This study describes the risk of thrombotic and hemorrhagic complications, both intraoperatively, and up to 1 month following visceral transplantation. Data from 48 adult visceral transplants performed between 2010 and 2017 were retrospectively studied [32 multivisceral (MVTx); 10 isolated intestine; six modified-MVTx]. Intraoperatively, intracardiac thrombosis (ICT)/pulmonary embolism (PE) occurred in 25%, 0% and 0% of MVTx, isolated intestine and modified MVTx, respectively, and was associated with 50% (4/8) mortality. Preoperative portal vein thrombosis (PVT) was a significant risk factor for ICT/PE (P = 0.0073). Thromboelastography resembling disseminated intravascular coagulation (DIC) (r time <4 mm combined with fibrinolysis or flat-line) was statistically associated with occurrence of ICT/PE (P < 0.0001). Compared to subgroup without ICT/PE, occurrence of ICT/PE was associated with an increased demand for all blood product components both overall, and each surgical stage. Hyperfibrinolysis (56%) was identified as cause of bleeding in MVTx. Incidence of postoperative thrombotic event at 1 month was 25%, 30% and 17% for MVTx, isolated intestine and modified MVTx, respectively. Incidence of postoperative bleeding complications at 1 month was 11%, 20% and 17% for MVTx, isolated intestine and modified MVTx. In conclusion, MVTx recipients with preoperative PVT are at an increased risk of developing intraoperative life-threatening ICT/PE events associated with DIC-like coagulopathy.
C ardiovascular complications are rampant after liver transplantation (LT). 1,2 Among this plethora of complications, systolic heart failure (HF) constitutes a distinct and important clinical entity in the first posttransplant year, with a reported incidence as high as 14% and associated mortality of 33%-45%. [3][4][5] Despite its devastating effect on the survival and quality of life of recipients, HF remains poorly understood. Regrettably, 2 decades of research into the diagnostic, therapeutic, and preventive strategies of post-LT myocardial dysfunction have provided scant data regarding its etiology, characteristics, and prognosis. 6,7 Thus, there remains a dire need to fill this knowledge gap so that the loss of both lives and grafts can be minimized.Systolic HF is also aptly referred to as HF with reduced ejection fraction (EF). The new universal definition of HF requires the left ventricular EF (LVEF) to be <50%, which includes reduced (<40%) and mildly reduced EF (41%-49%) categories. 8 Nonetheless, right ventricular (RV) dysfunction also plays a crucial role in the hemodynamics and prognosis of HF. 9 Although several etiologies and predictors of HF after LT has been proposed, 3,5,10 these reports mainly focused on early nonischemic systolic LV dysfunction and overlooked the roles of ischemic etiologies and RV in post-LT HF. [3][4][5]7,[10][11][12][13][14] An additional understanding of cardiac dysfunction after LT is
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