The Arrhythmic Burden in Patients Following Left Ventricular Assist Device Implantation - A Single Centre Retrospective Analysis

Abstracts S199 A temporary mechanical RV support has recently been reported as an interesting management. The described procedures require cannulating the pulmonary artery (PA) by an open chest approach, and removal require a resternotomy or cutting the tube-graft anastomosed on the PA at the skin level, with possible complications. We report our experience with a full percutaneous temporary RV support by a centrifugal pump in RV failure after LVAD implantation. Methods: Twenty-seven of the 69 patients undergoing LVAD implantation between May 2013 and June 2014 at the Pitie-Salpetriere Hospital in Paris had a severe postimplant RV failure requiring concomitant temporary right ventricular support that was performed percutaneously. 12 were already under ECLS before LVAD implantation (bridge to bridge). Our patients were at high risk of post implant RV failure (Michigan score =  5,1 ± 2.3). We analyzed preoperative data, complications and outcome of these patients. Results: Insertion was successful in all patients with no technical complications. The delay of RV support implantation was 2.1 ± 5.4 days and the mean duration was 12.9 ± 7.6 days. 12 patients had reoperations for bleeding and 2 patients had a cerebral hemorrhage. No patient had thromboembolic events or RV support infection. The mortality under RV support was 37% and the weaning rate was 63%. Three patients could be transplanted, and the 6 months mortality was 51.8%. Conclusion: Temporary percutaneous RV support is an acceptable approach to manage RV failure after LVAD implantation. The method we report, provides an efficient support, limiting haemorrhagic problems and eliminating the morbidity of surgical reoperation for weaning off. 5( 29) Left Atrial Pressure Monitoring for Early Post-Operative Management Following LVAD Implantation I. Rajapreyar , M. Petrovic, S. Nathan, M.H. Akay, B. Kar, P. Loyalka, M. Patel, I.D. Gregoric.  Center for Advanced Heart Failure, The University of Texas Health Science Center at Houston, Houston, TX. Purpose: Precise measurement of preload to the right (R) and left ventricle (LV) are main parameters that guide early postoperative management after LVAD implantation. RV failure due to overload can occur as the LV is near completely unloaded. Ramp-speed studies can be unreliable in the immediate postoperative period due to poor echocardiographic (ECHO) acoustic windows. We used short-term direct left atrial pressure (LAP) monitoring with the Mikro-Cath Pressure Catheter to optimize early hemodynamics of LVAD patients (pts). Methods: The Mikro-Cath accurately estimates dP/dt and gives true pressure readings at any fluid height.Twenty-one pts underwent implantation of LVAD (HMII or HVAD) with the concomitant placement of the Mikro-Cath.Average age was 53±12years;median INTERMACS score was 1 (range 1-3). Four patients had pre-LVAD severely reduced RV function by ECHO. The Mikro-Cath catheter was left in place for 48-72 hours and removed with PTT between 50-60 seconds. Results: At startup, for HMII the speed was set between 7400-8400 RPM and for HVAD between 2000-2400 RPM to allow pulsatility and avoid septal shifting. Upon arrival in ICU LAP,CVP and PAP parameters guided subsequent medical management. In HVAD pts, speed was increased by 100-500 RPM to a range of 2400-2700 RPM; in majority of HMII pts the speed was increased by 200-800 RPM to a range of 7800-9200 RPM. LAP monitoring guided the speed to keep LAP< 10 mmHg in addition to optimization when ECHO acoustic windows were poor during speed change studies (Table). We observed no complications associated with the use of LAP catheter. One catheter malfunctioned. Conclusion: Direct LAP monitoring with the Micro-Cath was safe and helped to optimize pts’ hemodynamics early after LVAD implantation. The LAP and CVP helped established the highest appropriate speed for each patient. Thus,we could avoid acute RV dysfunction and subsequent use of inotropes decreasing risk for inotrope-induced arrhythmias. Echocardiography and LAP-Guided LVAD Speed Optimization in Two Patients ---HVAD--Pump speed (RPM) LAP (mmHg) LVEDD (cm) CVP (mmHg) Pump flow (LPM) MAP (mmHg)

2200 19 6.3 21 2.5 78

----HM II---2700 10 5.1 13 4.1 85

8000 17 6.69 11 N/A 80

10000 10 5.57 9 N/A 88

5( 30) Cardiac Resynchronization Therapy Does Not Reduce Ventricular Arrhythmias After Left Ventricular Assist Device Implantation J.W. Schleifer ,1 F. Mookadam,1 E. Kransdorf,1 U. Nanda,2 S. Cha,3 O.E. Pajaro,4 D.E. Steidley,1 R.L. Scott,1 J.C. Adams,5 R. Saadiq,6 T.C. Carvajal,7 K. Srivathsan.1  1Cardiovascular Diseases, Mayo Clinic Arizona, Scottsdale, AZ; 2Internal Medicine, Maricopa Medical Center, Phoenix, AZ; 3Health Science Research, Mayo Clinic Rochester, Rochester, MN; 4Cardiothoracic Surgery, Mayo Clinic Arizona, Scottsdale, AZ; 5North Central Heart, Avera Heart Hospital of South Dakota, Sioux Falls, SD; 6Cardiology and Vascular Medicine, Mayo Clinic Rochester, Rochester, MN; 7General Surgery, Mayo Clinic Arizona, Scottsdale, AZ. Purpose: Cardiac resynchronization therapy (CRT) reduces ventricular arrhythmia (VA) burden and hospitalizations in some patients who have heart failure with reduced ejection fraction. The role of CRT in patients with left ventricular assist devices (LVAD) is unknown. We sought to determine whether continued biventricular (BiV) pacing after LVAD implantation reduced VA burden, implantable cardioverter-defibrillator (ICD) shocks, or hospitalizations for any cause. Methods: We conducted a retrospective analysis of 93 patients who were implanted with LVADs at a single center. Patients were grouped according to whether they received BiV pacing for 30 days or more after LVAD implantation (n= 39) or less than 30 days of BiV pacing (n= 54). The total number of sustained VA, ICD shocks, hospitalizations, and device related surgical interventions were compared between the two groups until death or heart transplantation. Results: Patients with BiV pacing 30 days or more after LVAD implantation had similar time to first VA, time to first ICD shock, or hospitalization for any cause compared to patients with less than 30 days of BiV pacing. There was a trend toward earlier VA and ICD shocks in patients who were BiV paced 30 days or more, even if VA events during the first 30 days after LVAD implantation were excluded. There were no statistically significant differences in LVAD pump exchanges or mean ICD pulse generator changes per patient between groups. Multivariate logistic regression analysis showed that VA after LVAD implantation was best predicted by VA prior to LVAD implantation, but did not correlate with continuation of CRT. Conclusion: In this study CRT after LVAD implantation does not appear to reduce VA burden, ICD shocks, or hospitalizations for any cause. There appeared to be no clinical detriment in patients where CRT was discontinued. 

5( 31) The Arrhythmic Burden in Patients Following Left Ventricular Assist Device Implantation - A Single Centre Retrospective Analysis K. Chua, Y. Go, C. Sivathasan, C. Lim, D.K. Sim, C. Ching, C. Ng .   Cardiology, National Heart Centre Singapore, Singapore, Singapore. Purpose: Patients who undergo left ventricular assist device (LVAD) implantation for end-stage heart failure experience significant ventricular arrhythmias (VA) post LVAD implantation. We aim to identify their potential predictors in a single tertiary referral centre. Methods: All patients who have undergone LVAD implantation for standard indications from May 2009 till October 2014 were included. A retrospective review of in-hospital records including telemetry monitoring, electrocardiograms and device interrogation reports was performed.

S200

The Journal of Heart and Lung Transplantation, Vol 34, No 4S, April 2015

Results: Fifty patients were identified, the majority being males (n= 38, 76.0%) with a mean age of 49.1 +/- 13.2 years. The etiology for heart failure was non-ischemic in 28 (56.0%) patients and 19 (38.0%) were in Intermacs Level 1. 37 (74.0%) patients received a HeartMate II while 13 (24.0%) received a HeartWare. The mean left ventricular ejection fraction (LVEF) based on echocardiography was 17.1% +/- 5.1%. Post-VAD implantation, 17 (34.0%) patients had atrial arrhythmis (AA), including supraventricular tachycardia (SVT), atrial fibrillation and atrial flutter, and 43 (86.0%) patients had VA, including non-sustained ventricular tachycardia (NSVT), ventricular tachycardia (VT) or ventricular fibrillation (VF), which seemed to occur within the first month post-surgery. Factors that were associated with an increased risk of VA post-implantation include an Intermacs level 1 status (RR 2.26, 95% CI 1.54-3.34, p< 0.001), the presence of AA pre-implantation (RR 1.87, 95% CI 1.39-2.50, p< 0.001), a QRS duration of more than 120ms pre- (RR 2.15, 95% CI 1.48-3.11, p< 0.001) or post-implantation (RR 1.39, 95% CI 1.08-1.78, p= 0.02), an increase in the QTc by more than 20ms post-implantation (RR 2.38, 95% CI 1.61-3.54, p< 0.001) and the use of Milrinone (RR 1.30, 95% CI 1.03-1.64, p= 0.04) or Dobutamine (RR 2.87, 95% CI 1.88-4.37, p< 0.001). Conclusion: There is a high prevalence of atrial and ventricular arrhythmias in the first month following LVAD implantation. Factors that were associated with an increased risk of VA post-implantation include an Intermacs level 1 status, the presence of AA pre-implantation, a QRS duration of more than 120ms pre- or post-implantation, an increase in the QTc by more than 20ms post-implantation and the use of Milrinone or Dobutamine. 5( 32) At Left Ventricular Assist Device (LVAD) Implantation, Morphologic Differences Are Observed Between Patients With Improved Cardiac Function Allowing LVAD Removal and Patients With Prolonged LVAD Support as a Bridge to Transplantation A. Segura ,1 A. Hernandez,2 A. Baldwin,3 S. Carranza,4 P. Odegaard,5 L. Buja,1 O. Frazier.6  1Cardiovascular Pathology Research, Texas Heart Institute, Houston, TX; 2Cardiology, St. Luke’s Hospital Medical Center, Houston, TX; 3Cardiothoracic Surgery, Texas Heart Institute, Houston, TX; 4Circulatory Support, Texas Heart Institute, Houston, TX; 5Center for Cardiac Support, CHI St. Luke’s Health, Houston, TX; 6Center for Cardiac Support, Cardiovascular Surgery Research, Texas Heart Institute, Houston, TX. Purpose: To evaluate differences in morphologic parameters of ventricular remodeling in tissue samples and echocardiograms obtained at left ventricular (LV) assist device (LVAD) implantation in patients who later had sufficient clinical improvement to undergo device explantation versus those who required prolonged continuous-flow (CF) LVAD support and subsequent orthotopic heart transplantation (OHT). Methods: We evaluated 25 CF-LVAD patients, 10 of whom had improved cardiac function allowing device removal and 15 of whom underwent long-term device support (> 24 months) and subsequent OHT. In all cases, myocardial tissue samples were collected from the LV core obtained at device implantation. Computerized morphometry was used to evaluate fibrosis and hypertrophy, including the cytoplasmic and nuclear diameter. Echocardiographic and hemodynamic parameters at the time of LVAD implantation were correlated with the histopathologic findings. Results: Ten patients (7 men, 3 women; age 30±10 years) had their LVAD (HeartMateII) explanted due to cardiac functional improvement. Fifteen patients (11 men, 4 women; age 46±15 years) underwent OHT after 33±8 months (range: 26-50 months) of CF-LVAD support (HeartMate II, 13 cases; HeartWare, 2 cases). Four patients had ischemic cardiomyopathy, and 11 had nonischemic disease. At LVAD implantation, the LV core from the explant group showed a smaller myocyte diameter (24.55±4.63 vs. 37.09±10.22µ; P= 0.0003), a smaller nuclear diameter (12.21±1.72 vs. 15.65±3.88µ; P= 0.003), and less fibrosis (10.24±4.03% vs. 17.5±10.36%; P= 0.014) than were observed in the transplant group. The left ventricular end-diastolic diameter (LVEDD) was smaller in the explant group than in the transplant group (6.37±0.63 vs. 7.18±1.11 cm; P= 0.017). Conclusion: Patients with clinical improvement allowing LVAD explantation had less hypertrophy, less fibrosis, and a smaller LVEDD at the time of LVAD implantation than did patients who required prolonged LVAD support and subsequent OHT. These findings suggest that less extensive morphologic

ventricular remodeling changes at LVAD implantation may help determine which subset of patients may have a potential for myocardial reconditioning. 5( 33) Inhibition of ADAMTS-13 By Hemoglobin Reinstates Normal von Willebrand Factor: A Contributor to LVAD Thrombosis? C.R. Bartoli , D.J. Restle, J. Kang, M.A. Acker, P. Atluri.  Cardiovascular Surgery, University of Pennsylvania, Philadelphia, PA. Purpose: Thrombosis is a devastating complication of left ventricular assist device (LVAD) support. Evidence suggests a relationship between hemolysis and thrombosis. However, a mechanistic link is not known. Plasma free hemoglobin, which increases during hemolysis, inhibits ADAMTS-13 (the von Willebrand factor [vWF] protease). We tested the hypothesis that inhibition of ADAMTS-13 with hemoglobin replenishes vWF multimers and causes a relative hypercoagulability through the vWF pathway. Methods: Whole blood was collected from human donors (n= 8). Plasma was exposed to LVAD-like supraphysiologic shear stress (4 hours, ~175 dynes/ cm2) in a vortexer with and without plasma free hemoglobin (30 mg/dL) to inhibit ADAMTS-13. Förester resonance energy transfer (FRET) quantified plasma ADAMTS-13 activity (n= 8). Large vWF multimers and 11 vWF degradation fragments were characterized with electrophoresis and immunoblotting (n= 6). Results: Supraphysiologic shear stress caused extensive degradation of vWF multimers and significantly (p< 0.05) increased 11/11 vWF degradation fragments. After exposure to shear stress, hemoglobin (30 mg/dL) decreased plasma ADAMTS-13 activity (432±23 to 411±16 ng/ml, p= 0.08). As a result, large vWF multimers returned and 10/11 vWF degradation fragments decreased by 8±2% (Figure), of which 4/11 were statistically significant (p< 0.05). Conclusion: Inhibition of ADAMTS-13 by plasma free hemoglobin decreased vWF degradation. These data support our novel hypothesis for LVAD thrombosis. Plasma free hemoglobin from hemolysis may reinstate hemostasis through the vWF pathway and contribute early to thrombogenesis and LVAD thrombosis.