BACKGROUND: Definite diagnosis of transudative or exudative pleural fluids often presents a diagnostic dilemma. The aim of this study was to evaluate whether amino-terminal brain natriuretic peptide (NT-proBNP) levels in pleural fluid has a diagnostic value for discriminating heart-failurerelated pleural effusions from non-heart-failure effusions. METHODS: Sixty-six subjects (40 male, mean age 61 ؎ 18 y) with pleural effusions were included. Samples of pleural fluid and serum were obtained simultaneously from each subject. Biochemical analysis, bacterial and fungal culture, acid-fast bacilli smear and culture, and cytology were performed on the pleural fluid. RESULTS: Subjects with heart-failure-related pleural effusion had significantly higher pleural NT-proBNP levels than other subjects (P < .001). Pleural and serum NT-proBNP measures were closely correlated (r ‫؍‬ 0.90, P < .001). An NT-proBNP cutoff value of > 2,300 pg/mL in pleural fluid had a sensitivity of 70.8%, a specificity of 97.6%, and positive and negative predictive values of 94.4% and 85.4%, respectively, for discriminating transudates caused by heart failure from exudates. Eight heart-failure subjects were misclassified as exudates by Light's criteria, 5 of whom received diuretics before thoracentesis. All misclassified subjects had pleural NT-proBNP levels higher than 1,165 pg/mL, which predicted heart-failure-associated transudates with 95.8% sensitivity and 85.7% specificity. CONCLUSIONS: Pleural fluid NT-proBNP measurement in the routine diagnostic panel may be useful in differentiation of heart-failure-related pleural effusions and exudative pleural fluids with reasonable accuracy, especially in heart-failure patients treated with diuretics.

Purpose: Degenerative mitral stenosis (DMS) is an increasingly recognized cause of mitral stenosis. The goal of this study was to compare echocardiographic differences between DMS and rheumatic mitral stenosis (RMS), identify echocardiographic variables reflective of DMS severity, and propose a dimensionless mitral stenosis index (DMSI) for assessment of DMS severity. Methods: This is a single-center, retrospective cohort study. We included patients with at least mild MS and a mean transmitral pressure gradient (TMPG) [?] 4 mmHg. Mitral valve area by the continuity equation (MVACEQ) was used as an independent reference. The DMSI was calculated as follows: DMSI = VTILVOT / VTIMV. All-cause mortality data were collected retrospectively. Results: A total of 64 patients with DMS and 24 patients with RMS were identified. MVACEQ was larger in patients with DMS (1.43 ? 0.4 cm2) than RMS (0.9 ? 0.3 cm2) by~0.5 cm2 (p = <0.001) and mean TMPG was lower in the DMS group (6.0? 2 vs. 7.9?3 mmHg, p=0.003). A DMSI of ? 0.50 and [?] 0.351 were associated with MVACEQ [?] 1.5 and MVACEQ [?] 1.0 cm2 (p<0.001), respectively. With the progression of DMS from severe to very severe, there was a significant drop in DMSI. There was a non-significant trend towards worse survival in patients with MVACEQ [?] 1.0 cm2 and DMSI [?] 0.35, suggesting severe stenosis severity. Conclusion: Our results show that TMPG correlates poorly with MVA in patients with DMS. Proposed DMSI may serve as a simple echocardiographic indicator of hemodynamically significant DMS.

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Purpose: Degenerative mitral stenosis (DMS) is an increasingly recognized cause of mitral stenosis. Echocardiographic evaluation of DMS severity is limited. The goal of this study was to compare echocardiographic differences between DMS and rheumatic mitral stenosis (RMS), identify echocardiographic variables reflective of DMS severity, and propose a dimensionless mitral stenosis index (DMSI) for assessment of DMS severity. Methods: This is a single-center, retrospective cohort study. We included patients with at least mild MS and a mean transmitral pressure gradient (TMPG) [?] 4 mmHg. Mitral valve area by the continuity equation (MVACEQ) was used as an independent reference. The DMSI was calculated as follows: DMSI = VTILVOT / VTIMV. Results: A total of 64 patients with DMS and 24 patients with RMS were identified. MVACEQ was larger in patients with DMS (1.43 ? 0.4 cm2) than RMS (0.9 ? 0.3 cm2) by~0.5 cm2 (p = <0.001) and mean TMPG was lower in the DMS group (6.0? 2 vs. 7.9?3 mmHg, p=0.003) despite similar left ventricular stroke volume, left atrial volume index and pulmonary arterial systolic pressure. A DMSI of ? 0.50 and [?] 0.351 were associated with MVACEQ [?] 1.5 and MVACEQ [?] 1.0 cm2 (p<0.001), respectively. With the progression of DMS from severe to very severe, there was a significant drop in DMSI. Conclusion: Our results show that TMPG correlates poorly with MVA in patients with DMS. Proposed DMSI may serve as a simple echocardiographic indicator of hemodynamically significant DMS. More extensive studies are needed to validate these findings.