Angiotensin II As A Natural Suppressor On Cardiac Natriuretic Peptide System: Molecular Insights And Novel Therapeutic Design
HFSA ePoster Library. Ma X. 09/10/21; 343538; 3
Xiao Ma
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Abstract
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Introduction: Left ventricular (LV) longitudinal strain and stroke volume are significant predictors of mortality in patients with transthyretin amyloid cardiomyopathy (ATTR-CM). In the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT), tafamidis significantly reduced mortality and CV-related hospitalizations. Further analysis of changes in echocardiographic measures in ATTR-ACT may provide additional insight into the efficacy of tafamidis.
Hypothesis: Treatment with tafamidis significantly reduces the worsening of echocardiographic variables including LV longitudinal strain and stroke volume in ATTR-CM patients.
Methods: In ATTR-ACT, ATTR-CM patients (variant or wild-type) were treated with tafamidis 80 mg (n=176) or placebo (n=177) for 30 months. Echocardiography was conducted at enrollment, and at Months 6, 18 and 30, using a standardized protocol and analyzed by an independent central laboratory. We compared changes in LV stroke volume (SV), global longitudinal strain (GLS) and mitral inflow E wave/annular diastolic early (e’) wave (E/e’) in patients treated with tafamidis 80 mg (the approved dose) vs placebo.
Results: Baseline mean (SD) SV (mL), GLS (%) and septal and lateral E/e’ were similar in the tafamidis and placebo groups (Table). Each measure worsened over the duration of the trial, as shown by least-squares (LS) mean (SE) change from baseline at Month 30 for each group (Table). This decline was more pronounced in placebo-treated patients, with a significant reduction in LS mean difference (95% CI) with tafamidis vs placebo for each measure (P<0.05 for all). Decline in SV and GLS was apparent from Month 6 in all patients; difference between tafamidis and placebo groups was apparent from Month 18. Decline in E/e’ (indicative of elevated LV filling pressures) was apparent from Month 6 with placebo but only minimally changed with tafamidis at each time point; difference between tafamidis and placebo was apparent from Month 6.
Conclusions: LV longitudinal strain and stroke volume are significant predictors of mortality in ATTR-CM patients. Treatment with tafamidis significantly reduced worsening progression of LV systolic (GLS, SV) and diastolic function (E/e’) over 30 months in ATTR-CM patients. These echocardiographic data provide additional insight into the efficacy of tafamidis.
Hypothesis: Treatment with tafamidis significantly reduces the worsening of echocardiographic variables including LV longitudinal strain and stroke volume in ATTR-CM patients.
Methods: In ATTR-ACT, ATTR-CM patients (variant or wild-type) were treated with tafamidis 80 mg (n=176) or placebo (n=177) for 30 months. Echocardiography was conducted at enrollment, and at Months 6, 18 and 30, using a standardized protocol and analyzed by an independent central laboratory. We compared changes in LV stroke volume (SV), global longitudinal strain (GLS) and mitral inflow E wave/annular diastolic early (e’) wave (E/e’) in patients treated with tafamidis 80 mg (the approved dose) vs placebo.
Results: Baseline mean (SD) SV (mL), GLS (%) and septal and lateral E/e’ were similar in the tafamidis and placebo groups (Table). Each measure worsened over the duration of the trial, as shown by least-squares (LS) mean (SE) change from baseline at Month 30 for each group (Table). This decline was more pronounced in placebo-treated patients, with a significant reduction in LS mean difference (95% CI) with tafamidis vs placebo for each measure (P<0.05 for all). Decline in SV and GLS was apparent from Month 6 in all patients; difference between tafamidis and placebo groups was apparent from Month 18. Decline in E/e’ (indicative of elevated LV filling pressures) was apparent from Month 6 with placebo but only minimally changed with tafamidis at each time point; difference between tafamidis and placebo was apparent from Month 6.
Conclusions: LV longitudinal strain and stroke volume are significant predictors of mortality in ATTR-CM patients. Treatment with tafamidis significantly reduced worsening progression of LV systolic (GLS, SV) and diastolic function (E/e’) over 30 months in ATTR-CM patients. These echocardiographic data provide additional insight into the efficacy of tafamidis.
| Tafamidis 80 mg (N=176) | Placebo (N=177) | |
| SV, baseline, mean (SD) | 45.5 (16.9) | 45.1 (16.9) |
| SV, change at Month 30, LS mean (SE) | –4.17 (1.30) | –11.19 (2.16) |
| SV, LS mean (95% CI) difference from placebo | 7.02 (2.55, 11.49); P=0.0021 | |
| GLS, baseline, mean (SD) | –9.3 (3.7) | –9.4 (3.6) |
| GLS, change at Month 30, LS mean (SE) | 1.13 (0.30) | 2.15 (0.34) |
| GLS, LS mean (95% CI) difference from placebo | –1.02 (–1.73, –0.31); P=0.0051 | |
| Septal E/e’, baseline, mean (SD) | 24.8 (11.0) | 24.2 (10.4) |
| Septal E/e’, change at Month 30, LS mean (SE) | 1.07 (0.97) | 4.18 (1.29) |
| Septal E/e’, LS mean (95% CI) difference from placebo | –3.11 (–5.50, –0.72); P=0.0109 | |
| Lateral E/e’, baseline, mean (SD) | 17.1 (7.7) | 17.2 (7.8) |
| Lateral E/e’, change at Month 30, LS mean (SE) | 0.04 (0.75) | 2.38 (0.61) |
| Lateral E/e’, LS mean (95% CI) difference from placebo | –2.35 (–4.01, –0.69); P=0.0057 |
Introduction: Left ventricular (LV) longitudinal strain and stroke volume are significant predictors of mortality in patients with transthyretin amyloid cardiomyopathy (ATTR-CM). In the Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT), tafamidis significantly reduced mortality and CV-related hospitalizations. Further analysis of changes in echocardiographic measures in ATTR-ACT may provide additional insight into the efficacy of tafamidis.
Hypothesis: Treatment with tafamidis significantly reduces the worsening of echocardiographic variables including LV longitudinal strain and stroke volume in ATTR-CM patients.
Methods: In ATTR-ACT, ATTR-CM patients (variant or wild-type) were treated with tafamidis 80 mg (n=176) or placebo (n=177) for 30 months. Echocardiography was conducted at enrollment, and at Months 6, 18 and 30, using a standardized protocol and analyzed by an independent central laboratory. We compared changes in LV stroke volume (SV), global longitudinal strain (GLS) and mitral inflow E wave/annular diastolic early (e’) wave (E/e’) in patients treated with tafamidis 80 mg (the approved dose) vs placebo.
Results: Baseline mean (SD) SV (mL), GLS (%) and septal and lateral E/e’ were similar in the tafamidis and placebo groups (Table). Each measure worsened over the duration of the trial, as shown by least-squares (LS) mean (SE) change from baseline at Month 30 for each group (Table). This decline was more pronounced in placebo-treated patients, with a significant reduction in LS mean difference (95% CI) with tafamidis vs placebo for each measure (P<0.05 for all). Decline in SV and GLS was apparent from Month 6 in all patients; difference between tafamidis and placebo groups was apparent from Month 18. Decline in E/e’ (indicative of elevated LV filling pressures) was apparent from Month 6 with placebo but only minimally changed with tafamidis at each time point; difference between tafamidis and placebo was apparent from Month 6.
Conclusions: LV longitudinal strain and stroke volume are significant predictors of mortality in ATTR-CM patients. Treatment with tafamidis significantly reduced worsening progression of LV systolic (GLS, SV) and diastolic function (E/e’) over 30 months in ATTR-CM patients. These echocardiographic data provide additional insight into the efficacy of tafamidis.
Hypothesis: Treatment with tafamidis significantly reduces the worsening of echocardiographic variables including LV longitudinal strain and stroke volume in ATTR-CM patients.
Methods: In ATTR-ACT, ATTR-CM patients (variant or wild-type) were treated with tafamidis 80 mg (n=176) or placebo (n=177) for 30 months. Echocardiography was conducted at enrollment, and at Months 6, 18 and 30, using a standardized protocol and analyzed by an independent central laboratory. We compared changes in LV stroke volume (SV), global longitudinal strain (GLS) and mitral inflow E wave/annular diastolic early (e’) wave (E/e’) in patients treated with tafamidis 80 mg (the approved dose) vs placebo.
Results: Baseline mean (SD) SV (mL), GLS (%) and septal and lateral E/e’ were similar in the tafamidis and placebo groups (Table). Each measure worsened over the duration of the trial, as shown by least-squares (LS) mean (SE) change from baseline at Month 30 for each group (Table). This decline was more pronounced in placebo-treated patients, with a significant reduction in LS mean difference (95% CI) with tafamidis vs placebo for each measure (P<0.05 for all). Decline in SV and GLS was apparent from Month 6 in all patients; difference between tafamidis and placebo groups was apparent from Month 18. Decline in E/e’ (indicative of elevated LV filling pressures) was apparent from Month 6 with placebo but only minimally changed with tafamidis at each time point; difference between tafamidis and placebo was apparent from Month 6.
Conclusions: LV longitudinal strain and stroke volume are significant predictors of mortality in ATTR-CM patients. Treatment with tafamidis significantly reduced worsening progression of LV systolic (GLS, SV) and diastolic function (E/e’) over 30 months in ATTR-CM patients. These echocardiographic data provide additional insight into the efficacy of tafamidis.
| Tafamidis 80 mg (N=176) | Placebo (N=177) | |
| SV, baseline, mean (SD) | 45.5 (16.9) | 45.1 (16.9) |
| SV, change at Month 30, LS mean (SE) | –4.17 (1.30) | –11.19 (2.16) |
| SV, LS mean (95% CI) difference from placebo | 7.02 (2.55, 11.49); P=0.0021 | |
| GLS, baseline, mean (SD) | –9.3 (3.7) | –9.4 (3.6) |
| GLS, change at Month 30, LS mean (SE) | 1.13 (0.30) | 2.15 (0.34) |
| GLS, LS mean (95% CI) difference from placebo | –1.02 (–1.73, –0.31); P=0.0051 | |
| Septal E/e’, baseline, mean (SD) | 24.8 (11.0) | 24.2 (10.4) |
| Septal E/e’, change at Month 30, LS mean (SE) | 1.07 (0.97) | 4.18 (1.29) |
| Septal E/e’, LS mean (95% CI) difference from placebo | –3.11 (–5.50, –0.72); P=0.0109 | |
| Lateral E/e’, baseline, mean (SD) | 17.1 (7.7) | 17.2 (7.8) |
| Lateral E/e’, change at Month 30, LS mean (SE) | 0.04 (0.75) | 2.38 (0.61) |
| Lateral E/e’, LS mean (95% CI) difference from placebo | –2.35 (–4.01, –0.69); P=0.0057 |
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