Radiofrequency ablation of supraventricular arrhythmias after orthotopic heart transplantation: Long-term follow-up of a single-center experience.

Background: Supraventricular arrhythmias (SVAs), commonly managed with radiofrequency ablation (RFA), may occur after orthotopic heart transplantation (OHT).

Methods: We retrospectively assessed 514 consecutive patients (pts.) undergoing OHT between January 1990 and July 2016 in a single-center.

Short-term mechanical circulatory support devices as bridge to heart transplantation: A prospective single-center experience in Argentina.

Background: Patients with cardiogenic shock may require hemodynamic stabilization with short-term mechanical circulatory support devices (ST-MCS) such as extracorporeal membrane oxygenation (ECMO) and centrifugal pump (CP) as bridge to transplantion (BTT). This study aimed to describe ECMO and CP during BTT and after heart transplant.

Methods: A cohort of patients on ECMO or CP as BTT between April 2006 and April 2018 in a single hospital.

Involvement of PI3K/Akt and p38 MAPK in the induction of COX-2 expression by bacterial lipopolysaccharide in murine adrenocortical cells.

Previous studies from our laboratory demonstrated the involvement of COX-2 in the stimulation of steroid production by LPS in murine adrenocortical Y1 cells, as well as in the adrenal cortex of male Wistar rats. In this paper we analyzed signaling pathways involved in the induction of this key regulatory enzyme in adrenocortical cells and demonstrated that LPS triggers an increase in COX-2 mRNA levels by mechanisms involving the stimulation of reactive oxygen species (ROS) generation and the activation of p38 MAPK and Akt, in addition to the previously demonstrated increase in NFκB activity. In this sense we showed that: (1) inhibition of p38 MAPK or PI3K/Akt (pharmacological or molecular) prevented the increase in COX-2 protein levels by LPS, (2) LPS induced p38 MAPK and Akt phosphorylation, (3) antioxidant treatment blocked the effect of LPS on p38 MAPK phosphorylation and in COX-2 protein levels, (4) PI3K inhibition with LY294002 prevented p38 MAPK phosphorylation and, (5) the activity of an NFκB reporter was decreased by p38 MAPK or PI3K inhibition.