| HW (kg) | BW (kg) | HW/BW (%) | LV vol (ml) |
---|
Control (n = 13)
| 0.018 ± 0.001 | 4.36# ± 0.16 | 0.4 ± 0.013 | 0.24• ± 0.04 |
Cont
1
(n = 11)
| 0.018 ± 0.001 | 5.3# ± 0.14 | 0.35 ± 0.016 | 0.37• ± 0.06 |
Cont
20
(n = 10)
| 0.02 ± 0.001 | 5.65# ± 0.09 | 0.35 ± 0.008 | 0.37• ± 0.04 |
DCM
0
(n = 18)
| 0.017 ± 0.001 | 2.61 ± 0.23 | 0.64 ± 0.049 | 9.36 ± 2.0 |
DCM
1
(n = 13)
| 0.019 ± 0.001 | 3.07# ± 0.29 | 0.60 ± 0.05 | 6.28• ± 2.54 |
DCM
20
(n = 12)
| 0.019 ± 0.001 | 3.26# ± 0.29 | 0.58 ± 0.078 | 5.38• ± 1.95 |
- HW: heart weight
p ≤ 0.01 compared to non-treated DCM group;BW: body weight #p < 0.001 compared to non-treated DCM group;HW/BW ratio
p < 0.04 compared to non-treated DCM group; LV vol: atria were removed and the left ventricles were arrested in diastole and filled with saline • p ≤ 0.008 compared to non-treated DCM. Note the increase in body weight and heart weight with carvedilol treatment. This resulted in a significant improvement in HW/BW ratio despite having heavier hearts. The reduction in heart weight seen in the non-treated DCM group was associated with a higher incidence of apoptosis while the increased heart weight in hearts from DCM animals treated with carvedilol was associated with a lower incidence of apoptosis.