Induction Immunosuppression with Anti-CD25 Monoclonal Antibody (Basiliximab) Allows Delayed Initiation and Uptitration of Calcineurin Inhibitor Post Cardiac Transplant

Induction Immunosuppression with Anti-CD25 Monoclonal Antibody (Basiliximab) Allows Delayed Initiation and Uptitration of Calcineurin Inhibitor Post Cardiac Transplant

S74 Heart, Lung and Circulation 2010;19S:S1–S268 Abstracts ABSTRACTS 173 174 Induction Immunosuppression with Anti-CD25 Monoclonal Antibody (Bas...

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S74

Heart, Lung and Circulation 2010;19S:S1–S268

Abstracts

ABSTRACTS

173

174

Induction Immunosuppression with Anti-CD25 Monoclonal Antibody (Basiliximab) Allows Delayed Initiation and Uptitration of Calcineurin Inhibitor Post Cardiac Transplant

Invasive Assessment of Changes in Continuous Flow Left Ventricular Assist Device Function Due to Exercise and Increased Pump Speed

G.

Grima ∗ ,

J.

Gan ∗ ,

G. Javorsky, M. Brown

Advanced Heart Failure and Transplant Unit, The Prince Charles Hospital, Australia Background: The role of anti-CD monoclonal antibodies in induction immunosuppression for cardiac transplantation remains unclear. This study sought to determine if basiliximab allows delayed commencement, slower uptitration and reduced nephrotoxicity or allograft rejection with cyclosporin. Methods: We performed retrospective analysis of cardiac transplant patients on cyclosporin, mycophenolate mofetil, and corticosteroids and compared the results depending on whether they received basiliximab post transplant. Data was collected for 21 days post transplant. Exclusion criteria: <18 yrs old, alternative immunosuppression, multi-organ transplant. Results: 39 patients studied (basiliximab: 22; nonbasiliximab: 17). More patients in the non-basiliximab group were ex-smokers (71% vs. 32%, p = 0.025) and type 2 diabetics (35% vs. 4.5%, p = 0.03) but had similar demographics for stroke, hypertension, mechanical support and indication for transplant. No patients received OKT3 or antithymocyte globulin. Time to cyclosporin initiation (mean ± 1SD) was 0.12 ± 0.35 days for non-basiliximab versus 1.50 ± 2.54 days for basiliximab (p = 0.003). Therapeutic cyclosporin levels (250–300 mg/L) were reached later in the basiliximab arm (11.1 ± 3.7 days) versus (17.1 ± 7.4 days) (p = 0.003). There was a trend to decreased Grade 3 rejection on day 14 in the basiliximab arm (p = 0.09). There were no significant differences in average creatinine clearance between the groups within the initial 21 days (p = 0.71). Conclusion: Post cardiac transplant, basiliximab allowed delayed initiation and time to therapeutic trough levels of cyclosporin with a trend to decreased severe rejection on day 14. Nephrotoxicity was not reduced. A larger study group is needed to evaluate basiliximab’s effect on rejection rate and renal function. doi:10.1016/j.hlc.2010.06.840

C. Hayward 1,∗ , R. Salamonsen 2 , A. Keogh 1 , P. 1 1 1 Macdonald , E. Kotlyar , R. Prichard , R. Walker 1 , J. Woodard 3 , P. Jansz 1 , P. Spratt 1 1 St.

Vincent’s Hospital, Sydney, Australia Alfred Hospital, Melbourne, Australia 3 John Woodard Associates, Sydney, Australia 2 The

Background: Pump flows from third-generation centrifugal LVAD (left ventricular assist devices) increase with exercise and faster pump speed. We examined haemodynamic differences of these interventions in patients supported by VentrAssist LVAD. Methods: Eight patients (39 ± 10 years, mean ± SD) underwent echocardiography, right heart catheterisation, mixed venous oxygen saturation (SVO2), heart rate (HR) and mean arterial pressure (MAP) monitoring. Pump speed was increased from baseline to maximum 2400 rpm every 5 min. After return of pump speed to baseline, patients underwent 20 min supine bicycle exercise. Results: Pump flow and cardiac output (CO) were closely related (r2 = 0.84, p < 0.001). Increasing the pump speed from 2075 ± 71 to 2333 ± 58 rpm increased pump flow (5.4 ± 1.0 to 6.2 ± 1.0 L/min), SVO2 (67 ± 6 to 73 ± 5%), power (4.9 ± 0.5 to 6.5 ± 0.9 W) and decreased PCWP (15 ± 7 to 9 ± 6 mm Hg, p < 0.002 for all). LV dimensions, MAP and HR did not change. Exercise also increased pump flow from 5.5 ± 1.0 to 6.6 ± 0.7 L/min but increased PCWP (16 ± 7 to 25 ± 6 mm Hg), HR (91 ± 11 to 125 ± 11 per min) and MAP (91 ± 16 to 98 ± 16 mm Hg). SVO2 decreased from 69 ± 7 to 32 ± 11% (p < 0.001 for all). Lactate increased with exercise (1.4 ± 0.4 to 3.2 ± 0.76 mmol/L, p = 0.001) but BNP did not change. Conclusions: LVAD flow was increased by faster pump speed and exercise to a similar extent. Because exercise elevated both preload and after load there was little change in intraventricular-aortic pressure gradient, and increased flow may reflect differential pre vs. after load pump sensitivity. Increased pressures and oxygen extraction may contribute to exercise intolerance in LVAD patients. Faster pump speeds need to be weighed against increased power consumption and assessed in the context of right ventricular function. doi:10.1016/j.hlc.2010.06.841