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 mgyl, 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.
Objective: We aimed to investigate effects of left ventricular diastolic dysfunction on left atrial appendage functions, spontaneous echo contrast and thrombus formation in patients with nonvalvular atrial fibrillation. Methods: In 58 patients with chronic nonvalvular atrial fibrilation and preserved left ventricular systolic function, left atrial appendage functions, left atrial spontaneous echo contrast grading and left ventricular diastolic functions were evaluated using transthoracic and transoesophageal echocardiogram. Patients divided in two groups: Group D (n=30): Patients with diastolic dysfunction, Group N (n=28): Patients without diastolic dysfunction. Categorical variables in two groups were evaluated with Pearson's chi-square or Fisher's exact test. The significance of the lineer correlation between the degree of spontaneous echo contrast (SEC) and clinical measurements was evaluated with Spearman's correlation analysis. Results: Peak pulmonary vein D velocity of the Group D was significantly higher than the Group N (p=0.006). However, left atrial appendage emptying velocity, left atrial appendage lateral wall velocity, peak pulmonary vein S, pulmonary vein S/D ratio were found to be significantly lower in Group D (p=0.028, p<0.001, p<0.001; p<0.001). Statistically significant negative correlation was found between SEC in left atrium and left atrial appendage emptying, filling, pulmonary vein S/D levels and lateral wall velocities respectively (r=-0.438, r=-0.328, r=-0.233, r=-0.447). Left atrial appendage emptying, filling, pulmonary vein S/D levels and lateral wall velocities were significantly lower in SEC 2-3-4 than SEC 1 (p=0.003, p=0.029, p<0.001, p=0.002). Conclusion: In patients with nonvalvular atrial fibrillation and preserved left ventricular ejection fraction, left atrial appendage functions are decreased in patients with left ventricular diastolic dysfunction. Left ventricular diastolic dysfunction may constitute a potential risk for formation of thrombus and stroke. (Anadolu Kardiyol Derg 2014; 14: 256-60
Background: Brain natriuretic peptide (BNP) is a cardiac hormone secreted from the ventricular myocardium as a response to ventricular volume expansion and pressure overload. Rheumatic heart disease (RHD) is still an important cause of heart failure in developing countries. Aims: To measure BNP levels in patients with RHD and to determine whether BNP concentrations correlate with clinical and echocardiographic findings. Methods: Eighty-eight patients with rheumatic valve disease and 24 age-and sex-matched healthy subjects were entered in the study. BNP was measured using the Triage B-Type Natriuretic Peptide test (Biosite Diagnostics, San Diego, CA). Transthoracic echocardiography was performed in all patients to assess the severity of the valve disease and for the measurement of pulmonary artery pressure. Results: The plasma concentrations of BNP were significantly higher in patients with rheumatic heart disease than in control subjects (232 F 294 vs. 14 F 12 pg/ml, p < 0.0001). The plasma BNP level was significantly higher in NYHA class III + IV than in class II (463 F 399 vs. 192 F 243 pg/ml, p < 0.0001) and in NYHA class II than in class I (192 F 243 vs. 112 F 135 pg/ml, p < 0.001). The independent determinants of higher BNP levels were NYHA functional class and systolic pulmonary artery pressure in multivariate analysis. Conclusion: We found increased plasma BNP levels in patients with rheumatic heart disease compared with healthy subjects.
In this study we found elevated plasma BNP levels in patients with pure MS in sinus rhythm. Plasma BNP levels correlated with disease severity and this can have potential clinical implications, for example in patients undergoing percutaneous balloon mitral valvuloplasty or in patients with poor echocardiographic windows.
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