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This article, published in the journal Thoracic & Cardiovascular Surgeon, explores the predictive value of the preoperative right-to-left ventricular filling pressures (CVP/PCWP) ratio on the development of right-sided heart failure (RSHF) after left ventricular assist device (LVAD) implantation. The study analyzed data from 134 patients who received a continuous flow LVAD with a centrifugal pump, with 40 patients initially evaluated using a right-sided heart catheter. The results showed that a high CVP/PCWP ratio was associated with a higher incidence of RSHF after LVAD implantation. The study suggests that monitoring the CVP/PCWP ratio could help predict the risk of RSHF and guide treatment decisions. [Extracted from the article]

Ischemia-induced apoptosis of endothelial cells may contribute to tissue injury, organ failure, and transplantation rejection. However, little is known about survival mechanisms capable to counteract endothelial apoptosis. This study investigated the potential role of an endogenous anti-apoptotic response elicited by transient hypoxia, capable to avert ongoing apoptosis in endothelial cells. Experiments were carried out in three different types of cultured endothelial cells (human umbilical vein, pig aorta, and from rat coronary microvasculature). As a pro-apoptotic challenge endothelial cells were cultured in serum-free medium and subjected to hypoxia for 2 h. We found that transient hypoxia reduced caspase 3 activation within 1 h of hypoxia. Accordingly, the number of apoptotic cells was reduced after 24 h of reoxygenation. This was true for all three cell types analyzed. Analysis of Akt and mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathways revealed that hypoxia induced a transient activation of ERK 2 but not of Akt. ERK 2 phosphorylation preceded the phosphorylation of pro-apoptotic molecule Bad at Ser112, an inhibitory phosphorylation site specific for ERK. The protective effects of hypoxia regarding Bad phosphorylation, caspase 3 activation, and apoptosis were abolished by MEK 1/2 inhibitors, PD98059 or UO126, as well as by antisense oligonucleotides directed against ERK 1/2. Furthermore, inhibition of this pathway inhibited hypoxia-induced increase in mitochondrial membrane potential. The present study demonstrates that transient hypoxia induces a novel survival mechanism that protects endothelial cells against apoptosis. This endogenous process involves MEK/ERK-mediated inhibition of the pro-apoptotic molecule Bad and caspase 3. anti-apoptosis; Bad; extracellular signal-regulated kinases; phosphoinositide 3-kinase/Akt doi: 10.1152/ajpcell.00333.2009.