Challenges in Long-Term Mechanical Circulatory Support and Biological Replacement of the Failing Heart

Solid organ transplantation and gut microbiota: a review of the potential immunomodulatory properties of short-chain fatty acids in graft maintenance

“…Hyperacute rejection occurs in the first minutes to hours after transplantation and is due to a preformed antibodies that react with alloantigens (e.g., ABO blood type antigens, major histocompatibility complex -MHC-antigens) present on the surface of grafted cells leading to endothelial damage, platelet accumulation and thrombosis in capillaries (Solez et al, 1993). Indeed, pre-existing donor-specific antibodies (DSA) in the recipient induce complement system activation and massive inflammatory response with recruitment and activation of polymorphonuclear neutrophils leading to thrombosis, ischemia and graft necrosis (Lala et al, 2014) (Figure 1). Nowadays, this type of graft rejection is very rare due to prior investigations of tissue compatibility between the donor and the recipient (Tittelbach-Helmrich et al, 2014).…”

The Registry Report of Heart Transplantation in Japan (1999–2014)

“…10 Although the revised Organ Transplant Law cleared the way for organ harvesting from child donors in Japan, the number of pediatric cases is still low. A heart transplant was performed on a pediatric patient on BTT with an extracorporeal LVAD in 2014.…”

Vulnerable Brain and Ventricular Assist Devices

“…1 Despite generational shifts in engineering of such devices, from large pulsatile mechanisms to smaller continuous flow devices, the complications related to neurological adverse effects have not improved substantially. 2,3 Hemorrhagic and ischemic strokes continue to occur, with a frequency greater than that observed in patients with advanced heart failure.…”

“…Thus, it is clear that the brain remains a highly vulnerable organ even as the heart is well supported with LVAS. 15 The causes of strokes with newer LVADs are unclear and could relate to (1) clots that pass through the device (as with atrial fibrillation in patients with a device or with clots that form within the device or in the proximate ventricle), (2) vascular changes as a result of nonpulsatile flow (we know that reduced pulse pressure with the newer devices increases vascular fragility, so even lower levels of blood pressure can cause vascular loss of integrity), and (3) rheological causes (new devices create an acquired von Willebrand syndrome and can predispose to bleeding). 16,17 Debilitating stroke is a disastrous situation that diminishes the gains from application of LVAS therapy and occurs with enough frequency and is intertwined with other complications of LVAS, that it is a major concern, especially in older patients who are receiving these devices as lifetime therapy without the option of a transplant.…”