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Objective: The purpose of this study was to evaluate the use of echocardiographic parameters as predictors of rehospitalization in scleroderma patients. Methods : Echocardiographic studies were conducted in 38 patients with systolic scleroderma (SSc) to assess cardiopulmonary function. Forty-five age-matched volunteers without any sign of heart failure served as the control group. Transmitral flow pattern, tricuspid annular plane systolic excursion (TAPSE), left ventricular ejection fraction (LVEF), and right ventricular ejection fraction (RVEF) were evaluated. All patients were subsequently followed for one year. Results : Peak transmitral early-diastolic velocity (mitral E) and TAPSE measurements were significantly different between SSc and control patients (mitral E: 74.1 ± 16.3 vs. 83.5 ± 17.0 cm/s with P = 0.012; TAPSE: 2.4 ± 0.43 vs. 1.9 ± 0.39 cm with P < 0.0001). LVEF was similar, but RVEF was lower in the SSc group (LVEF: 61.7 ± 9.7 vs. 61.7 ± 5.8% with P = 0.962; RVEF: 49.6 ± 6.8 vs. 39.2 ± 6.7% with P < 0.0001). A strong correlation was found between TAPSE and RVEF. A TAPSE less than 1.96 cm indicted a RVEF less than 40% with a sensitivity of 81% and specificity of 78%. Contrary to expectation, pulmonary artery systolic pressure (PASP) did not correlate well with RV function (r = 0.261, r2= 0.068, P = 0.016). Finally, the frequency of rehospitalization was inversely correlated with RVEF and TAPSE in SSc patients. Conclusions: We can predict the rehospitalization rate of SSc patients by TAPSE and RVEF, suggesting the involvement of heart, skin, lung, and other organs in scleroderma patients. [ABSTRACT FROM AUTHOR]

Objective: This study investigates the change in new diastolic indices in uremic patients who undergo regular hemodialysis (H/D). Materials and Methods: We studied uremic patients receiving regular H/D. All patients were sinus rhythm before H/D. They had normal left ventricular systolic performance without regional wall motion abnormality. Patients were separated into two groups according to whether they had significant aortic or mitral regurgitation (AR or MR) or not. They received complete transthoracic echocardiographic examinations. Stroke volume (SV) was calculated as the product of the time-velocity integral (TVI) and cross-sectional area of aortic annulus. Flow propagation velocity (FPV) was measured by color M-mode echocardiography in apical four-chamber view. Mitral annulus tissue Doppler velocities—peak systolic (Sa), early diastolic, and late diastolic—were measured from septal and lateral wall. All these parameters were obtained immediately before and after H/D. Paired data were compared. Result: H/D amount was strongly correlated with the change of SV. After H/D, the reduction of SV in patients without AR or MR (control group) was obvious but it was not significant in patients with significant AR or MR (study group). There were significant differences in mitral inflow velocities, FPV, and mitral annular velocities (except septal Sa) in the control group. In the study group, predialytic and postdialytic parameters of new diastolic indexes had no statistical difference. Conclusion: New echocardiographic indexes of uremic patients with significant AR or MR were relatively preload-independent. The phenomenon was possibly related to insignificant change of SV after H/D. [ABSTRACT FROM AUTHOR]

Objective: This study investigates the change in flow propagation velocity (FPV) in uremic patients who undergo regular hemodialysis (H/D). Materials and Methods: We studied 93 uremic patients (44 men and 49 women; 59 ± 14-years-old) receiving regular hemodialysis. Patients were separated by baseline left ventricular ejection fraction (LVEF): 71 patients with LVEF > 50% (group 1), 13 patients with LVEF 35–50% (group 2), 7 patients with LVEF < 35% (group 3). All patients were in sinus rhythm before H/D. They received complete transthoracic echocardiographic examinations. Flow propagation velocity was measured by color M-mode echocardiography in apical four chambers view. All these parameters were obtained before and after H/D. Paired data were compared. According to different H/D amounts, we viewed the FPV response after H/D in variant baseline LVEF groups. Result: The baseline FPV became lower in patients with low LVEF. After H/D, obvious decrement of FPV occurred in group 1, but there were no obvious changes in groups 2 and 3. In fact, a slight increment of FPV was found in group 3. In patients with baseline LVEF > 50%, FPV after H/D was almost always lower, regardless of H/D amount. But there was different response in patients with baseline LVEF < 50%. Conclusion: Flow propagation velocity is preload independent in patients with LVEF < 50%, but it is preload-dependent in patients with LVEF > 50%. (ECHOCARDIOGRAPHY, Volume 22, September 2005) [ABSTRACT FROM AUTHOR]

Carvedilol is a useful cardiovascular drug for treating heart failure, however, thein vitroeffect on many cell types is unclear. In human MG63 osteosarcoma cells, the effect of carvedilol on intracellular Ca2+ concentrations ([Ca2+]i) and cytotoxicity was explored by using fura-2 and tetrazolium, respectively. Carvedilol at concentrations greater than 1μM caused a rapid rise in[Ca2+]i in a concentration-dependent manner (EC50=15μM). Carvedilol-induced[Ca2+]i rise was reduced by 60% by removal of extracellular Ca2+. Carvedilol-induced Mn2+-associated quench of intracellular fura-2 fluorescence also suggests that carvedilol induced extracellular Ca2+ influx. In Ca2+-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca2+-ATPase, caused a monophasic[Ca2+]i rise, after which the increasing effect of carvedilol on[Ca2+]i was inhibited by 50%. Conversely, pretreatment with carvedilol to deplete intracellular Ca2+ stores totally prevented thapsigargin from releasing more Ca2+. U73122, an inhibitor of phospholipase C, abolished histamine (an inositol 1,4,5-trisphosphate-dependent Ca2+ mobilizer)-induced, but not carvedilol-induced,[Ca2+]i rise. Pretreatment with phorbol 12-myristate 13-acetate and forskolin to activate protein kinase C and adenylate cyclase, respectively, did not alter carvedilol-induced[Ca2+]i rise. Separately, overnight treatment with 0.1–30μM carvedilol inhibited cell proliferation in a concentration-dependent manner. These findings suggest that in human MG63 osteosarcoma cells, carvedilol increases[Ca2+]i by stimulating extracellular Ca2+ influx and also by causing intracellular Ca2+ release from the endoplasmic reticulum and other stores via a phospholipase C-independent manner. Carvedilol may be cytotoxic to osteoblasts. [ABSTRACT FROM AUTHOR]

Evaluation of the severity of valvular mitral stenosis and measurements of the effective rheumatic mitral valve area by noninvasive echocardiography has been well accepted. The area is measured by the two-dimensional planimetry (PLM) method and the Doppler pressure half-time (PHT) method. Recently, the proximal isovelocity surface area (PISA) by color Doppler technique has been used as a quantitaive measurement for valvular heart disease. However, this method needs more validation. The aim of this study was therefore to investigate the clinical applicability of the PISA method in the measurements of effective mitral valve area in patients with rheumatic valvular heart disease. Forty-seven patients aged from 23 to 71 years, with a mean age of 53 ± 13 (25 male and 22 female, 15 with sinus rhythm, mean heart rate of 83 ± 14 beats per minute, with rheumatic valvular mitral stenosis without hemodynamically significant mitral regurgitation) were included in the study. Effective mitral valve area (MVA) derived by the PISA method was calculated as follows: 2 ×Π× (proximal aliasing color zone radius)2× aliasing velocity/peak velocity across mitral orifice. Effective mitral valve areas measured by three different methods (PLM, PHT, and PISA) were compared and correlated with those calculated by the “gold standard” invasive Gorlin's formula. The MVA derived from PHT, PLM, PISA and Gorlin's formula were 1.00 ± 0.31cm2, 0.99 ± 0.30 cm2, 0.95 ± 0.30 cm2 and 0.91 ± 0.29 cm2, respectively. The correlation coefficients (r value) between PHT, PLM, PISA, and Gorlin's formula, respectively, were 0.66 (P = 0.032, SEE = 0.64), 0.67 (P = 0.25, SEE = 0.72) and 0.80 (P = 0.002, SEE = 0.53). In conclusion, the PISA method is useful clinically in the measurement of effective mitral valve area in patients with rheumatic mitral valve stenosis. The technique is relatively simple, highly feasible and accurate when compared with the PHT, PLM, and Gorlin's formula. Therefore, this method could be a promising supplement to methods already in use. (ECHOCARDIOGRAPHY, Volume 21, January 2004) [ABSTRACT FROM AUTHOR]