Sated: 1338 (562?5000) pg/mL; decompensated: 8765 (4610?7804) pg/mL; P.0.05]. Troponin T was available in 23 patients (compensated: 0.03 (0.01?.07) ng/mL; decompensated: 0.12 (0.05?.20) ng/mL; P.0.05). Eight patients received digitalis therapy for the purpose of rate control and/or for heart failure therapy. Thicker LV walls, smaller LV cavities, and enlarged left atria were present in patients compared to controls. EF and FS were similar between the controls and compensated patients but significantly reduced in decompensated patients. MAD_sept, MAD_lat, and TAPSE were significantly reduced in both patient groups. Table 3 showed that the proportion of pericardial effusion and advanced diastolic dysfunction were significantly higher in decompensated group than those in compensated group (all P,0.05).(anteroseptal) LE was documented in 1 decompensated patient. Figure 1 shows example of diffuse LE in a patient. LV longitudinal strain rate and strain data are shown in tables 4 and 5. LSRsys and LSsys were similar among groups in apical segments and significantly reduced in both patient groups in basal segments. LSsys at the mid segment was significantly reduced in all walls of the decompensated group. In general, LSRsys and LSsys at mid and basal segments were significantly lower in the decompensated group compared to the compensated group. ENMD-2076 Global circumferential systolic strain was significantly reduced in both patient groups. Radial Ssys in all 6 walls was similar between controls and the compensated group, but was significantly reduced in the decompensated group (table 5).Base-to-apex Deformation GradientThere was a base-to-apex deformation gradient with higher apical LSRsys and LSsys values and lower mid and basal LSRsys and LSsys values in both patient groups as well as in the controls. Accordingly, we established a ratio to quantify this base-to-apex gradient. The ratio was obtained by dividing apical LSsys with the sum of basal, mid, and apical LSsys (LSsys_api/(LSsys_bas+LSsys_mid+LSsys_api)), ratio 0.45 (0.45 represents the maximal ratio of the control group) indicates pathological gradient. The prevalence of pathological gradient in the septum was 73 (32/ 44) in all patients [9 (50 ) compensated patients, 23 (88 ) decompensated patients, P,0.05] (figure 2).Cardiac Magnetic Resonance DataLE, a possible sign of myocardial interstitial deposition of amyloid fibrils, was detected by cMRI in 17 patients. Diffuse LE was documented in 11 patients and equally distributed in compensated (n = 6) and decompensated (n = 5) patients, localizedMyocardial Strain in Systemic Amyloidosis PatientsTable 5. Longitudinal, circumferential, and radial peak systolic strain ( ).Controls n = 30 Longitudinal systolic 15900046 strain (LSsys, ) Septum Apical Mid Basal Lateral wall Apical Mid Basal Global LSsys of the 6 segments in the 42chamber view Inferior wall Apical Mid Basal SQ 34676 Anterior wall Apical Mid Basal Global LSsys of the 6 segments in the 22chamber view Posterior wall Apical Mid Basal Anteroseptal wall Apical Mid Basal Global LSsys of the 6 segments in the apical long axis view Circumferential systolic strain (CSsys, ) Anteroseptal wall Anterior wall Lateral wall Posterior wall Inferior wall Septum Global Radial systolic strain (RSsys, ) Anteroseptal wall Anterior wall Lateral wall Posterior wall Inferior wall Septum 39.2619.1 46.2619.0 52.5620.4 54.7619.9 51.2618.4 42.7619.9 225.264.9 222.764.3 216.464.5 214.066.4 215.465.5 220.763.9 218.062.5 221.264.8.Sated: 1338 (562?5000) pg/mL; decompensated: 8765 (4610?7804) pg/mL; P.0.05]. Troponin T was available in 23 patients (compensated: 0.03 (0.01?.07) ng/mL; decompensated: 0.12 (0.05?.20) ng/mL; P.0.05). Eight patients received digitalis therapy for the purpose of rate control and/or for heart failure therapy. Thicker LV walls, smaller LV cavities, and enlarged left atria were present in patients compared to controls. EF and FS were similar between the controls and compensated patients but significantly reduced in decompensated patients. MAD_sept, MAD_lat, and TAPSE were significantly reduced in both patient groups. Table 3 showed that the proportion of pericardial effusion and advanced diastolic dysfunction were significantly higher in decompensated group than those in compensated group (all P,0.05).(anteroseptal) LE was documented in 1 decompensated patient. Figure 1 shows example of diffuse LE in a patient. LV longitudinal strain rate and strain data are shown in tables 4 and 5. LSRsys and LSsys were similar among groups in apical segments and significantly reduced in both patient groups in basal segments. LSsys at the mid segment was significantly reduced in all walls of the decompensated group. In general, LSRsys and LSsys at mid and basal segments were significantly lower in the decompensated group compared to the compensated group. Global circumferential systolic strain was significantly reduced in both patient groups. Radial Ssys in all 6 walls was similar between controls and the compensated group, but was significantly reduced in the decompensated group (table 5).Base-to-apex Deformation GradientThere was a base-to-apex deformation gradient with higher apical LSRsys and LSsys values and lower mid and basal LSRsys and LSsys values in both patient groups as well as in the controls. Accordingly, we established a ratio to quantify this base-to-apex gradient. The ratio was obtained by dividing apical LSsys with the sum of basal, mid, and apical LSsys (LSsys_api/(LSsys_bas+LSsys_mid+LSsys_api)), ratio 0.45 (0.45 represents the maximal ratio of the control group) indicates pathological gradient. The prevalence of pathological gradient in the septum was 73 (32/ 44) in all patients [9 (50 ) compensated patients, 23 (88 ) decompensated patients, P,0.05] (figure 2).Cardiac Magnetic Resonance DataLE, a possible sign of myocardial interstitial deposition of amyloid fibrils, was detected by cMRI in 17 patients. Diffuse LE was documented in 11 patients and equally distributed in compensated (n = 6) and decompensated (n = 5) patients, localizedMyocardial Strain in Systemic Amyloidosis PatientsTable 5. Longitudinal, circumferential, and radial peak systolic strain ( ).Controls n = 30 Longitudinal systolic 15900046 strain (LSsys, ) Septum Apical Mid Basal Lateral wall Apical Mid Basal Global LSsys of the 6 segments in the 42chamber view Inferior wall Apical Mid Basal Anterior wall Apical Mid Basal Global LSsys of the 6 segments in the 22chamber view Posterior wall Apical Mid Basal Anteroseptal wall Apical Mid Basal Global LSsys of the 6 segments in the apical long axis view Circumferential systolic strain (CSsys, ) Anteroseptal wall Anterior wall Lateral wall Posterior wall Inferior wall Septum Global Radial systolic strain (RSsys, ) Anteroseptal wall Anterior wall Lateral wall Posterior wall Inferior wall Septum 39.2619.1 46.2619.0 52.5620.4 54.7619.9 51.2618.4 42.7619.9 225.264.9 222.764.3 216.464.5 214.066.4 215.465.5 220.763.9 218.062.5 221.264.8.
