Abstract
Background High sensitive C-Reactive Protein (hs-CRP) predicts morbidity and mortality in various clinical conditions. The effect of hsCRP on progression of chronic rheumatic mitral stenosis (CRMS) has not been demonstrated. Methods and results A total of 132 patients with CRMS (95 female, 37 male) and 145 control (100 female, 45 male) were included in the study. Baseline clinical, echocardiographic, hematologic and hs-CRP measurements were collected prospectively. Mean mitral valve area (MVA) was 1.4 ± 0.3 cm2, mean wilkins valve score value was 8.9 ± 1.7, left atrial diameter was 5.0 ± 0.7 cm, left atrial area was 37.2 ± 12.6 cm2, and systolic pulmonary arterial pressure (SPAP) was 44 ± 11 mmHg in patients with CRMS. The mean levels of hs-CRP value, fibrinogen, and mean platelet volume (MPV) were significantly higher in CRMS group compared to control group. The levels of hsCRP were found to be positively correlated with mean Wilkins valve score value, SPAP, presence of atrial fibrillation (AF), left atrial diameter, left atrial area, presence of LASEC(+), fibrinogen, and MPV and inversely correlated with MVA in patients with CRMS. Linear regression analysis revealed that the hsCRP level independently affects mean Wilkins valve score value, left atrial area (LAA), LASEC(+) and AF in the patients with CRMS. Conclusions These results suggest that increased hsCRP levels are associated with CRMS severity. These association may be important when treating patients with CRMS.
Similar content being viewed by others
References
Goldstein I, Rebeyrotte P, Parlebas J et al (1968) Isolation from heart valves of glycopeptides which share Immunologic properties with streptococcus haemolyticus group A polysaccharides. Nature 219:866–868
Soler-Soler J, Galve E (2000) Worldwide perspective of valve disease. Heart 83:721–725
Ridker PM, Glynn RJ, Hennekens CH (1998) C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. Circulation 97:2007–2011
Yeun JY, Levine RA, Mantadilok V et al (2000) C-Reactive protein predicts all-cause and cardiovascular mortality in hemodialysis patients. Am J Kidney Dis 35:469–476
Haverkate F, Thompson SG, Pyke SD et al (1997) Production of C-reactive protein and risk of coronary events in stable and unstable angina. Europen concerted action in thrombolisis and disabilities angina pectoris study group. Lancet 349:462–466
Ridker PM, Cushman M, Stampfer MJ et al (1998) Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 97:425–428
Ridker PM, Buring JE, Shih J et al (1998) Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women. Circulation 98:731–733
Schoen FJ, St.John M (1991) Contemporary pathologic considerations in valvular disease. In: Virmani B, Atkinson JB, Feuoglio JJ (eds) Cardiovascular pathology. Saunders, Philadelphia, pp 334–353
Edep ME, Shirani J, Wolf P et al (2000) Matrix matalloproteinase expression in nonrheumatic aortic stenosis. Cardiovasc Pathol 9:281–286
Otto CM, Kuusisto J, Reichenback DD et al (1994) Characterization of the early lesion of valvular aortic stenosis. Histological and immunohistochemical studies. Circulation 90:844–853
Danesh J, Whincup P, Walker M et al (2000) Low grade inflammation and coronary heart disease: Prospective study and updated meta-analyses. BMJ 321:199–204
Chiu-Braga YY, Hayashi SY, Schafranski M et al (2006) Further evidence of inflammation in chronic rheumatic valve disease (CRVD): High levels of advanced oxidation protein products (AOPP) and high sensitive C-reactive protein. Int J Cardiol 109:275–276
Gölbasi Z, Ucar O, Keles T et al (2002) Increased levels of high sensitive C-reactive protein in patients with chronic rheumatic valve disease evidence of ongoing inflammation. Eur J Heart Fail 4:593–595
Krasuski RA, Bush A, Kay JE et al (2003) C-reactive protein elevation independently influences the procedural success of percutaneous balloon mitral valve commissurotomy. Am Heart J 146:1099–1104
Yetkin E, Erbay AR, Ileri M et al (2001) Levels of circulating adhesion molecules in rheumatic mitral stenosis. Am J Cardiol 88:1209–1211
Sahn DJ, DeMaria A, Kisslo J et al (1978) Recommendation regarding quantitation in M-mode echocardiography: results of a survey of echocardiographic measurement. Circulation 58:1072–1083
Wilkins GT, Weyman AE, Abascal VM et al (1988) Percutaneous balloon dilatationof the mitral valve. An analysisof echocardiographic variables related to outcome and the mechanism of dilatation. Br Heart J 60:299–308
Hatle L, Angelsen B, Tromsdal A (1979) Noninvasive assessment of atrioventricular pressure half-time by Doppler ultrasound. Circulation 60:1096–1104
Helmcke F, Nanda NC, Hsiung MC et al (1987) Color Doppler assessment of mitral regurgitation with orthogonal planes. Circulation 75:175–183
Guilherme L, Cunha-neto E, Coelho V et al (1995) Human heart-infiltrating T-cell clones from rheumatic heart disease patients recognize both streptococcal and cardiac proteins. Circulation 92:415–420
Stollerman GH (1991) Rheumatologic streptococci and autoimmunity. Clin Immunol Immunopathol 61:131–142
Lagrand WK, Visser CA, Hermens WT et al (1999) C-reactive protein as a cardiovascular risk factor: more than an epiphenomenon? Circulation 100:96–102
Venugopal SK, Devaraj S, Yuhanna I et al (2002) Demonstration that C-reactive protein decreases eNOS expression and bioactivity in human aortic endothelial cells. Circulation 106:1439–1441
Venugopal SK, Devaraj S, Jialal I (2003) C-reactive protein decreases prostacyclin release from human aortic endothelial cells. Circulation 108:1676–1678
Gerber IL, Stewart RA, Hammett CJ et al (2003) Effect of aortic valve replacement on c-reactive protein in nonrheumatic aortic stenosis. Am J Cardiol 92:1129–1132
Buffon A, Liuzzo G, Biasucci LM et al (1999) Preprocedural serum levels of c-reactive protein predict early complications and late restenosis after coronary angioplasty. J Am Coll Cardiol 34:1512–1521
Boeken U, Feindt P, Zimmermann N et al (1998) Increased preoperative C-reactive protein values without signs of an infection and complicated course after cardiopulmonary bypass (CPB)-operations. Eur J Cardiothorac Surg 13:541–545
Sanchez PL, Santos JL, Kaski JC et al (2006) Grupo AORTICA (Grupo de Estudio de la Estenosis Aortica): relation of circulating C-reactive protein to progression of aortic valve stenosis. Am J Cardiol 97:90–93
Olsson M, Dalsgaard CJ, Haegerstrand A et al (1994) Accumulation of T lymphocytes and expression of interleukin–2 receptors in nonrheumatic stenotic aortic valves. J Am Coll Cardiol 23:1162–1170
Mohler ERI, Gannon F, Reynolds C et al (2001) Bone formation and inflammation in cardiac valves. Circulation 103:1522–1528
Warrier B, Mallipeddi R, Karla PK et al (2005) The functional role of C-reactive protein in aortic wall calcification. Cardiology 104:57–64
Lefer DJ (2002) Statins as potent anti-inflammatory drugs. Circulation 106:2041–2042
Rosenson RS, Tangney CC, Casey LC (1999) Inhibition of proinflammatory cytokine production by pravastatin. Lancet 353:983–984
Novaro GM, Tiong IY, Pearce GL et al (2001) Effect of hydroxymethylglutaryl coenzyme a reductase inhibitors on the progression of calcific aortic stenosis. Circulation 104:2205–2209
Rosenhek R, Rader F, Loho N et al (2004) Statins but not angiotensinconverting enzyme inhibitors delay progression of aortic stenosis. Circulation 110:1291–1295
Moura LM, Ramos SF, Zamorano JL et al (2007) Rosuvastatin affecting aortic valve endothelium to slow the progression of aortic stenosis. J Am Coll Cardiol 49:554–561
Bruins P, Velthuis H, Yazdanbakhsh AP et al (1997) Activation of the complement system during and after cardiopulmonary bypass surgery: postsurgery activation involves C-reactive protein and is associated with postoperative arrhythmia. Circulation 96:3542–3548
Fontes ML, Mathew JP, Rinder HM et al (2005) Multicenter Study of Perioperative Ischemia (McSPI) Research Group. Atrial fibrillation after cardiac surgery/cardiopulmonary bypass is associated with monocyte activation. Anesth Analg 101:17–23
Hatzinikolaou-Kotsakou EH, Tziakas D, Hotidis A et al (2006) Relation of C-reactive protein to the first onset and the recurrence rate in lone atrial fibrillation. Am J Cardiol 97:659–661
Merino A, Hauptman P, Badimon L et al (1992) Echocardiographic “smoke” is produced by an interaction of erythrocytes and plasma proteins modulated by shear forces. J Am Coll Cardiol 20:1661–1668
Black IW, Hopkins AP, Lee LC et al (1991) Left atrial spontaneous echo contrast: a clinical and echocardiographic analysis. J Am Coll Cardiol 18:398–404
Bernstein NE, Demopoulos LA, Tunick PA et al (1994) Correlates of spontaneous echo contrast in patients with mitral stenosis and normal sinus rhythm. Am Heart J 128:287–292
Goswami KC, Yadav R, Rao MB et al (2000) Clinical and echocardiographic predictors of left atrial clot and spontaneous echo contrast in patients with severe rheumatic mitral stenosis: a prospective study in 200 patients by transesophageal echocardiography. Int J Cardiol 73:273–279
Vincelj J, Sokol I, Jaksic O (2002) Prevalence and clinical significance of left atrial spontaneous echo contrast detected by transesophageal echocardiography. Echocardiography 19(4):319–324
Yuan YW, Shumg KK (1988) Ultrasonic backscatter from flowing whole blood:II. Dependence on frequency and fibrinogen concentrations. J Acoust Soc Am 84:1195–1200
Karthikeyan G, Thachil A, Sharma S et al (2007) Elevated high sensitivity CRP levels in patients with mitral stenosis and left atrial thrombus. Int J Cardiol 122:252–254
Ileri M, Buyukasik Y, Ileri NS et al (1998) Activation of blood coagulation in patients with mitral stenosis and sinus ritm. Am J Cardiol 81:795–797
Author information
Authors and Affiliations
Corresponding author
Rights and permissions
About this article
Cite this article
Alyan, O., Metin, F., Kacmaz, F. et al. High levels of high sensitivity C-reactive protein predict the progression of chronic rheumatic mitral stenosis. J Thromb Thrombolysis 28, 63–69 (2009). https://doi.org/10.1007/s11239-008-0245-7
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s11239-008-0245-7