Effects of Left Ventricular Assist Device (LVAD) Placement on Myocardial Oxidative Stress Markers

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.