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As treatments for hematologic malignancies continue to advance, many patients with active disease and many more in remission will present for cardiac surgical procedures. Radiation and chemotherapeutic therapies for hematologic malignancies often result in cardiopulmonary injury. Evidence demonstrates that patients with hematologic malignancies undergoing cardiac surgery are at risk for perioperative adverse events, including bleeding, clotting, infection, and immunomodulation. However, short- and long-term mortality has been found to be acceptable. This review will distinguish the important points of characterizing, understanding, and managing hematologic malignancies in the cardiac surgical patient.

Background Inferior vena cava (IVC) obstruction is a rare complication of orthotopic heart transplantation (OHT) and is unique to bicaval surgical technique. The clinical significance, diagnosis, complications, and management of post-operative IVC anastomotic obstruction have not been adequately described. Case summary Two patients with end-stage heart failure presented for bicaval OHT. Post-operative course was complicated with shock refractory to fluid resuscitation and inotropic/vasopressor support. Obstruction at the IVC-right atrial (RA) anastomosis was diagnosed on transoesophageal echocardiography (TOE), prompting emergent reoperation. In both cases, a large donor Eustachian valve was found to be restricting flow across the IVC-RA anastomosis. Resection of the valve resulted in relief of obstruction across the anastomosis and subsequent improvement in haemodynamics and clinical outcome. Discussion Presumably rare, we present two cases of IVC obstruction post-bicaval OHT. Inferior vena cava obstruction is an under-recognized cause of refractory hypotension and shock in the post-operative setting. Prompt recognition using TOE is crucial for immediate surgical correction and prevention of multi-organ failure. Obstruction can be caused by a thickened Eustachian valve caught in the suture line at the IVC anastomosis, which would require surgical resection.

As perioperative bleeding continues to be a major source of morbidity and mortality in cardiac surgery, the search continues for an ideal hemostatic agent for use in this patient population. Transfusion of blood products has been associated both with increased costs and risks, such as infection, prolonged mechanical ventilation, increased length of stay, and decreased survival. Recombinant-activated factor VII (rFVIIa) first was approved for the US market in 1999 and since that time has been used in a variety of clinical settings. This review summarizes the existing literature pertaining to perioperative rFVIIa, in addition to society recommendations and current guidelines regarding its use in cardiac surgery.

Objectives Renal hypoperfusion is a common mechanism of cardiac surgery–related acute kidney injury (CS-AKI). However, the optimal amount of volume resuscitation to correct systemic hypoperfusion and prevent the postoperative development of CS-AKI has been a subject of debate. The goal of this study was to assess the association of volume responsiveness determined by stroke volume variation using the passive leg raise test (PLRT) at chest closure, with the development of CS-AKI according to the Kidney Disease Improving Global Outcomes criteria. Design Single-center, prospective observational study. Setting Tertiary hospital. Interventions None. Measurements and Main Results A total of 131 patients were studied from January 2015 until May 2017. All patients underwent cardiac surgery that required cardiopulmonary bypass. Volume responsiveness was assessed at chest closure using the PRLT. Stroke volume variation from the sitting to the recumbent positions was measured by transesophageal echocardiography. Fluid responsiveness was defined as an increase of >12% of stroke volume from sitting to recumbent positions. A total of 82 (68.3%) patients were fluid-responsive versus 38 (31.6%) who were fluid-unresponsive. CS-AKI occurred in 30% of patients. There was no difference in CS-AKI between fluid-responsive and fluid-nonresponsive groups. However, CS-AKI was associated independently with an increases in body mass index and preoperative diastolic blood pressure. CS-AKI also was associated with prolonged intensive care unit length of stay. Conclusion End-of-procedure volume responsiveness is not associated with a high risk for postoperative CS-AKI.

Introduction Bicaval anastomosis is the most adopted surgical technique for OHT. We present a case of IVC stenosis following bicaval OHT; a rare but potentially catastrophic complication. Case Report A 59-year-old woman with ischemic cardiomyopathy presented for OHT. Her intraoperative course was unremarkable. She was on stable doses of inotropes/vasopressors postoperatively. Four hours later, she became tachycardic and hypotensive requiring escalating vasopressor support. Swan-Ganz catheterization revealed low cardiac indices and filling pressures. She was resuscitated with 5 L of crystalloid and albumin without improvement in hypotension. She notably developed progressive abdominal distention corresponding with fluid resuscitation. TEE showed a small hyperdynamic LV and a small underfilled RV (Figure 1A). Flow acceleration was noted at the IVC-RA junction with velocity of 2 m/s (Figure 1B). The gradient across the junction was 16 mmHg (Figure 1C). A femoral CVC was placed and transduced to measure pressure in the IVC. The transduced gradient across the SVC and IVC was 18 mmHg; consistent with that found on TEE. She was emergently taken to the operating room. Evidently, the IVC anastomosis was obstructed by presence of a thickened eustachian valve. The valve was completely excised. The IVC orifice and anastomosis were confirmed to be widely patent and the anterior wall of the anastomosis was closed. TEE following resection showed resolution of IVC-RA pressure gradient (Figure 1D). Her hemodynamics subsequently showed hypervolemia for which aggressive diuresis was started. She was slowly weaned off vasopressor support. Her cardiac index improved to >2.0. She later had an uncomplicated course and overall recovery. Summary IVC stenosis is an underrecognized cause of hypotension following bicaval OHT. Prompt recognition using TEE is crucial for immediate repair and prevention of multi-organ failure. A thickened donor eustachian valve can result in IVC stenosis and may require surgical resection if hemodynamically significant.

Previous reports have demonstrated that increased levels of reactive oxygen species (ROS) and alterations in cell signaling characterize aging in the Fischer 344 X Brown Norway (FBN) rat aorta. Other work has suggested that increases in ROS may be related to vascular wall thickening and the development of hypertension. Paracetamol (acetaminophen) is a potent antioxidant that has been found to diminish free radicals in ischemia-reperfusion studies. However, it remains unclear whether chronic paracetamol administration influences signaling or ROS accumulation in the aging aorta. FBN rats (27 months old; n=8) were subjected to 6 months of treatment with a therapeutic dose of paracetamol (30 mg/kg/day) and compared to age-matched untreated FBN rat controls (n=8). Compared to measurements in the aortae of 6-month old animals, tunica media thickness, tissue superoxide levels, and protein oxidation levels were 38 ± 7%, 92 ± 31%, and 7 ± 2% higher in the aortae of 33-month control animals (p ≤0.05). Chronic paracetamol treatment decreased tunica media thickness and the amount of oxidized protein by 13 ± 4% and 30 ± 1%, respectively (p ≤0.05). This finding of diminished aortic thickening was associated with increased phosphorylation (activation) of the mitogen activated protein kinases and diminished levels of the anti-apoptotic protein Bcl-2. Taken together, these data suggest that chronic paracetamol treatment may decrease the deleterious effects of aging in the FBN rat aorta.

Abstract 1996 Poster Board I-1018 Background: Iron overload occurs under conditions such as primary (hereditary) hemochromatosis and secondary iron overload (hemosiderosis) and is associated with an increased risk of developing liver fibrosis, cirrhosis, and hepatocellular carcinoma. Deferasirox is a novel oral chelator with high iron-binding potency and selectivity. Here we investigate the ability of deferasirox to remove excessive hepatic iron and prevent or reverse iron induced hepatic injury. Methods: Adult male Mongolian Gerbils were randomly divided into three groups: control, iron overload, and iron overload + deferasirox treatment (n = 8 / group). Iron overload animals received iron dextran 100mg/kg i.p /5d for 10 wks while deferasirox was given 100mg/kg/d p.o for 1-,3-, or 9- months. Hepatic iron levels were determined by inductively coupled plasma atomic emission spectrometry and Prussian blue staining was performed to examine iron deposition in the corresponding tissues. Immunoblot and immunohistochemical analyses for markers of oxidative stress were employed to assess effects of deferasirox treatment on hepatic protein oxidation and superoxide levels. TUNEL assay was employed to examine the extent of hepatic apoptosis. Results: Compared to the non-treated iron overload group, deferasirox treatment reduced hepatic iron levels by 21.3%, 43.5%, and 47.4% after 1, 3, and 9 months of treatment, respectively (p Conclusions: These findings suggest that chronic deferasirox treatment may decrease iron-induced hepatic oxidative stress and apoptosis. Decrease in ROS accumulation in the liver may be the possible mechanism of this protective effect. Further studies are underway to delineate specific mechanisms. Disclosures: No relevant conflicts of interest to declare.