Purpose: The primary purpose of this study was to examine the changes in myocardial oxidative stress during the support of a left ventricular assist device (LVAD). Methods: Myocardial tissue was collected from the lower left ventricle of 15 adult subjects with class IV heart failure (HF) during LVAD placement (n=9) or LVAD removal (Post-LVAD; n=6). Each tissue sample was separated into cytosolic and myofibrillar subfractions and analysed for protein content and carbonylation. Results: The myofibrillar proteins in the HF subjects had a significantly lower (p= 0.008) level of protein carbonylation when compared to the myofibrillar proteins in Post-LVAD patients at 1.630 ± 0.277 and 3.075 ± 0.413 optical density, respectively. The level of protein carbonylation in myosin and actin were lower in HF (myosin: 1406.22 ± 218.45, actin: 436 ± 79.72 optical density) subjects compared to Post-LVAD (myosin: 2280.5 ± 441.26, actin: 804.67 ± 155.71 optical density) subjects (p= 0.035 and p= 0.018, respectively). However, once the extent of carbonylation in the myosin and actin bands were normalised to the amount of protein content, all significant difference was lost (HF moysin: 1823.89 ± 413.42, Post-LVAD myosin: 1330.33 ± 297.10 optical density, p= 0.199 and HF actin: 3755.78 ± 349.59, Post-LVAD actin: 4402.83 ± 666.51 optical density, p= 0.182). There was no significant difference in the cytosolic subfractions before or after normalisation of protein content. Conclusion: Carbonylation is elevated in the myocardium of HF and Post-LVAD subjects and it appears that LVAD support does not affect the level of myocardial oxidative stress.
- Heart failure
- Left ventricular assist device
- Oxidative stress