Ients with AL amyloidosis, 15 normal controls) and blinded to the initial results by one investigator (DL). Interobserver variation was done on the same datasets by two observers (DL and KH). Reproducibility was assessed using Bland and Altman analysis.Data AnalysisData are presented as mean6standard deviation (SD) or median (quartiles), as appropriate. Differences on continuous data among 3 groups were compared using one-way order 11089-65-9 analysis of variance (ANOVA) followed by either Tukeys or Games-Howell multiple comparison post hoc tests as appropriate. Serum level of NT-proBNP and Troponin T showed a significant skewed distribution, difference between groups was compared using the Mann-Whitney U-statistic test. Multiple linear regression analysis was performed to identify predictors for the reduction of LSsys. Survival curves were calculated by the Kaplan-Meier method, and compared by 23727046 Mantel-Cox log-rank tests. The end point was date of death or heart transplantation during follow-up. The mortality hazard ratios (HR) were calculated using univariate proportionalhazards regression analysis. The major determinants of mortalityFigure 1. Cardiac magnetic resonance imaging in a patient with AL amyloidosis and LV hypertrophy. A (transverse T2 haste image) and B (short axis cine image) demonstrate left ventricular hypertrophy and minor pericardial effusion (dash arrow). C and D show late gadolinium enhancement images (short axis and horizontal long axis) presenting diffuse LE (solid arrows) in the left ventricular walls. LE: late enhancement; PE: pericardial effusion. doi:10.1371/journal.pone.0056923.gMyocardial Strain in Systemic Amyloidosis PatientsTable 4. Longitudinal peak systolic strain rate (LSRsys, s21).Controls n = 30 Septum Apical Mid Basal Lateral wall Apical Mid Basal Peptide M site Global LSRsys of the 6 segments in the 42chamber view Inferior wall Apical Mid Basal Anterior wall Apical Mid Basal Global LSRsys of the 6 segments in the 22chamber view Posterior wall Apical Mid Basal Anteroseptal wall Apical Mid Basal Global LSRsys of the 6 segments in the apical long axis view 21.2660.34 21.0260.22{ 20.9460.19{ 21.2460.27 21.0860.31 21.2060.26 20.9660.13 21.3060.40 21.1060.28{ 21.2260.21 21.2460.51 21.1160.36 21.1660.40 21.0660.30 21.2160.33 21.1760.31 21.3560.27 21.2860.37 21.0960.23{ 20.9260.14{ 21.0460.Compensated group n = 18 21.3060.48 20.8060.27*{ 20.6060.24*{ 21.2760.44 21.0060.35 21.0160.52 20.9460.29 20.9960.37 20.8660.28* 20.9460.32* 20.9560.46 20.8260.34* 20.7860.41* 20.8060.27* 21.1360.37 20.9660.29 20.9260.33* 21.4460.53 20.9260.37{ 20.5460.27*{ 20.9260.Decompensated group n = 26 21.1860.47 15900046 20.5960.31*{{ 20.4160.25*{{ 21.1560.42 20.6860.29*{{ 20.4960.31*{{ 20.6860.28*{ 21.0060.52* 20.6160.34*{{ 20.6660.31*{ 21.2860.52 20.8160.38*{ 20.5860.29*{ 20.6960.29* 20.9860.42 20.6260.33*{{ 20.6460.29*{{ 21.2760.51 20.9660.42{ 20.5060.30*{1 20.7260.28*{*P,0.05 vs. Controls; { P,0.05 vs. Compensated group; { P,0.05 vs. apical; 1 P,0.05 vs. Mid. doi:10.1371/journal.pone.0056923.tHigh-dose melphalan plus autologous stem-cell transplantation regimen was more frequently used while oral melphalan plus prednisone regimen was less frequently applied in compensated group than in decompensated group. Cardiac associated clinical data and standard echocardiographic data of the cohort are presented in table 2, specific echocardiographic and electrocardiographic parameters were shown in table 3. Serum NT-proBNP was available in 20 patients [median (quartiles), compen.Ients with AL amyloidosis, 15 normal controls) and blinded to the initial results by one investigator (DL). Interobserver variation was done on the same datasets by two observers (DL and KH). Reproducibility was assessed using Bland and Altman analysis.Data AnalysisData are presented as mean6standard deviation (SD) or median (quartiles), as appropriate. Differences on continuous data among 3 groups were compared using one-way analysis of variance (ANOVA) followed by either Tukeys or Games-Howell multiple comparison post hoc tests as appropriate. Serum level of NT-proBNP and Troponin T showed a significant skewed distribution, difference between groups was compared using the Mann-Whitney U-statistic test. Multiple linear regression analysis was performed to identify predictors for the reduction of LSsys. Survival curves were calculated by the Kaplan-Meier method, and compared by 23727046 Mantel-Cox log-rank tests. The end point was date of death or heart transplantation during follow-up. The mortality hazard ratios (HR) were calculated using univariate proportionalhazards regression analysis. The major determinants of mortalityFigure 1. Cardiac magnetic resonance imaging in a patient with AL amyloidosis and LV hypertrophy. A (transverse T2 haste image) and B (short axis cine image) demonstrate left ventricular hypertrophy and minor pericardial effusion (dash arrow). C and D show late gadolinium enhancement images (short axis and horizontal long axis) presenting diffuse LE (solid arrows) in the left ventricular walls. LE: late enhancement; PE: pericardial effusion. doi:10.1371/journal.pone.0056923.gMyocardial Strain in Systemic Amyloidosis PatientsTable 4. Longitudinal peak systolic strain rate (LSRsys, s21).Controls n = 30 Septum Apical Mid Basal Lateral wall Apical Mid Basal Global LSRsys of the 6 segments in the 42chamber view Inferior wall Apical Mid Basal Anterior wall Apical Mid Basal Global LSRsys of the 6 segments in the 22chamber view Posterior wall Apical Mid Basal Anteroseptal wall Apical Mid Basal Global LSRsys of the 6 segments in the apical long axis view 21.2660.34 21.0260.22{ 20.9460.19{ 21.2460.27 21.0860.31 21.2060.26 20.9660.13 21.3060.40 21.1060.28{ 21.2260.21 21.2460.51 21.1160.36 21.1660.40 21.0660.30 21.2160.33 21.1760.31 21.3560.27 21.2860.37 21.0960.23{ 20.9260.14{ 21.0460.Compensated group n = 18 21.3060.48 20.8060.27*{ 20.6060.24*{ 21.2760.44 21.0060.35 21.0160.52 20.9460.29 20.9960.37 20.8660.28* 20.9460.32* 20.9560.46 20.8260.34* 20.7860.41* 20.8060.27* 21.1360.37 20.9660.29 20.9260.33* 21.4460.53 20.9260.37{ 20.5460.27*{ 20.9260.Decompensated group n = 26 21.1860.47 15900046 20.5960.31*{{ 20.4160.25*{{ 21.1560.42 20.6860.29*{{ 20.4960.31*{{ 20.6860.28*{ 21.0060.52* 20.6160.34*{{ 20.6660.31*{ 21.2860.52 20.8160.38*{ 20.5860.29*{ 20.6960.29* 20.9860.42 20.6260.33*{{ 20.6460.29*{{ 21.2760.51 20.9660.42{ 20.5060.30*{1 20.7260.28*{*P,0.05 vs. Controls; { P,0.05 vs. Compensated group; { P,0.05 vs. apical; 1 P,0.05 vs. Mid. doi:10.1371/journal.pone.0056923.tHigh-dose melphalan plus autologous stem-cell transplantation regimen was more frequently used while oral melphalan plus prednisone regimen was less frequently applied in compensated group than in decompensated group. Cardiac associated clinical data and standard echocardiographic data of the cohort are presented in table 2, specific echocardiographic and electrocardiographic parameters were shown in table 3. Serum NT-proBNP was available in 20 patients [median (quartiles), compen.
Related Posts
Eir flanking regions (Figure S2). Even so, we couldn't amplify MENAEir flanking regions (Figure S2).
Eir flanking regions (Figure S2). Even so, we couldn’t amplify MENAEir flanking regions (Figure S2). Even so, we couldn’t amplify MENA (3136 bp). We did not attempt to amplify the corresponding gene for PHYLLO (15.7 kb) for the reason that it was also long to be amplified by PCR. menb cells and mene cells had […]
Uted from wear-time was shorter. In contrast, we found no distinction in duration of activity
Uted from wear-time was shorter. In contrast, we found no distinction in duration of activity bouts, variety of activity bouts every day, or intensity of your activity bouts when non-wear time was computed applying either 20, 30 or 60 consecutive minutes of zero counts around the accelerometer (see Table two). This suggests study cohorts and […]
Culture. N . Conidiophores with verticillately placed conidiogenous cells bearing conidia at their guidelines. R
Culture. N . Conidiophores with verticillately placed conidiogenous cells bearing conidia at their guidelines. R . Conidia. U. Hyphae turning from initial yellow to purple in KOH. V, W. Chlamydospores. (A, H, I. TU 112902; B, G, J. BPI 749247; C, K. TFC 97-138; D, E. Holotype, BPI 748258; F. TU 112903; L, M. TU […]