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Implantable Cardioverter Defibrillator Malfunction Following LVAD Implantation
The 17th Annual Scientific Meeting enrolled if they had a change in clinical status or for pre-transplant screening. The primary endpoint of device malfunction was defined as (1) suspected pump thrombosis with clinical evidence of hemolysis and HF or death; (2) confirmed thrombosis at the time of device exchange. Comprehensive echocardiographic evaluation was performed at baseline pump speed, and at each 1,000 rpm interval from the lowest setting of 8,000 rpm to the highest setting of 11,000 rpm. ANOVA was performed to determine differences between 8-11,000 rpm and ROC curves were constructed for optimal cut-off for the delta change. A stepwise logistic regression analysis was used to construct the prediction model (LVAD score), p-values ! 0.05 were considered significant. Results: Of 46 patients who underwent echocardiography-guided pump speed testing, 8 met the criteria for device malfunction. The diagnostic model included changes in LV end-diastolic diameter (LVEDd) (!0.6 cm), aortic valve opening duration (AVOD) (!86 ms) and deceleration time (DT) of mitral inflow (!73 ms). The LV.A.D. score, calculated as the sum of the points for each of these echo variables, provides 100% sensitivity and 95% specificity for diagnosing pump malfunction if at least 2 of 3 parameters are met. Conclusions: The LV.A.D. score, composed of change in LVEDd, AVOD, DT of mitral inflow between the lowest and highest pump speed settings during echocardiography-guided pump speed change testing, is highly accurate in diagnosing device malfunction in the setting of pump thrombosis among patients supported with CF- LVADs. Table. Proposed LVAD Pump Thrombosis Score to detect device malfunction Echocardiographic parameter D LVEDd ! 0.6 cm D AVOD !86 ms D Mitral DT ! 73 ms
Point 1 1 1
D 5 difference from lowest to highest pump speed
175 High Dose Aspirin Is Associated with Increased Risk of Gastrointestinal Bleeding in Patients with Left Ventricular Assist Devices David S. Raymer, Michael E. Nassif, Timothy J. Fendler, Eric Novak, Shane J. LaRue, Gregory A. Ewald; Washington University, St. Louis, MO
Introduction: Aspirin (ASA) is recommended to prevent thrombosis in patients with continuous-flow left ventricular assist devices (LVADs). Gastrointestinal bleeding (GIB) is a common complication in these patients, occurring in approximately a third of patients with continuous-flow devices. Studies to determine optimal dosing of ASA therapy have not been performed. Methods: We performed a retrospective cohort study of patients who survived their index admission for continuous-flow LVAD implantation. We identified 237 patients that received either a Heart Mate II (n 5 219) or Heartware HVAD (n 5 18) LVAD between 1/2005 and 1/2013. Patients receiving ASA 81 mg were compared to those receiving ASA 325 mg. The primary outcome was GIB at one year. Group differences were balanced with propensity score adjusted weights. Hypothesis: ASA 325 mg is associated with increased GIB compared with ASA 81 mg in patients with LVADs. Results: The majority of patients in both groups were male (81%) and categorized with a median INTERMACS profile of 2 at the time of LVAD implant. There were no significant differences in either cohort with respect to demographics (age, race, BMI) baseline laboratories (HgB, CrCl, INR), or past medical history (CAD, A-fib, Smoking). All patients received either ASA 81 mg (n 5 148), or 325 (n 5 89) during their index hospitalization and were discharged on the same dose. There were 71 patients with GIB events: 31 out of 89 (34.8%) in ASA 325 mg vs. 40 out of 148 (27.1%) in ASA 81 mg, p 5 0.24. A significant difference was found between KM curves, p 5 0.004 (see figure). At 1 year, the event-free rates were 53.9% in ASA 325 mg vs. 72.4% in ASA 81 mg (p 5 0.025). After inverse propensity score weighted adjustment, the ASA 325 mg
HFSA
S61
was associated with significantly higher rates of GIBs (HR 1.642, 95% CI 1.163-2.318; p 5 0.005). There was no difference in the rates of pump thrombosis or hemolysis between the ASA 325 mg and ASA 81 mg groups (OR 0.843, 95% CI 0.493-1.441; p 5 0.53. Discussion: In this sample of patients supported with LVADs, ASA 81 mg was associated with a lower incidence of GIB during the first year than ASA 325 mg, without a statistically significant difference in the incidence of LVAD pump thrombosis. These results suggest ASA 81 mg may decrease the incidence of GIB, while still affording anti-thrombotic protection.
176 Role of C4d Staining in Endomyocardial Biopsies after Cardiac Transplantation Geetha Bhat, Tasneem Siddiqua, Ashim Aggarwal, Joseph Pyle, John Hamilton; Advocate Christ Medical Center, Oak Lawn, IL Introduction: Cardiac transplant antibody mediated rejection is a challenging diagnostic and therapeutic problem. C4d staining of interstitial capillaries on endomyocardial biopsies (EMB) has been associated with antibody mediated rejection (AMR) in cardiac allografts. The role of routine C4d staining by immunohistochemistry or immunofluorescence in all endomyocardial biopsies after transplantation is unclear. The goal of our study was to determine clinical significance of C4d capillary staining on serial biopsies in cardiac transplant recipients. Methods: Preand post-transplant donor specific antibodies (DSA) by Luminex assay, pre-transplant panel reactive antibodies (PRA), flow cytometry crossmatch, echocardiographic/hemodynamic variables, data on acute cellular rejection (ACR) and antibody mediated rejection (AMR) episodes on 36 patients was retrospectively reviewed. Peak HLA-DSA Luminex mean fluorescence intensity (MFI) pre- and posttransplant was analyzed. C4d was considered positive if diffuse capillary staining was present by immunoperoxidase or immunofluorescence. C4d was tested in conjunction with routine hematoxylin and eosin staining of all endomyocardial biopsies (EMB) for diagnosis of acute cellular rejection. Clinical suspicion of AMR was based on graft dysfunction by echo and abnormal hemodynamics. Results: 36 consecutive cardiac transplant recipients underwent 583 endomyocardial biopsies (EMB) over one year. Group I (n58) [50% male, 50% Caucasian, mean age 45.6 6 19.9 years] with C4d positive biopsies at median of 65 days (20-250) post-transplant, was compared to Group II with C4d negative biopsies (Table). ACR was present in a significantly higher number of patients in Group I compared to Group II (p 5 0.003). Clinical suspicion of AMR was also significantly higher in Group I. There was a trend toward a greater number of patients with post-transplant DSA in Group I. Conclusion: More C4d positive patients (Group I) had post-transplant DSA and clinical suggestion of AMR supporting C4d association with AMR. In addition, our study showed that ACR was significantly higher in C4d positive patients. C4d in association with acute cellular rejection, therefore, may be a biomarker for early or subclinical form of antibody mediated rejection. Routine use of C4d staining in a larger group of cardiac transplant patients may provide a biomarker for prospectively evaluating prognosis and clinical outcomes.
Characteristic Age: (years) Male (%) Caucasian (%) Number of EMB per patient Patients bridged with Left Ventricular Assist Device (%) Pre-Transplant DSA (DSA with MFI O2000) Post-Transplant DSA (DSA with MFI O2000) Pre-Transplant PRA positive patients (PRA Level O 10) Mean PRA level Acute Cellular Rejection [$1R] Clinical suspicion of AMR Mortality
Group I (C4d+) N5 8
Group II (C4d-) N5 28
p Value
45.63 6 19.92 4 (50) 4 (50) 17.13 6 3.79
52.82 6 12.34 20 (71.4) 14 (50) 15.93 6 5.55
0.35 0.39 0.48 0.49
4 (50)
16 (57.1)
0.51
3 (37.5%)
10 (35.7%)
0.61
5 (62.5%)
8(28.6%)
0.09
3 (37.5%)
8 (28.6%)
0.67
21.25 6 31.59 5 (62.5%) 3 (37.5%) 2 (25%)
6.57 6 10.20 2 (7.1%) 1 (3.6%) 6 (21.4%)
0.23 0.003 0.02 0.83
177 Implantable Cardioverter Defibrillator Malfunction Following LVAD Implantation Yuhning L. Hu1, Vigneshwar Kasirajan2, Daniel G. Tang2, Keyur B. Shah3, Kenneth A. Ellenbogen4, Jordana Kron4; 1Virginia Commonwealth University, Richmond, VA; 2Virginia Commonwealth University, Richmond, VA; 3Virginia Commonwealth University, Richmond, VA; 4Virginia Commonwealth University, Richmond, VA
Introduction: Implantable cardioverter defibrillator (ICD) lead malfunction has been reported after left ventricular assist device (LVAD) implantation, however
S62 Journal of Cardiac Failure Vol. 19 No. 8S August 2013 the incidence and mechanism are not known. Hypothesis: The mechanism of RV lead malfunction following LVAD implantation may be related to changes in LV and RV geometry, rather than decrease in LV mass. Methods: In this prospective single center study, we collected ICD lead data before, during and after LVAD implantation, including 12 time points during implantation. Results: Data were collected prospectively on 29 patients, including 24 patients undergoing LVAD implantation (ICD implanted 35634.9 months earlier) and 5 control patients who had LVAD implanted initially followed by ICD implantation. Of the 24 LVAD patients, 17 were male, 15 had coronary artery disease, 15 had LVAD implanted as destination therapy, and mean age was 57.6613 years. Fifty-four leads were tested before, during, 1 week and 3 months after LVAD implantation, including 18 right atrial, 24 right ventricular (RV), and 12 left ventricular (LV) leads. In 16 patients, ICD leads were tested at 12 intraoperative steps. RV sensing was O50% decreased from baseline in 6 patients (25%) immediately post-op, with RV sensing improving at 1 week in 3 patients (50%). In 2 patients (8%) who also had decreased sensing, RV pacing threshold was O50% elevated from baseline immediately post-op (n51) and at 1 week (n51). One RV pacing threshold returned to baseline at 3 months. Of the 4 patients with significant decreases in RV sensing in whom lead function was tested at serial time points during VAD implantation, an RV sensing decrease was not detected until immediately following weaning off cardiopulmonary bypass. One RV lead was turned off and one was replaced due to non-capture. Time from lead implant to LVAD was 77.6657.9 months in the patients with decreased RV lead sensing (n56) vs. 33.3643 months in patients with no decreased RV sensing (n518). Post-operatively, 14 (58%) patients had ventricular arrhythmias, new onset in 8 (33%); and 15 (63%) had atrial arrhythmias, new onset in 7 (29%). On ECG, sensed QRS width decreased after LVAD (126.5636.7 vs. 100635.5ms). Of the 5 control patients, none had O50% decreased RV sensing and 1 had O50% elevation in pacing threshold from the day of implant to 1 year post-implant. Of 29 patients, 6 died (4.966.8 months) and 1 underwent cardiac transplant (3 months). Conclusions: ICD lead malfunction can occur following LVAD implantation, but may improve over time. Intraoperative RV sensing problems were not detected until weaning of cardiopulmonary bypass, suggesting the mechanism of RV lead malfunction may be related to changes in LV and RV geometry from LVAD implantation. Ventricular arrhythmias are common in the LVAD population, even in patients who did not have them pre-operatively.
178 Telemetry Capable, Implantable Pulsatile Controller (IPC) for Left Ventricular Assist Devices (LVAD) Sam Siavash Asgari, Pramod Bonde; Yale School of Medicine, New Haven, CT Introduction: Recent generations of continuous-flow LVADs require a transcutaneous driveline to conduct power, controller algorithms, and data between the pump and extracorporeal controller unit. Driveline associated infections are a common complication which impart significant negative impact on quality of life and increase medical cost of LVAD treatment. Furthermore, continuous flow circulation has been implicated in gastrointestinal bleeding, limited cardiac unloading, and aortic incompetence. Hypothesis: We have earlier demonstrated the feasibility of wireless energy transfer to power an LVAD controller. In the current investigation, we present an ultra-compact implantable controller (IPC) to entirely free patients from the LVAD driveline and considerably reduce the extracorporeal hardware and weight. Since physiological flow, especially in the patient category of destination therapy, is of significance, we have embedded a pulsatile algorithm in the IPC. Methods: The controller has been designed to drive an LVAD with required safety and back up measures. The IPC embraces a reliable wireless algorithm to communicate to an external platform based Graphical User Interface (GUI) embedded in an iPhone, iPad, or a computer. The controller couples to a receiver coil to wirelessly obtain power. Furthermore, we have employed signal processing methods to analyze an ECG signal and modulate the pump speed during systole and diastole for co/counter-pulsation or fixed mode operation. When used with ECG gating, the IPC allows on-demand customization of operation with instantaneous flow and RPM changes, resulting in a pulsatile flow with adjustable pulse pressure. Telemetry has also been achieved by an embedded antenna. Initially, the controller was
Figure 1. A&B show the HVAD and IPC; C&D show the smart platform; E&F show the in -vivo data; G&H show the in vitro results; I&J show high speed during systole and Diastole. respectively (ECG Gated).
tested with an HVAD and HMII in an in-vitro setup to test its reliability. Ultimately, the controller has been implanted in two animals to wirelessly drive an HVAD in continuous and pulsatile modes. Results: Our tests results prove the system to be remarkably safe, accurate and efficient. The IPC operated continuously for two weeks in a mock circulation loop and 3 hours in each animal experiment. We have demonstrated the versatility of a controller that can create physiological flow. In terms of efficiency, IPC consumes less power to obtain the same pump speed and flow rate as compared with the HVAD controller. Conclusions: The combination of wireless powering, communicating with a user-friendly GUI and a very small footprint makes this an ideal totally implantable LVAD system. Patients are therefore liberated from the risk of driveline infection and are able to shower, swim, and perform physical activities with improved hygiene and mobility.
179 A Multi-Modailty Approach to Antibody Mediated Rejection Steven Geier1, Hemant Parekh1, Yanhau Li1, Rene Alvarez2, Eman Hamad2, Emily Tsai2, James Fitzpatrick2, Lazaros Nikolaidis2, Mustafa Ahmed2; 1Temple University School of Medicine, Philadelphia, PA; 2Temple University School of Medicine, Philadelphia, PA Introduction: Antibody mediated rejection remains a difficult problem in orthotopic heart transplant recipients. Treatment with solitary therapeutic targets often result in incomplete success. We describe our experience using a multi-targeted therapeutic approach. Case: A 41 year-old female who underwent orthotopic heart transplantation in 2007 presented with signs and symptoms of heart failure. She was treated with high dose corticosteroids while awaiting results of endomyocardial biopsy, which reveled no cellular rejection, but C4d and C1q evidence for antibody mediated rejection. Multiple donor specific antibodies were identified. She was initially treated with plasmapharesis and rituximab. This resulted in clinical improvement, but no change in her serologic or immunohistochemical markers of AMR. Several weeks later, she presented with symptomatic bradycardia and hypotension, requiring dobutamine infusion for hemodynamic stability. Endomyocardial biopsy once again was C4d and C1q positive, and serum was noted to have multiple DSAs with elevated MFIs. She therefore was treated with a combination of plasmapharesis, IVIG, and subcutaneous bortezomib [Figure 1] which resulted in clinical stabilization and improvement in donor specific antibodies [Figure 2]. Conclusions: A combination, multi-targeted approach to antibody mediated rejection may prove to be more effective in regards to clinical improvement, and resolution of serologic and immunohistochemical markers of rejection. Additional study to define an optimal approach is required.
Point 1 1 1
D 5 difference from lowest to highest pump speed
175 High Dose Aspirin Is Associated with Increased Risk of Gastrointestinal Bleeding in Patients with Left Ventricular Assist Devices David S. Raymer, Michael E. Nassif, Timothy J. Fendler, Eric Novak, Shane J. LaRue, Gregory A. Ewald; Washington University, St. Louis, MO
Introduction: Aspirin (ASA) is recommended to prevent thrombosis in patients with continuous-flow left ventricular assist devices (LVADs). Gastrointestinal bleeding (GIB) is a common complication in these patients, occurring in approximately a third of patients with continuous-flow devices. Studies to determine optimal dosing of ASA therapy have not been performed. Methods: We performed a retrospective cohort study of patients who survived their index admission for continuous-flow LVAD implantation. We identified 237 patients that received either a Heart Mate II (n 5 219) or Heartware HVAD (n 5 18) LVAD between 1/2005 and 1/2013. Patients receiving ASA 81 mg were compared to those receiving ASA 325 mg. The primary outcome was GIB at one year. Group differences were balanced with propensity score adjusted weights. Hypothesis: ASA 325 mg is associated with increased GIB compared with ASA 81 mg in patients with LVADs. Results: The majority of patients in both groups were male (81%) and categorized with a median INTERMACS profile of 2 at the time of LVAD implant. There were no significant differences in either cohort with respect to demographics (age, race, BMI) baseline laboratories (HgB, CrCl, INR), or past medical history (CAD, A-fib, Smoking). All patients received either ASA 81 mg (n 5 148), or 325 (n 5 89) during their index hospitalization and were discharged on the same dose. There were 71 patients with GIB events: 31 out of 89 (34.8%) in ASA 325 mg vs. 40 out of 148 (27.1%) in ASA 81 mg, p 5 0.24. A significant difference was found between KM curves, p 5 0.004 (see figure). At 1 year, the event-free rates were 53.9% in ASA 325 mg vs. 72.4% in ASA 81 mg (p 5 0.025). After inverse propensity score weighted adjustment, the ASA 325 mg
HFSA
S61
was associated with significantly higher rates of GIBs (HR 1.642, 95% CI 1.163-2.318; p 5 0.005). There was no difference in the rates of pump thrombosis or hemolysis between the ASA 325 mg and ASA 81 mg groups (OR 0.843, 95% CI 0.493-1.441; p 5 0.53. Discussion: In this sample of patients supported with LVADs, ASA 81 mg was associated with a lower incidence of GIB during the first year than ASA 325 mg, without a statistically significant difference in the incidence of LVAD pump thrombosis. These results suggest ASA 81 mg may decrease the incidence of GIB, while still affording anti-thrombotic protection.
176 Role of C4d Staining in Endomyocardial Biopsies after Cardiac Transplantation Geetha Bhat, Tasneem Siddiqua, Ashim Aggarwal, Joseph Pyle, John Hamilton; Advocate Christ Medical Center, Oak Lawn, IL Introduction: Cardiac transplant antibody mediated rejection is a challenging diagnostic and therapeutic problem. C4d staining of interstitial capillaries on endomyocardial biopsies (EMB) has been associated with antibody mediated rejection (AMR) in cardiac allografts. The role of routine C4d staining by immunohistochemistry or immunofluorescence in all endomyocardial biopsies after transplantation is unclear. The goal of our study was to determine clinical significance of C4d capillary staining on serial biopsies in cardiac transplant recipients. Methods: Preand post-transplant donor specific antibodies (DSA) by Luminex assay, pre-transplant panel reactive antibodies (PRA), flow cytometry crossmatch, echocardiographic/hemodynamic variables, data on acute cellular rejection (ACR) and antibody mediated rejection (AMR) episodes on 36 patients was retrospectively reviewed. Peak HLA-DSA Luminex mean fluorescence intensity (MFI) pre- and posttransplant was analyzed. C4d was considered positive if diffuse capillary staining was present by immunoperoxidase or immunofluorescence. C4d was tested in conjunction with routine hematoxylin and eosin staining of all endomyocardial biopsies (EMB) for diagnosis of acute cellular rejection. Clinical suspicion of AMR was based on graft dysfunction by echo and abnormal hemodynamics. Results: 36 consecutive cardiac transplant recipients underwent 583 endomyocardial biopsies (EMB) over one year. Group I (n58) [50% male, 50% Caucasian, mean age 45.6 6 19.9 years] with C4d positive biopsies at median of 65 days (20-250) post-transplant, was compared to Group II with C4d negative biopsies (Table). ACR was present in a significantly higher number of patients in Group I compared to Group II (p 5 0.003). Clinical suspicion of AMR was also significantly higher in Group I. There was a trend toward a greater number of patients with post-transplant DSA in Group I. Conclusion: More C4d positive patients (Group I) had post-transplant DSA and clinical suggestion of AMR supporting C4d association with AMR. In addition, our study showed that ACR was significantly higher in C4d positive patients. C4d in association with acute cellular rejection, therefore, may be a biomarker for early or subclinical form of antibody mediated rejection. Routine use of C4d staining in a larger group of cardiac transplant patients may provide a biomarker for prospectively evaluating prognosis and clinical outcomes.
Characteristic Age: (years) Male (%) Caucasian (%) Number of EMB per patient Patients bridged with Left Ventricular Assist Device (%) Pre-Transplant DSA (DSA with MFI O2000) Post-Transplant DSA (DSA with MFI O2000) Pre-Transplant PRA positive patients (PRA Level O 10) Mean PRA level Acute Cellular Rejection [$1R] Clinical suspicion of AMR Mortality
Group I (C4d+) N5 8
Group II (C4d-) N5 28
p Value
45.63 6 19.92 4 (50) 4 (50) 17.13 6 3.79
52.82 6 12.34 20 (71.4) 14 (50) 15.93 6 5.55
0.35 0.39 0.48 0.49
4 (50)
16 (57.1)
0.51
3 (37.5%)
10 (35.7%)
0.61
5 (62.5%)
8(28.6%)
0.09
3 (37.5%)
8 (28.6%)
0.67
21.25 6 31.59 5 (62.5%) 3 (37.5%) 2 (25%)
6.57 6 10.20 2 (7.1%) 1 (3.6%) 6 (21.4%)
0.23 0.003 0.02 0.83
177 Implantable Cardioverter Defibrillator Malfunction Following LVAD Implantation Yuhning L. Hu1, Vigneshwar Kasirajan2, Daniel G. Tang2, Keyur B. Shah3, Kenneth A. Ellenbogen4, Jordana Kron4; 1Virginia Commonwealth University, Richmond, VA; 2Virginia Commonwealth University, Richmond, VA; 3Virginia Commonwealth University, Richmond, VA; 4Virginia Commonwealth University, Richmond, VA
Introduction: Implantable cardioverter defibrillator (ICD) lead malfunction has been reported after left ventricular assist device (LVAD) implantation, however
S62 Journal of Cardiac Failure Vol. 19 No. 8S August 2013 the incidence and mechanism are not known. Hypothesis: The mechanism of RV lead malfunction following LVAD implantation may be related to changes in LV and RV geometry, rather than decrease in LV mass. Methods: In this prospective single center study, we collected ICD lead data before, during and after LVAD implantation, including 12 time points during implantation. Results: Data were collected prospectively on 29 patients, including 24 patients undergoing LVAD implantation (ICD implanted 35634.9 months earlier) and 5 control patients who had LVAD implanted initially followed by ICD implantation. Of the 24 LVAD patients, 17 were male, 15 had coronary artery disease, 15 had LVAD implanted as destination therapy, and mean age was 57.6613 years. Fifty-four leads were tested before, during, 1 week and 3 months after LVAD implantation, including 18 right atrial, 24 right ventricular (RV), and 12 left ventricular (LV) leads. In 16 patients, ICD leads were tested at 12 intraoperative steps. RV sensing was O50% decreased from baseline in 6 patients (25%) immediately post-op, with RV sensing improving at 1 week in 3 patients (50%). In 2 patients (8%) who also had decreased sensing, RV pacing threshold was O50% elevated from baseline immediately post-op (n51) and at 1 week (n51). One RV pacing threshold returned to baseline at 3 months. Of the 4 patients with significant decreases in RV sensing in whom lead function was tested at serial time points during VAD implantation, an RV sensing decrease was not detected until immediately following weaning off cardiopulmonary bypass. One RV lead was turned off and one was replaced due to non-capture. Time from lead implant to LVAD was 77.6657.9 months in the patients with decreased RV lead sensing (n56) vs. 33.3643 months in patients with no decreased RV sensing (n518). Post-operatively, 14 (58%) patients had ventricular arrhythmias, new onset in 8 (33%); and 15 (63%) had atrial arrhythmias, new onset in 7 (29%). On ECG, sensed QRS width decreased after LVAD (126.5636.7 vs. 100635.5ms). Of the 5 control patients, none had O50% decreased RV sensing and 1 had O50% elevation in pacing threshold from the day of implant to 1 year post-implant. Of 29 patients, 6 died (4.966.8 months) and 1 underwent cardiac transplant (3 months). Conclusions: ICD lead malfunction can occur following LVAD implantation, but may improve over time. Intraoperative RV sensing problems were not detected until weaning of cardiopulmonary bypass, suggesting the mechanism of RV lead malfunction may be related to changes in LV and RV geometry from LVAD implantation. Ventricular arrhythmias are common in the LVAD population, even in patients who did not have them pre-operatively.
178 Telemetry Capable, Implantable Pulsatile Controller (IPC) for Left Ventricular Assist Devices (LVAD) Sam Siavash Asgari, Pramod Bonde; Yale School of Medicine, New Haven, CT Introduction: Recent generations of continuous-flow LVADs require a transcutaneous driveline to conduct power, controller algorithms, and data between the pump and extracorporeal controller unit. Driveline associated infections are a common complication which impart significant negative impact on quality of life and increase medical cost of LVAD treatment. Furthermore, continuous flow circulation has been implicated in gastrointestinal bleeding, limited cardiac unloading, and aortic incompetence. Hypothesis: We have earlier demonstrated the feasibility of wireless energy transfer to power an LVAD controller. In the current investigation, we present an ultra-compact implantable controller (IPC) to entirely free patients from the LVAD driveline and considerably reduce the extracorporeal hardware and weight. Since physiological flow, especially in the patient category of destination therapy, is of significance, we have embedded a pulsatile algorithm in the IPC. Methods: The controller has been designed to drive an LVAD with required safety and back up measures. The IPC embraces a reliable wireless algorithm to communicate to an external platform based Graphical User Interface (GUI) embedded in an iPhone, iPad, or a computer. The controller couples to a receiver coil to wirelessly obtain power. Furthermore, we have employed signal processing methods to analyze an ECG signal and modulate the pump speed during systole and diastole for co/counter-pulsation or fixed mode operation. When used with ECG gating, the IPC allows on-demand customization of operation with instantaneous flow and RPM changes, resulting in a pulsatile flow with adjustable pulse pressure. Telemetry has also been achieved by an embedded antenna. Initially, the controller was
Figure 1. A&B show the HVAD and IPC; C&D show the smart platform; E&F show the in -vivo data; G&H show the in vitro results; I&J show high speed during systole and Diastole. respectively (ECG Gated).
tested with an HVAD and HMII in an in-vitro setup to test its reliability. Ultimately, the controller has been implanted in two animals to wirelessly drive an HVAD in continuous and pulsatile modes. Results: Our tests results prove the system to be remarkably safe, accurate and efficient. The IPC operated continuously for two weeks in a mock circulation loop and 3 hours in each animal experiment. We have demonstrated the versatility of a controller that can create physiological flow. In terms of efficiency, IPC consumes less power to obtain the same pump speed and flow rate as compared with the HVAD controller. Conclusions: The combination of wireless powering, communicating with a user-friendly GUI and a very small footprint makes this an ideal totally implantable LVAD system. Patients are therefore liberated from the risk of driveline infection and are able to shower, swim, and perform physical activities with improved hygiene and mobility.
179 A Multi-Modailty Approach to Antibody Mediated Rejection Steven Geier1, Hemant Parekh1, Yanhau Li1, Rene Alvarez2, Eman Hamad2, Emily Tsai2, James Fitzpatrick2, Lazaros Nikolaidis2, Mustafa Ahmed2; 1Temple University School of Medicine, Philadelphia, PA; 2Temple University School of Medicine, Philadelphia, PA Introduction: Antibody mediated rejection remains a difficult problem in orthotopic heart transplant recipients. Treatment with solitary therapeutic targets often result in incomplete success. We describe our experience using a multi-targeted therapeutic approach. Case: A 41 year-old female who underwent orthotopic heart transplantation in 2007 presented with signs and symptoms of heart failure. She was treated with high dose corticosteroids while awaiting results of endomyocardial biopsy, which reveled no cellular rejection, but C4d and C1q evidence for antibody mediated rejection. Multiple donor specific antibodies were identified. She was initially treated with plasmapharesis and rituximab. This resulted in clinical improvement, but no change in her serologic or immunohistochemical markers of AMR. Several weeks later, she presented with symptomatic bradycardia and hypotension, requiring dobutamine infusion for hemodynamic stability. Endomyocardial biopsy once again was C4d and C1q positive, and serum was noted to have multiple DSAs with elevated MFIs. She therefore was treated with a combination of plasmapharesis, IVIG, and subcutaneous bortezomib [Figure 1] which resulted in clinical stabilization and improvement in donor specific antibodies [Figure 2]. Conclusions: A combination, multi-targeted approach to antibody mediated rejection may prove to be more effective in regards to clinical improvement, and resolution of serologic and immunohistochemical markers of rejection. Additional study to define an optimal approach is required.