Gölbasi, Zehra, Uçar, Özgül, Keles, Telat, Sahin, Ahmet, Çagli, Kerim, Çamsari, Ahmet, Diker, Erdem, Aydogdu, Sinan, Gölbasi, Zehra, Uçar, Ozgül, Cagli, Kerim, and Camsari, Ahmet
The precise pathogenetic mechanism(s) of rheumatic fever and rheumatic heart disease have never been defined. C-reactive protein (CRP) is increased in patients with acute rheumatic fever, but it is not known whether plasma levels increase in patients with chronic rheumatic valve disease. The aim of this study was to determine the role of inflammation detected by high sensitivity CRP (hs-CRP) levels in the progression of chronic rheumatic valve disease. A total of 113 patients with chronic rheumatic valve disease (81 women, 32 men; mean age 40±14 years, range 13–70), 51 patients with prosthetic valve(s) (31 women, 20 men; mean age 48±13 years, range 21–71) and 102 healthy subjects (68 women, 34 men, mean age 41±12 years, range 25–73), as a control group, were assessed. Patients with acute rheumatic fever, acute infection, inflammatory disease, malignancy, acute myocardial infarction and trauma were excluded. hs-CRP was determined using latex-enhanced immunonephelometric assays on a BN II analyzer (Behring). Transthoracic echocardiography was performed in all patients in order to evaluate valvular disease. Levels of hs-CRP were significantly higher in patients with chronic rheumatic heart disease than in patients with prosthetic valve(s) and healthy subjects (0.62±0.64 vs. 0.35±0.41 vs. 0.24±0.18 mg/l, P<0.01 and P<0.001 respectively). No correlation was observed between CRP and age, sex or functional capacity. We found that hs-CRP is increased in chronic rheumatic heart disease; this may indicate that inflammatory response still persists in the chronic phase. [Copyright &y& Elsevier]