The Journal of Heart and Lung Transplantation, Vol 35, No 4S, April 2016
Conclusion: The presence of NC-CAF in pediatric HTx recipients is correlated with decreased duration of exercise, increased ectopy during exercise, and increased antihypertensive use. The study may be underpowered to detect a significant association with multivariable analysis. We suggest that the presence of NC-CAF may be associated with altered myocardial perfusion and could impact exercise ability in children after HTx. These findings suggest that more research is needed regarding the hemodynamic impact and clinical significance of NC-CAF. 1( 149) Coronary Flow Reserve Predicts Graft Loss in Pediatric Heart Transplant Patients J.A. Kleinman ,1 S.M. Stack,1 J. Gralla,2 S.M. Miyamoto,1 B.A. Pietra,3 M.D. Everitt,1 S.R. Auerbach.1 1Pediatrics, Division of Cardiology, Children’s Hospital Colorado, University of Colorado School of Medicine, Aurora, CO; 2Pediatrics, Children’s Hospital Research Institute, University of Colorado School of Medicine, Aurora, CO; 3Pediatrics, Division of Cardiology, University of Florida, Gainesville, FL. Purpose: Cardiac allograft vasculopathy (CAV) is a common cause of graft loss (GL) in heart transplant (HT) patients (pt). Coronary flow reserve (CFR) quantifies coronary microcirculatory function. We aimed to determine the utility of CFR for predicting GL. Methods: We reviewed pediatric HT pt at our center with CFR measurements from 1993-2008. Normal CFR was defined as change in coronary flow with adenosine 2 times above the baseline measurement. Pt were grouped based on CFR < 2X baseline (abnormal) or ≥ 2X baseline (normal). GL was defined as repeat-HT or death. Statistical analysis included the Mann-Whitney U and Fisher exact tests for descriptive purposes. Freedom from graft loss was analyzed using the log rank test and multivariable Cox proportional hazards modeling with time varying covariates to account for time to CFR measurement. Results: There were 185 pediatric HT pt and 499 CFR measurements; 62% were male, 70% had a pre-HT diagnosis of congenital heart disease, and median [IQR] age at HT was 0.8 yr [IQR 0.26-7.7]. The cohort mean CFR was 2.9X ± 0.8. CFR was < 2X in 21 pt and time from HT to CFR measurement was longer for CFR< 2X vs CFR≥ 2X, 7.03 [3.18-7.69] vs 1.51 yr [1.04-5.24], respectively; p< 0.001). There was no difference in the proportion of pt with biopsy proven 2R acute cellular rejection (ACR) between CFR≥ 2X vs CFR < 2X (11 vs 14%, respectively; p= 0.71); Only 3/21 pt with CFR< 2X had ACR at that time. Incidence of GL was higher for CFR< 2X from time of CFR measurement and from time of HT (Figure 1A and 1B, respectively). Cox modeling with time varying covariates showed higher risk of GL for CFR< 2X (HR= 4.36 95%CI 2.07-9.20) and older age at HT (HR= 1.05, CI 1.01-1.08). Conclusion: Abnormal CFR is suggestive of microvascular CAV and can predict risk of GL. CFR may aid in risk stratification, assessing CAV severity, response to CAV-directed medical therapy, and in timing of re-listing for HT.
1( 150) The End-of-Life Experience in Pediatric Heart Transplant Recipients S.A. Hollander ,1 J.C. Dykes,1 S. Chen,1 L.M. Barkoff,2 D.N. Rosenthal,1 D. Bernstein,1 B.D. Kaufman.1 1Pediatrics (Cardiology), Stanford University, Palo Alto, CA; 2Solid Organ Transplant Services, Lucile Packard Children’s Hospital, Stanford, Palo Alto, CA. Purpose: The causes of death following pediatric heart transplant (pHtx) are well characterized, however, the context in which post-transplant deaths occur, especially in the modern era, is not well described. We analyzed the circumstances surrounding death in a recent cohort of pHtx patients.
Methods: Retrospective review of all deaths occurring in pHtx patients between 3/14/2009-7/9/2015 at a single center. The causes, location, and level of support at the time of death were analyzed, as was the incidence of sudden cardiac arrest occurring out of hospital or in the emergency department (ED). Deaths that occurred prior to transplant hospitalization discharge were excluded. Results: Twenty-two patient deaths were analyzed. The median age of death was 12 (IQR 6,18) years. 18/22 (82%) died of cardiac causes, 3 (14%) died of infection, and 1 (5%) died of primary pulmonary disease. Of those who died of cardiac causes, 12 (67%) had no evidence of graft dysfunction or coronary vasculopathy at their most recent assessments, which occurred a median of 54 (IQR 24, 119) days before death. Fifteen (68%) of patients died in an ICU, 17 (77%) were intubated, and 8 (36%) died on mechanical support (VAD or ECMO). 11/22 (50%) patients suffered sudden cardiac arrest at home or in the ED prior to hospital admission. Conclusion: Most deaths following pHtx occur in the ICU while receiving advanced life-sustaining therapies. This may be due in part to the rapid evolution of life-threatening cardiac complications that manifest despite little evidence of preceding cardiac disease and often result in sudden death or outof-hospital/ED resuscitations. As a result, families may be left unprepared for end-of-life decision-making. These findings suggest the need for advanced care directives and ongoing discussions regarding resuscitative wishes for all pHtx patients, even in the absence of graft dysfunction. 1( 151) Milrinone Use for Inotropic Support in Pediatric Acute Heart Failure: Utilization, Safety and Markers of Efficacy S.R. Deshpande ,1 L. Smitley,1 M. Carroll,2 K. LaPorte,2 W.T. Mahle,1 K.O. Maher.1 1Pediatric Cardiology, Emory University Children’s Healthcare of Atlanta, Atlanta, GA; 2Children’s Healthcare of Atlanta, Atlanta, GA. Purpose: Data for Milrinone use in non-surgical pediatric acute heart failure (AHF) patients is extremely limited. We present a large, single center cohort of AHF patients treated with milrinone and assess safety and efficacy of the therapy. Methods: Retrospective study (2008-15). Results: 90 patients with a mean age of 82.04 months (range 0-251 months) were admitted for non-surgical, decompensated AHF majority with cardiomyopathy. Milrinone was initiated in the CICU, dose range of 0.5-1.0 mcg/kg/min. Gender distribution was even (45/45). 34/90 (37.8%) were intubated for cardiorespiratory failure. 47 (52.2%) patients required parental nutritional supplementation. Weaning attempt was made in all patients based on clinical assessment and stabilization of AHF. 63/91 (70%) were successfully weaned off milrinone (fig 1). Mean duration of support was 29.26 days (1-205 days). Age, weight, gender, ejection fraction (EF), fractional shortening (SF), BNP, renal function, liver function were similar at baseline in the two groups. Use of additional HF therapies were similar. Serial measurements were performed to assess treatment efficacy. In patients with successful wean, there was a statistically significant reduction in BNP, lactate, BUN, creatinine, AST, ALT and significant increase in EF and SF (all p lt 0.05) with therapy. Absence of such response was associated with poor outcome. There were no side effects directly attributable to milrinone, especially arrhythmias. Milrinone was not discontinued in any of the patients for adverse events. Overall outcomes for the cohort were: weaned (63/90, 70%), home milrinone (3/90, 3.3%), transplanted (20/90, 22.2%), death (4/90, 4.4%). Conclusion: Initiation of milrinone was associated with improvement in AHF symptoms and markers of severity with significant changes within two weeks of therapy. Therapy was well tolerated. Study supports continued use of milrinone in therapy of pediatric AHF and needs a large scale validation.