Effect of mechanical assist devices for ischemic myocardial damage-cardiomyocyte apoptosis and TNFalpha-.

It has been demonstrated that tumor necrosis factor-alpha (TNFalpha) induces cardiomyocyte apoptosis. Apoptosis has been elucidated as playing an important role as one of the mechanisms of myocardial disorders. However, it is not known whether mechanical support with a left ventricular assist device (LVAD) and percutaneous cardiopulmonary support (PCPS) influence cardiomyocyte apoptosis. The aim of this study was to examine cardiomyocyte apoptosis and TNFalpha in an experimental acute myocardial infarction model after mechanical support in pigs.The animals were divided into three groups: the CONT group, LVAD group, and PCPS group. The CONT group was left unassisted after ligation, while the LVAD group was assisted by LVAD and the PCPS group by venoarterial bypass. Acute myocardial infarction was induced by ligation of the left anterior descending coronary artery. As hemodynamic data, aortic pressure (AoP), end-systolic pressure volume relationship (ESPVR), and pressure volume area (PVA) were calculated. The serum TNFalpha level was measured and terminal deoxynucleotidyl transferase-mediated dUTP in situ nick end labeling (TUNEL) was performed in sections.ESPVR in the LVAD group and PCPS group was improved (p<0.05 versus the CONT group). Cardiomyocyte apoptosis was restrained by mechanical support (p<0.05 versus the CONT group). TNFalpha in the LVAD group showed a low value (p<0.05 versus the CONT group). These results were statistically significant.This study suggests that VADs participate in proinflammatory cytokines and depression of apoptosis, and are effective in recovery from myocardial injury.