Dr. Roberta Keller has nothing to disclose.
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1 Vascular reactivity and onary hypertension in congenital diaphragmatic hernia Roberta L. Keller, MD UCSF Benioff Children s Hospital March 12, 211 Dr. Roberta Keller has nothing to disclose. Outline Lung hypoplasia Antenatal + neonatal vascular assessment Growth and function of the vascular bed Approach to treatment Pathophysiology of CDH parenchymal and vascular hypoplasia abnormal lung structure + function abnormal vascular structure + function poor transition/pphn varying severity postnatal lung + vascular growth critical for survival Kitagawa 1971; Naeye 1976; Levin 1978; Geggel 1985 MRA in 3 ½ week old term male with severe left CDH Pathophysiology: lung protection & survival Management era CDH survival by site Boston (n=235) Toronto (n=316) Gainesville (n=89) Emergent repair 45% 53% 15% ECMO/delayed repair 43% 55% 44% Permissive hypercapnia (PHC) 69%* PHC & lung protection 92% 75% 78%** Wilson 1997; Azarow 1997; Kays 1999; Bohn 22; Downward 23 Vascular hypoplasia: structure/function Post-mortem Antenatal Neonatal Lung Vasculature Lung weight/body weight Pulmonary artery (PA) size Vasculature Pulmonary blood flow Pulmonary hypertensive Vascular reactivity changes no size criteria Vasculature Elevated PA or right ventricle (RV) pressure Vascular reactivity 1
2 ANTENATAL VASCULAR ASSESSMENT Fetal vascular assessment in CDH Abnormal resistance pulsatility index (PI) + peak earlydiastolic reversed flow (PEDRF) improve mortality prediction over measure of lung hypoplasia alone (observed-expected LHR) Abnormal function: maternal hyperoxygenation decrease PI (2%) predicts survival in lung hypoplasia: PPV 79%, NPV 93% change in PI after fetal intervention associated with survival Moreno-Alavarez 28; Cruz-Martinez 2; Broth 22; Done 211 Biochemical effectors in fetal CDH ET1 interacts + antagonizes NO-cGMP signaling system maternal endothelin converting enzyme inhibitor in rat model mitigates lung hypoplasia ET1: smooth muscle cell mitogen ET1 infusion endothelial dysfunction in rat due to ROS decreasing NO bioavailability Endothelin-1 (ET1) Kelly 24; Kavanagh 2; Migneault 25 N C Fetal (cord) blood: control vs. CDH Acute PH + the honeymoon Endothelin-1/NO metabolites P=.38 Control CDH n=15 n=16 ET1/NO metabolites 3.5 (.84, 4.3) vs (1.95, 6.48) Plasma cgmp (pmol/ml) P=.2 Control CDH n=18 n=15 Plasma cyclic GMP 2.96 (1.51, 4.66) vs (3.73, 8.62) NEONATAL VASCULAR ASSESSMENT: acute onary hypertension Left lung from infant with left CDH and severe PPHN who died in 1 st day of life physiology (PPHN in 79%, 11/14) (Vacanti 1984) honeymoon group characterized by post-ductal PO 2 within normal range + higher Q p :Q s morphometry (Geggel 1985) honeymoon group had decreased medial wall thickness + no distal muscle extension 2
3 Acute PH: prior + current FiO hyperventilation (Bos 1993) PPHN (46%, 21/46) vasodilator challenge: 2/4 responders vs. /5 nonresponders survived permissive hypercapnia/ gentle ventilation PPHN (56%, 22/39) ino reactivity may be altered with different management approach Keller Peds Research 24 Echo assessment of P PA Patent ductus arteriosus flow direction + velocity Interventricular septal (IVS) position normal flattened D-shaped Tricuspid regurgitant (TR) jet velocity RVsp = 4 * velocity 2 + RAp 144 echocardiograms classified in 39 infants < 2/3 systemic 2/3 systemic systemic systemic suprasystemic indeterminate n=4 (3%) TR jet less common with lower pressure estimate (P=.8) < 2/3 systemic: 17/44 (39%) 2/3 systemic: 29/47 (62%) suprasystemic: 34/49 (69%) Right ventricular performance in CDH 2D + M-mode indices at 24 h: abnormal function (Baptista et al 28) higher myocardial performance (Tei) index (global) decreased tricuspid E/A ratio (diastolic) Pulse-wave tissue doppler imaging (Patel et al 29) decreased RV + septal E wave (impaired relaxation) decreased RV isovolumic + peak systolic ejection velocity Persistent suprasystemic PH Persistent suprasystemic PH NEONATAL VASCULAR ASSESSMENT: persistent onary hypertension < 48 hours 1 week 2 weeks 3 weeks 4 weeks Poor outcome Sensitivity 48 (26, 7) 41 (18, 67) 37 (16, 62) 47 (21, 73) 24 (7, 5) Specificity 33 (13, 59) 86 (57, 98) (74, ) (29, ) (4, ) PPV 45 (24, 68) 78 (4, 97) (59, ) (59, ) (4, ) NPV 35 (14, 62) 55 (32, 76) 5 (29, 71) 27 (6, 61) 23 (7, 5) Death Sensitivity 5 (19, 81) 43 (, 82) 75 (35, 97) 83 (36, ) 5 (12, 88) Specificity 41 (24, 61) 75 (53, 9) 96 (78, ) 83 (52, 98) 93 (68, ) PPV 23 (8, 45) 67 (3, 93) 86 (42, ) 71 (29, 96) 75 (19, 99) NPV 71 (44, 9) 82 (6, 95) 92 (73, 99) 91 (59, ) 82 (57, 96) < 48 hours 1 week 2 weeks 3 weeks 4 weeks Poor outcome Sensitivity 48 (26, 7) 41 (18, 67) 37 (16, 62) 47 (21, 73) 24 (7, 5) Specificity 33 (13, 59) 86 (57, 98) (74, ) (29, ) (4, ) PPV 45 (24, 68) 78 (4, 97) (59, ) (59, ) (4, ) NPV 35 (14, 62) 55 (32, 76) 5 (29, 71) 27 (6, 61) 23 (7, 5) Death Sensitivity 5 (19, 81) 43 (, 82) 75 (35, 97) 83 (36, ) 5 (12, 88) Specificity 41 (24, 61) 75 (53, 9) 96 (78, ) 83 (52, 98) 93 (68, ) PPV 23 (8, 45) 67 (3, 93) 86 (42, ) 71 (29, 96) 75 (19, 99) NPV 71 (44, 9) 82 (6, 95) 92 (73, 99) 91 (59, ) 82 (57, 96) 3
4 Estimated P PA 2/3 systemic Poor outcome & estimated P PA 1-2 d 1 week 2 weeks 3 weeks 4 weeks DC on RA P<.1 Poor outcome P=.4 n = Biochemical alterations in CDH + PH: abnormalities in vascular tone Inflammation (Okawada 27) increased monocyte chemotactic protein-1 (MCP-1) Endothelial activation increased circulating ICAM-1, VCAM-1 + ELAM-1 (Kobayashi 24) altered thromboxane (TBXB 2 ) + prostacyclin (6-keto- PGF 1α ) metabolites + TBX/PGF ratios TBXB 2 higher in PH (Bos 199) inversely correlated with A-a ratio (Nakayama 1992) ET1 levels: discharge on room air (DC RA) vs. poor outcome 2 3 Age (days) DC RA (n=18) Age (days) Poor outcome (n=19) ET1 levels: DC on RA vs. poor outcome Estimated P PA & plasma ET-1 at 2 weeks Transonary ET1 gradient Sample time DC RA ET1 (pg/ml) 1-2 d 19.6 ± 6.3 (n=18) 1 week 21.6 ± 9.5 (n=18) 2 weeks 17.5 ± 4.8 (n=14) 4 weeks 15.8 ± 4.1 (n=8) Poor Outcome ET1 (pg/ml) 23.1 ± 11.5 (n=19) 27.5 ± 11.4 (n=19) 32.1 ± 19.8 (n=19) 2. ± 8.9 (n=17) P value *P=.26 n = < 2/3 SBP 2/3 SBP-systemic Systemic-suprasystemic *nonparametric test for trends mean ET1 -.5 pg/ml, P=.6 Pre-onary circulation Post-onary circulation 4
5 Trans-onary ET1 gradient Trans-onary ET1 gradient Trans-onary ET1 gradient 1./ NO /3 36 1L 1./ NO / L 1./ NO 4 1./ NO /3 36 1L 1./ NO / L 1./ NO 4 1./ NO /3 36 1L 1./ NO / L 1./ NO 4 Trans-onary ET1 gradient 1./ NO /3 36 1L 1./ NO / L 1./ NO 4 Pulmonary vascular resistance (Woods units) Baseline conditions Vasoreactivity in CDH *P=.17 Vasodilator 6 ± 16 d (41-89 d) 6/7 with PVR decrease by 2% (median 44%) Baseline conditions RA 56 and 89 d PVR increase and 39% GROWTH + LATER FUNCTION OF THE VASCULAR BED 5
6 Vascular development: pruning Lung development: growth arrest Vascular development: growth arrest Left CDH: 1 month Left lung perfusion 22% R R L Left CDH: 2 months Left lung perfusion 2% Left CDH: 15 days Hemorrhagic complications on ECMO Left CDH: 2 ½ months Chronic lung disease & onary hypertension 5 months 2 years APPROACH TO TREATMENT: onary vascular disease Lung + vascular hypoplasia Hyperoxia Localized hypoxia Barotrauma Volutrauma Inflammation Oxidative injury Chronic endothelial stress (vascular injury) Growth arrest Lung + vascular dysplasia Approach to treatment Prevention gentle ventilation, permissive oxygenation careful monitoring + assessment of RV function Time Interventions to consider maintenance of ductal patency to unload RV specific onary vasodilator therapy Assessment for long-term therapy 6-8 weeks of age cardiac catheterization 6
7 Acknowledgements Funding K23 HL79922 (Keller) Pulmonary Hypertension Association (Keller) HL (Fineman) UL RR (CTSI/PCRC) Research mentors Sam Hawgood Jeff Fineman Pediatric Echocardiography Lab Faculty, fellows & staff of UCSF William H. Tooley Intensive Care Nursery, Fetal Treatment Center + Pediatric Surgeons Later vascular assessments: children + adults ECMO survivors (Schwartz 1999) age 3.2 ± 1.4 y 8/21 with PH by echo (2/3 criteria for increased RV ejection time) 6/8 with mid-systolic notch 2/5 desaturated 5% with exercise Older children/adults decreased left PA flow/ volume (Abolmaali 2) decreased maximum V O2, work load, duration in 2/3 studies in children (Zaccara 1996, Trachsel 26, Peetsold 27) no echo evidence of PH maximum V O2 + workload within normal limits in adults (Peetsold 29) 7
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