Role of pulmonary vasodilators in the Fontan setting. Michael Cheung Melbourne
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1 Role of pulmonary vasodilators in the Fontan setting Michael Cheung Melbourne
2 Fontan circuit Low resistance to adequate pulmonary blood flow is critical Central PA anatomy (size and distortion) Intrapulmonary vessel (arborisation and flow) Unobstructed pulmonary venous flow (anatomical/physiological) Normal capillary bed
3 Elevated resistance to flow? Goldilocks and her bears We know excessive PBF is bad Low/non-pulsatile flow also bad PVR Group A; Right lung PVR 2x greater than left lung Group B; Left/right lungs PVR no different Pig model, 3 months enos Right lung I; sham II; Non-pulsatile III; Slight pulsatility Henaine et al J Thorac Cardiovasc Surg 2013;146:522-9
4 Endothelial function Initial procedure 15 Fontan patients aged 7-17 years PA band BT shunt All subjects; fall in PVR (p=0.016) Greater effect of NO in pts with previous pulsatile flow (p=0.006) Khambadkone et al Circulation 2001
5 Pulmonary arterial hypertension specific therapy Supportive therapy hydration anticoagulation Iron supplementation NO PDE5 inhibition sildenafil/vardenafil/tadalafil soluble Guanylate Cyclase stimulation Riociguat ERA bosentan/ambrisentan/macitentan PGI Prostacyclin (IV/subcut/nebulised) Selexipag N Engl J Med 2004; 351:
6 Pulmonary arterial hypertension specific therapy 2015 ESC/ERS Guidelines for the diagnosis and treatment of PAH
7 Prostacyclin; Studies in Fontan patients 2 exercise tests done 1/12 apart Randomised to single dose inhaled prostacyclin vs placebo Improved VO2max All patients with baseline VO2 <30ml/kg/min improved with iloprost c/f placebo No change in spirometry Median VO2max 30.2 vs 27.6 ml/min/kg p=0.004 Rhodes Int J Card 2013
8 Sildenafil; Studies in Fontan patients 27 patients Mean age 15 +/-5 years 6 weeks of sildenafil,/placebo crossover trial CPET assessment Mean VO2 baseline 30.5ml/kg/min Whole group data Improved ventilatory AT (p=0.03) Greater effect in those with BNP>100 pg/ml No change in VO2 max Circulation 2011;123:1185
9 Sildenafil; Studies in Fontan patients Adults (n=10) Single dose of sildenafil (50mg) pre-exercise Exercise MRI and SVC/radial artery catheter Improved cardiac Reduced PVR Restored exercise SVR greater fall output induced cgmp release Circ CV Imaging 2014;7:
10 ERAs; Studies in Fontan patients Eur J Heat Failure 2013 CITY 2009 N=9, median age 12 years (4-33 years) Failing Fontan 4 months of Bosentan treatment No difference in 6MWT/functional class N=32, median age 29 years (18-56 years) 6 months of treatment No change in VO2 max, SF-36 QoL, NT-proBNP
11 ERAs; Studies in Fontan patients AmJ Card 2016 Circ 2014 n=69, mean age 20 +/-7 years 14 weeks of treatment Increase in VO2 max +1.4 ml/kg/min (~+5%) Improved endurance +24 seconds Reduced NT-proBNP n=19, aged years 8 with reduced systolic function Randomised to ambrisentan or placebo12 weeks Improved VO2 max and Ve/VO2 Improved FC in 9/32 Rx, 0/37 controls No change in QoL (SF-36)
12 ERAs; Studies in Fontan patients All had PVRi>2 Woods units 6 children (9 yo) 8 adolescents (17 yo) 7 adults (26 yo) Bosentan in under 18, macitentan in adults 6/12 treatment Reduced PVR in >70% of subjects Improved FEV1 and FVC in under 18s Adolescents and adults increase cardiac output JTCVS 2017;153:1468
13 Combination therapy; Studies in Fontan patients Children PVR >2.5 WU Sildenafil added to Rx Group 1 shunted; mean 1 year old Group 2 Glenn; mean 7 years old Group 3 Fontan; mean 13 years old Significant fall in PVR in all 3 groups Int Journal of Cardiology 221 (2016)
14 IPAH; histology Thickened intima and media Eccentric intimal thickening Muscularised small artery
15 Histology of vessels; postmortem lung specimens PAH Fontan Control Thicker More Thin layer Minimal walls collagen of actin smooth muscle Intrapulmonary arteries of Fontan patients (aged years) Acellular fibrosis with collagen deposition Ridderbos JHLTx 2015
16 Histology of vessels; pulmonary veins Low flow lung Control lung Pulmonary veins; pig model of low flow A subpleural venous hyperplasia B venous hyperplasia between alveolar Pulmonary veins humans A control B Fontan; fibromuscular intimal proliferation and medial muscularisation (yellow arrow) Hays et al Heart 2017 lobules C control lung Henaine et al JTCVS 2013;146:522-9
17 Summary Lack of pulsatile/low pulmonary blood flow induces endothelial dysfunction structural changes arteries and veins Changes seem different to pulmonary arterial hypertension with acellular fibrosis and collagen deposition Variable results of studies Which patients benefit and why? Baseline PVR > 2 WU showed greater response to NO Khambadkone Previously banded patients greater response Khambadkone 71% of patients had fall in PVR with ERAs, all subjects had baseline PVR > 2 WU Agnoletti BNP > 100 had greater response to sildenafil Goldberg VO2 max < 30mL/min/kg had greater response to nebulised prostacyclin Rhodes Perhaps improved Ve/VCO2 is opening capillaries and improving V/Q mismatch? Goldberg Is some of the effect is in altering systemic vascular resistance? Van De Bruane
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