldman ME: Association of coronary risk factors and use of statins with progression of mild valvular aortic stenosis in older persons. Am J Cardiol. 2001, 88: 693-695.
Novaro GM, Tiong IY, Pearce GL, Lauer MS, Sprecher DL, Griffin BP: Effect of hydroxymethylglutaryl coenzyme A reductase inhibitors on the progression of calcific aortic stenosis. Circulation. 2001, 104: 2205-2209.
Shavelle DM, Takasu J, Budoff MJ, Mao S, Zhao XQ, O'Brien KD: HMG CoA reductase inhibitor (statin) and aortic valve calcium. Lancet. 2002, 359: 1125-6.
Bellamy MF, Pellikka PA, Klarich KW, Tajik AJ, Enriquez-Sarano M: Association of cholesterol levels, hydroxymethylglutaryl conezyme-A reductase treatment, and progression of aortic stenosis in the community. J Am Coll Cardiol. 2002, 40: 1723-30.
Rosenhek R, Rader F, Loho N, Gabriel H, Heger M, Klaar U, Schemper M, Binder T, Maurer G, Baumgartner H: Statins but not angiotensinconverting enzyme inhibitors delay progression of aortic stenosis. Circulation. 2004, 110: 1291-5.
Cowell SJ, Newby DE, Prescott RJ, Bloomfield P, Reid J, Northridge DB, Boon NA, : A randomized trial of intensive lipid-lowering therapy in calcific aortic stenosis. N Engl J Med. 2005, 352: 2389-97.