Outcomes of transfemoral transcatheter aortic valve implantation (TAVI) and predictors of thirty-day major adverse cardiovascular events (MACE) and one-year mortality.

Objective: TAVI is more frequently used to treat aortic stenosis with the mandate to have a low as possible rate of adverse events. We present our 30-day outcomes and one-year mortality and examine the factors associated with them.

Methods: A prospective evaluation was performed of all patients who underwent transfemoral TAVI in Nicosia General Hospital from January 2015 until March 2020.

Complement depletion protects lupus-prone mice from ischemia-reperfusion-initiated organ injury.

Ischemia-reperfusion (IR) injury causes a vigorous immune response that is amplified by complement activation, leading to local and remote tissue damage. Using MRL/lpr mice, which are known to experience accelerated tissue damage after mesenteric IR injury, we sought to evaluate whether complement inhibition mitigates organ damage. We found that complement depletion with cobra venom factor protected mice from local and remote lung tissue damage.

Platelets, complement and tissue inflammation.

The release of immunoregulatory and inflammatory molecules following platelet activation has been invariably associated with the expression of tissue injury in several clinical conditions including trauma, organ transplantation, inflammatory bowel diseases and autoimmune diseases. We present a thorough review of the available information on the role of platelets and their interaction with complement cascade on the expression of tissue inflammation and organ damage. We propose that in autoimmune diseases and conditions associated with ischemia/reperfusion, platelets are decorated with complement, become activated and lodge tissues inappropriately to spread the inflammatory process.

The role of platelet factor 4 in local and remote tissue damage in a mouse model of mesenteric ischemia/reperfusion injury.

The robust inflammatory response that occurs during ischemia reperfusion (IR) injury recruits factors from both the innate and adaptive immune systems. However the contribution of platelets and their products such as Platelet Factor 4 (PF4; CXCL4), during the pathogenesis of IR injury has not been thoroughly investigated. We show that a deficiency in PF4 protects mice from local and remote tissue damage after 30 minutes of mesenteric ischemia and 3 hours of reperfusion in PF4-/- mice compared to control B6 mice.

Inhibition of Syk activity by R788 in platelets prevents remote lung tissue damage after mesenteric ischemia-reperfusion injury.

Tissue injury following ischemia-reperfusion (I/R) occurs as a consequence of actions of soluble factors and immune cells. Growing evidence supports a role for platelets in the manifestation of tissue damage following I/R. Spleen tyrosine kinase has been well documented to be important in lymphocyte activation and more recently in platelet activation.

Platelet-associated CD40/CD154 mediates remote tissue damage after mesenteric ischemia/reperfusion injury.

Several innate and adaptive immune cell types participate in ischemia/reperfusion induced tissue injury. Amongst them, platelets have received little attention as contributors in the process of tissue damage after ischemia reperfusion (I/R) injury. It is currently unknown whether platelets participate through the immunologically important molecules including, CD40 and when activated, CD154 (CD40L), in the pathogenesis of I/R injury.

Platelets orchestrate remote tissue damage after mesenteric ischemia-reperfusion.

Ischemia-reperfusion (I/R) injury is a leading cause of morbidity and mortality. A functional role for platelets in tissue damage after mesenteric I/R is largely unknown. The hypothesis that mesenteric I/R local and remote injury are platelet dependent was tested.

Immunopathogenesis of ischemia/reperfusion-associated tissue damage.

Ischemia/reperfusion (IR) instigates a complex array of inflammatory events which result in damage to the local tissue. IR-related organ damage occurs invariably in several clinical conditions including trauma, organ transplantation, autoimmune diseases and revascularization procedures. We critically review available pre-clinical experimental information on the role of immune response in the expression of tissue damage following IR.

Infections in patients with traumatic brain injury who undergo neurosurgery.

Objective: Several factors place victims with traumatic brain injury (TBI) at increased risk for infection. The purpose of this study was to delineate the frequency, types and risk factors for infection in patients with TBI who undergo neurosurgery.

Materials And Methods: Retrospective surveillance of infections in patients with TBI, aged  ≥18 years who underwent neurosurgery in University of Crete between 1999 and 2005.