Cardiopathies,acquises - Dr Daniela Laux Cardiopédiatre associée - UE3C -Paris Médecin hospitalier temps partiel - Arcothova
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Cardiopathies,acquises Dr Daniela Laux Cardiopédiatre associée – UE3C –Paris Médecin hospitalier temps partiel Centre Chirurgical Marie Lannelongue Le Plessis Robinson
Kawasaki – Les points clés • Maladie(décrite(en(1967(–(seulement(50(ans(de(recul(!( • Vascularite, systémique, qui( touche( essen4ellement( les, artères, de, moyen, calibre, avec( un( tropisme( élec4f( pour( les, artères,coronaires,(gravité(de(la(maladie)(( • Les(complica4ons(coronaires(surviennent(dans(15,à,25,%,des( cas(chez(les(enfants(non(traités( • L'administra4on( précoce( d'immunoglobulines( humaines( par( voie( intraveineuse( a( transformé( le( pronos4c( en, diminuant, par,5,le(risque(d'anévrisme(coronaire( • Risque, de, mortalité, 0,015, %, (Japon),( surtout( entre( le( 15N45eme( jour( (thrombocytose( concomiQante( avec( la( vascularite)(
Epidémiologie( • Première,cause,de,cardiopathie,acquise,de,l'enfant,dans,les, pays,développés, ( • Tous,les,âges,pédiatriques,(80,%,des,cas,avant,5,ans)( • Les(pa4ents(de(moins,de,1,an,ou(de,plus,de,8,ans,sont(rares( mais(ont(un(risque(plus(élevé(d'anévrisme(coronaire( • Formes,de,l'adulte:,première(fois(décrite(en(1977( • symptômes(majeurs(décrits(iden4ques( ( • Kawasaki,aOeint,chaque,année:, – 265/100.00(enfants(
CaractérisTques,cliniques:,critères,majeurs, La,fièvre,de,plus,de,5,jours,et,au,moins,4,critères,suivants, ( N(La(conjoncTvite(bulbaire(non(purulente( N(L’aOeinte,muqueuse(:(la(pharyngite,(la(chéilite,(la(langue(framboisée,(la(stoma4te( N(L'exanthème,polymorphe,du,tronc, N(L'aOeinte,des,extrémités(:(un(érythème(des(paumes(des(mains(et/ou(des(plantes( des(pieds,(l'œdème(palmoNplantaire,(la(desquama4on(palmoNplantaire(secondaire(( N(L'aOeinte,unilatérale,des,ganglions,cervicaux,(de(plus(de(( (1.5(cm(de(diamètre(( ( Critères majeurs définis par l'American Heart Association Committee On Rheumatic Fever, Endocarditis, and Kawasaki Disease
AQeinte(cardiovasculaire( • Pas,d’aOeinte,coronaire,dans,75%,des,cas,!, • Anomalie,ECG,ou,échocardiographique:, – DilataTon,des,artères,coronaires,(20%), – Anévrismes(coronaires( – Infarctus( – Myocardite(avec(possible(insuffisance(ventriculaire(gauche( sévère( – Péricardite,(épanchement(péricardique( – Fuites(valvulaires(par(inflamma4on(des(valves(cardiaques(et( par4culièrement(la(valve(mitrale((1(%)( – Troubles(conduc4fs(et(troubles(du(rythme(par(inflamma4on( du(4ssu(de(conduc4on(
Les(anévrismes(coronaires( • ( Entre,le,10 ,et,le,25 ,jour,d'évoluTon, ème ème • 5(%(lorsque(le(traitement(est(fait(précocement(( (=(,2,,2,5,,10,ou,>,8,mm, ( Newburger JACC 2016
Formes(atypiques( Tableau,clinique,dominé,par,un,symptôme,inhabituel:( ( «(convulsions,(œdème(pulmonaire,(diarrhée(sanglante,(ascite,( obstruc4on(des(voies(aériennes(supérieures,(épiglonte,( adénopathies(cervicales(compressives(ou(hémolyse(et( défaillance(mul4Nviscérale,(syndrome(néphro4que,( hyponatrémie….(»( ( Formes,de,l'adulte, • (Troubles(diges4fs,(aQeinte(hépa4que,(signes( (ar4culaires(et(encéphalites(sont(plus(fréquent(
Les(formes(incomplètes( , Pa4ents(ayant(eu(une(fièvre(depuis(au,moins,5,jours,et(( au(moins,deux,critères,cliniques,de,Kawasaki,(sans(cause(évidente,(( et(des(critères(biologiques(en(faveur(d'une(inflamma4on(systémique( ( • Différent,de,la,«,forme,atypique,», , • Manque(un(ou(plusieurs,des,cinq,critères,diagnos4ques(majeurs( (, • Plus,fréquentes,chez,les,enfants,les,plus,jeunes,,à,risque,, ,,,,,d'anomalies,coronaires( (( Diagramme(décisionnel(proposé(par(l'American(Academy(( of(Paediatrics(pour(aider(à(la(prescrip4on(d’IgG(dans(les(formes( incomplètes(( Newburger JW et al., Circulation. 2004
Critères,cliniques,et,biologiques,supplémentaires, Cardiovasculaires,:(dilata4on(des(artères(coronaires,(anévrismes(coronaires,( infarctus,(myocardite(avec(possible(insuffisance(cardiaque(conges4ve,(péricardite,( épanchement(péricardique,(fuites(valvulaires,(troubles(conduc4fs(et(troubles(du( rythme,(anévrismes(des(vaisseaux(du(cou,(des(artères(rénales,(spléniques,( hépa4ques,(pancréa4ques,(génitales,(gangrènes(distales(et(pseudoNRaynaud( ( DigesTfs,:,diarrhées,(vomissements,(douleurs(abdominales,(hydrocholécyste,( dysfonc4on(hépa4que( ( Respiratoires(:(toux(et(rhinorrhée(( ( Neuroaméningés(:(troubles(de(la(conscience(avec(irritabilité,(apathie,(état(grognon,( hypoacousie( ( ArTculaires,:(arthrite,(arthralgies( Autres,:(uvéite,(érythème(au(niveau(de(la(cicatrice(de(BCG,(desquama4on(de(l’aine( ( Albumine(
secondaire en « doigt de gant » Atteinte unilatérale des ganglions cervicaux, de plus de 1,5 cm de diamètre, ferme Formes incomplètes upplémentaires Fièvre de plus de 5 jours et 2 ou 3 critères cliniques e, péricardite, état de choc, ou ronaire, anévrismes extra- Fièvre de plus de 7 jours sans cause retrouvée (enfants ≤ 6 mois+++) (vaisseaux du cou, artères s, pancréatiques, génitales), du culot aortique Faire un bilan biologique s, vomissements, douleurs e, dysfonction hépatique, te/méatite, hydrocèle CRP < 30 mg/l et VS < 40 mm/h CRP ≥ 30 mg/l et/ou VS ≥ 40 mm/h ribronchique et interstitiel, monaires conscience avec irritabilité aralysie faciale, hypoacousie Réexaminer et contrôler le bilan Au moins 3 critères biologiques ou plus : ies (hyperleucocytose du biologique si la fièvre persiste novial) Anémie pour l’âge eau de la cicatrice de BCG, Échocardiographie en cas de Plaquettes ≥ 450 000/mm3 Non hlegmon rétropharyngé desquamation en doigt de gant Albumine ≤ 30 g/l typique ALAT augmentées Globules blancs ≥ 15 000/mm3 ECBU ≥ 10 globules blancs/champ stics différentiels Oui ou ntérovirus, EBV, rougeole Traiter Échocardiographie positive ine se staphylococcique hoc toxique Échocardiographie positive actérienne x médicaments Z-score IVA ou CD ≥ 2,5 vens-Johnson Ou anévrisme coronaire (Z-score ≥ 2,5) juvénile Ou plus de 3 critères : rose - dysfonction ventriculaire gauche - fuite mitrale - épanchement péricardique oronaire élevé si score ≥ 5) - Z-score IVA ou CD compris entre 2 et 2,5 Bajolle et al. 2018 EMC (1 point) Description coronaire s jours de fièvre (2 points)
Evolu4on(naturelle( ( 1°)(La(phase(aiguë((J0NJ10)(:(aOeinte,cardiaque,rare, ( 2°)(La(phase(subaiguë((J10NJ20)(:(diagnosTc,de,complicaTon, coronaire, ( 3°)(La(phase(de(convalescence((J20NJ70)(:(constataTon,d’anévrysmes, et,de,sténoses,cicatricielles,en(cas(de(complica4on(coronaire(à(la( deuxième(phase(
Exemples(d’aQeinte(coronaires(
Dilata4on(anévrysmale(des(artères(coronaires( Aorte IVA =6.9 mm Thrombus Aorte dans l’IVA (A)(IVA=interventriculaire(antérieure( (B)(thrombus(dans(l’IVA(
Dysfonc4on(ventriculaire(gauche(sévère(en( échographie( Etat de choc dans 7% des cas de maladie de Kawasaki VG dilaté VG dilaté
Dilata4on(anévrysmale(des(artères( coronaires(au(scanner( CD =4.7 mm Aorte IVA =6.9 mm
Dilata4on(anévrysmale(de(l’IVA(en( chapelet(au(scanner( Aorte Aorte Chapelet anévrysmal Chapelet anévrysmal
Anévrysme(coronaire(avec(sténose( coronaire(au(cathétérisme(cardiaque( Sténose Anévrysmes et sténoses coronaire multiples des coronaires
AQeinte(diffuse(des(axes(vasculaires( A B Foie Dilatation fusiforme Aorte (A)(épaississement(pariétal(hyperéchogène(de(l’aorte,(de(l’artère(mésentérique(supérieure(et(du(tronc( coeliaque(en(échographie(( (B)(dilata4on(fusiforme(de(l’artère(mésentérique(supérieure,(du(tronc(caeliaque(au(scanner(
Le(traitement(de(1ère(inten4on( Immunoglobulines,intraveineuses:( • 2g/kg(en(8(à(12(heures,(à(posologie(progressive( ( En,associaTon(à(de(l’acide,acétylsalicylique,(AAS),:, • à( fortes( doses( pour( ses( effets( an4Ninflammatoires( et( an4N thrombo4ques((30a50,mg/kg/j,en,4,fois),à(la(phase(aiguë(( • puis( à( dose, anTaaggrégante, plaqueOaire, rapidement( 48N72( h( après(l’apyrexie((3N5(mg/kg/jour)( De Graeff et al 2019, Newburger 2016
CE NTRAL ILL USTRATIO N Management of Kawasaki Disease Diagnosis of Kawasaki disease according to American Heart Association criteria* Anti-inflammatory therapy with intravenous immunoglobulin (IVIG) and ASA (acetylsalicylic acid or aspirin). Echocardiogram to assess coronary arteries and determine Z score. Defervescence with no coronary dilation (Z score
Kawasaki Disease APRIL 12, 2016:1738–49 Recommanda4ons(américaines( TABLE 1 Principles in Acute Management of KD 1. The goal of therapy is to reduce systemic and tissue-level inflammation as rapidly as possible. For this reason, patients should be treated as soon as diagnosis can be confidently established. 2. All patients within the first 10 days of fever onset should be treated with IVIG. Patients diagnosed after 10 days should receive IVIG treatment if they are still febrile, have markedly elevated inflammatory parameters, or have coronary artery dilation. 3. Recrudescent fever at least 36 h after the end of IVIG infusion without other explanation is a marker for persistent inflammation and should prompt immediate and aggressive anti-inflammatory therapy a. Antibody-mediated hemolysis has become common in KD patients who have received IVIG retreatment and have type A or B blood; rescue therapies other than IVIG (e.g., infliximab, corticosteroids) should be considered. 4. Patients with coronary artery dilation (z-score >2.0) should be followed with a repeat echocardiogram at least twice a week until dimensions stabilize; additional anti-inflammatory therapy should be considered. 5. Patients with giant aneurysms should have frequent echocardiograms in the first 3 months of illness for thrombus surveillance, even after dimensions stabilize. 6. Infants under 6 months of age are at extremely high risk of aneurysm formation, even with timely therapy. They require echocardiograms every few days until dimensions have stabilized. 7. Patients with giant CAA (z-score $10) are at highest risk for thrombosis during the first 3 months after fever onset a. Systemic anticoagulation together with an antiplatelet agent should be administered until coronary dimensions improve. b. Low-molecular-weight heparin is easier to regulate than warfarin in infants, as well as in patients of any age, during the acute phase of illness or until hsCRP normalizes. CAA ¼ coronary artery aneurysm; hsCRP ¼ high-sensitivity C-reactive protein; IVIG ¼ intravenous immunoglobulin; KD ¼ Kawasaki disease. Newburger JACC 2016 The progression of aneurysm formation in some Children With Kawasaki Disease and Coronary Artery
Surveillance(à(court(terme(( Pour,les,paTents,sans,complicaTon,coronaire:, • 1(echo(entre(1N2(semaines(et(1(echo(entre(4N6(semaines((Classe(1)( Pour,les,paTents,avec,Z,score,coronaire,>,2,0,à,la,phase,aigue:, • 2(echos(par(semaines(jusqu’à(l’arret(de(la(progression( ( Pour,les,paTents,avec,anévrismes,géants:, • 2(échos(par(semaine(tant(que(les(lésions(progressent( • 1(écho/sem(pdt(45(jours(puis( • 1(écho/mois(pendant(3(mois((Casse(IIA)( Newburger JACC 2016
An4agréga4on(et(an4coagula4on( PaTents,sans,aOeinte,coronaire:, • Aspirine(pendant(6(semaines((Cl(1)( ( PaTents,avec,aOeinte,coronaire,d’aggravaTon,rapide:, • Hospitalisa4on(pour(mise(sous(heparine((An4Xa(0,5N1)( • Arret(si(stabilisa4on;(Z(score(
Que(faire(en(cas(de(persistance(de(la(fièvre( après(une(première(cure(d’IgIV?( • Résistants:,15(à(20(%(des(cas( • Associée(à(un(risque(plus(élevé(d'aQeinte(coronaire( • Deuxième(dose(d’IVG(( • associée(à(un(bolus(de(cor4coides((20N30(mg/kg/jour(IV( methylprednisolone)( • Discuter:,prednisolone(p.o.(plus(prolongé(2N3(semaines( • Alterna4ve:(infliximab( • En(cas(d’échec:(ciclosporine( Newburger(JW(et(al.,(Circula4on.(2004( Egami&K&et&al.,&J&Pediatr&2006&
Qui sont les patients à haut risque? Comment identifier les résistants ? • Score issu de la littérature de patients japonais!! Score d’Egami (2006) Score de Kobayashi (2006) Score de Sano (2007) Age ≤ 6 mois (2 points) Age ≤ 12 mois (1 point) Bilirubine totale ≥ 0.9mg/dL (1 point) ≤ 4 jours de fièvre (1 point) Traitement dans les 4 premiers CRP ≥ 7mg/dL (1 point) jours de fièvre (2 points) Plaquettes ≤ 300.109/L (1 Plaquettes ≤ 300.109/L (1 ASAT ≥ 200 U/L (1 point) point) point) CRP ≥ 8mg/dL(1 point) CRP ≥ 10mg/dL (1 point) ALAT > 100 U/L (1 point) ASAT ≥ 100 U/L (1 point) ≥ 80% neutrophiles (2 points) Na+ ≤ 133 mmol/L (2 points) Haut risque si ≥ 3 points Haut risque si ≥ 5 points Haut risque si ≥ 2 points Scores issus de la population japonaise, spécifique mais non sensible Shohai O et al., Pediatrics 2011; Egami K et al., J Pediatr 2006 ; Chen S, et al. JAMA 2016; Mc Crindle Circ 2017
2. Treatment of KD should include IVIG at a dose of 2 g/kg as a single infusion. 1A A 3. In non-Japanese patients, the Kobayashi criteria may indicate risk of IVIG resistance if ‘positive’ (score 2A C Original article 54) but may not reliably exclude IVIG resistance if ‘negative’ (score
Quelle,est,l’histoire,naturelle,des,complicaTons, coronaires,de,la,MK?, • Dispari4on(complète(dans(plus(de(50%(des(cas(même( en(cas(d’anévrysme((sauf(géant)(dans(les(2(ans( • Occlusion(coronaire;(sténoses(localisées(ou(mul4ples( parfois(très(tardives…( • Gravité(des(lésions(tardives(car(mul4ples(et(chirurgie( difficile(
Anévrysme(géants((1%)( • Mortalité(et(morbidité(+++( • Survie(à(30(ans:(88N90%( • Cardiac(event(free(à(30(ans(:(30%( • 26%(infarctus(myocardique( Adapted with permission from Newburger et al. (99). • Risque(accru(dans(les(2(ans(après(le(diagnos4c(( • 50%(de(bypass(coronaire(à(30(ans(
Surveillance à long terme 19-1800 ! Maladie de Kawasaki Immunoglobulines IV à 2 g/kg sur 12 h Aspirine à dose anti-inflammatoire 60 mg/kg/j jusqu’à disparition de la fièvre Puis relais par AAP 3–5 mg/kg/j 75 % 20 % 4% 1% Anévrisme géant Coronaires Petit anévrisme Anévrisme moyen Dilatation Z-score ≥ 10 ou ≥ 8 mm normales 2,5 ≤ Z-score < 5 5 ≤ Z-score < 10 2 ≤ Z-score < 2,5 AAP à vie Z-score < 2 AAP 1 an AAP à vie AAP 6 semaines AVK pour INR 2-3 AAP 6 semaines Cs à M3, M6, M12 Cs à M3, M6, M12 Cs à 6 semaines Cs à M1, M2, M3, M6, M9, M12 Cs à 6 semaines Coroscanner à 1 an Coroscanner à 1 an Coronarographie à 1 an Même Si Normali- Si Normali- Si Arrêt Normali- Si si persistance sation persistance sation persistance aspirine sation persistance normalisation Aspirine Aspirine Aspirine à vie Arrêt Maintien Clôture Arrêt Maintien Aspirine à vie à vie à vie Maintien AVK aspirine aspirine du aspirine aspirine ± double ± double ± double ± double AAP Clôture du Cs/2–5 dossier Cs/1–3 ans Cs/an AAP AAP AAP ± BB dossier ans Cs/an Cs/an Cs/an Cs/6 mois Prévention des FDRCV pour tous ! Figure 2. Arbre décisionnel. Prise en charge proposée par le centre de référence Malformations Cardiaques Congénitales Complexes (M3C) Necker. IV : par voie intraveineuse ; AAP : aspirine à dose antiagrégante plaquettaire ; Cs : consultation ; AVK : antivitamine K ; INR : international normalized ratio ; FDRCV : facteurs de risques cardiovasculaires. ! Formes incomplètes lines est le plus souvent excellente. La recommandation est une perfusion lente de 12 heures pour éviter tout effet secondaire Lorsqu’on a une forme incomplète de maladie de Kawasaki (flush, hypertension, malaise,Bajolle et al.etc.). hypotension, 2018 Les EMC immuno- (fièvre d’au moins cinq jours associée à deux ou trois critères cli- globulines humaines sont des médicaments dérivés du sang. À
iffness testing should minimize risks of anesthesia and North ionizing radiation. Children too young to exercise in pe- , reas- Devenir(à(long(terme( of late T A B L E 2 Principles in the Long-Term Management of Patients With KD nifesta- 1. On the basis of available data, patients with no demonstrated coronary artery always- dilation by echocardiogram with excellent visualization of all arterial segments ears of during the first weeks of illness appear to have normal cardiovascular status in early adulthood. 2. Remodeling (so-called regression) of aneurysms, especially if moderate or large, to normal internal lumen diameter is often accompanied by luminal myofibroblastic proliferation and abnormal vascular reactivity. 3. Patients with persistent CAA are at lifelong risk of progressive coronary artery stenosis or occlusion and worsening ischemia. ifelong 4. Patients with CAA documented at any stage require lifelong cardiovascular are to surveillance tailored to disease severity and age. 5. Testing should minimize exposure to ionizing radiation whenever possible. cardial 6. Sedentary life-style should be avoided. ble 2). 7. Women with coronary aneurysms can carry pregnancy successfully, but should de the have reproductive counseling. testing 8. Monitoring and counseling regarding traditional CV risk factors is appropriate to reduce the likelihood of later atherosclerosis. d upon Newburger JACC 2016 athero-
Endocardite(
Endocardite(infec4euse( ( Def:(Infec4on/inflamma4on(de(l’endocarde(=(valves(cardiaques( Dg:,Echographie(transNthoracique(voire(ETO( (N(EI(des(VAV:(sur(le(versant(auriculaire( (N(EI(des(valves(sigmoïdes:(sur(le(versant(ventriculaire( • Hémocultures:(au(moins(3!!!!!!!!!!!((au(mieux(6)( • Pas(d’ATB(à(l’aveugle( • Scanner(total(body((cérébral,(thoracique(et(abdominal)( • Examen(ophtalmologique,(bandeleQe(urinaire( • Recherche(porte(d’entrée:(examen(dentaire,(ORL,(cutané,(diges4f,( urinaire,(KTC…( (
Endocardite:(germes(
Endocardite:(Traitement(médical(
Endocardite:(Traitement(chirurgical(
Endocardite:(préven4on(
Endocardite:(préven4on(
Endocardite:(préven4on( - Bonne hygiène dentaire quotidienne - Consultation dentaire tous les 6 mois Indispensable pour diminuer le risque d’endocardite
POPULATION CONGENITALE(N(ENFANTS( 34 279 enfants avec CC suivis de 0 à 18 ans Incidence annualisée = 4.1 / 10 000 pt-année Rushani et al. Circulation 2013
POPULATION CONGENITALE(N(ADULTES( Registre CONCOR (14 224 patients>18 ans) Incidence EI : 1.33/1000 pt-years Prothèse valvulaire: HR=3.57(2.58–5.36) Kuijpers et al. Eur Heart Jour 2017
INCIDENCES(COMPARATIVES( Valve Melody : 0.8 – 3% pt-année Valves/conduits pulmonaire chir : 0.5 - 3% pt-année TAVI: 0.67 – 2.1% pt-année Valves Ao/mitrale chir : 0.3 – 1.2% pt-année Dispositifs electroniques implantables : 1.9/1000,deviceaannée,, Patients avec CC: 0.4 – 1.33 / 1000 pt-année Miranda et al. Eur Heart Jour 2016 Wang et al. JAMA 2007 Rushani et al. Circulation 2013 Population générale : 30 -100/ million pt-année Habib et al. Eur Heart Jour 2015 Dayer et al. Lancet 2015
COMPARER(CE(QUI(EST(COMPARABLE( 50
VALVES(PERCUTANÉES(VS(CHIRURGICALES( p=0.1 3 134 chir et 208 percut (33 Sapien) 195 chir et 93 percut (0 Sapien) 631 chir et 107 percut (0 Sapien) Incidence IE: 0.5 vs 1.5 %pt/années Incidence IE: 1.2 vs 3.9 %pt/années Incidence IE: 0.8 vs 2.7 vs 3% %pt/années Lluri et al. CCI 2017 Malekzadeh-Milani et al. JTCS 2014 Van(Dijck(et(al.(Heart(2014(
SUBSTRAT(VALVULAIRE( Author Year n Substrate EI EI Annualized Median Cumulative Incidence Follow-up incidence (% pt-year) (years) Albanesi, 2014 12/106 Contegra 11.3 7.6 Malekzadeh 2014 5/190 Homografts 2.6 1.2 2 Contegra Ramanan 2015 6/115 Freestyle 5.4 - 4.3 Mery 2016 23/586 Homograft 4 - 7 Contegra Porcine valve Ugaki 2016 21/298 Contegra 7 - 3.4 Homograft Tous les dispositifs valvulaires sont susceptibles d’être le siège d’une EI Avec une incidence variable mais significative Albanesi(et(al.(EJCTS(2014( Ramanan et al. Ann Thorac Surg 2015 Ugaki et al. Ann Thorac Surg 2016( Mery(et(al.(JTCS(2016(
SUBSTRAT(VALVULAIRE( • EI plus fréquente chez les patients avec VJB • Quelle que soit la techniqued’implantation (i.e. Contegra et Melody) • Comparés aux homogreffes RR=8.7 and 9.7 pour Melody et Contegra MalekzadehNMilani(et(al.(JTCS(2014( (Mery et(al.(JTCS(2016( Van(Dijck(et(al.(Heart(2014( Ugaki(et(al.(Ann Thorac Surg 2015
SUBSTRAT(VALVULAIRE( Méta-analyse sur IE chez les patients avec RVP chirurgical ou percutané 7063 patients Incidence cumulative globale = 2.5% VJB vs autres substituts : 5.4% vs 1.2%; p < 0.0001 Sharma et al. JACC Int. 2017
VALVE(SAPIEN( JACC: CARDIOVASCULAR INTERVENTIONS VOL. 10, NO. 5, 2017 ª 2017 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 1936-8798/$36.00 PUBLISHED BY ELSEVIER http://dx.doi.org/10.1016/j.jcin.2016.12.012 512 Hascoet et al. JACC: CARDIOVASCULAR INTERVENTIONS VOL. 10, NO. 5, 2017 Endocarditis After PPVI: Melody Versus Sapien Infective Endocarditis Risk After MARCH 13, 2017:510–7 JACC: CARDIOVASCULAR INTERVENTIONS VOL. 10, NO. 5, 2017 Percutaneous Pulmonary Hascoet et al.Valve513 MARCH 13, 2017:510–7 Endocarditis After PPVI: Melody Versus Sapien Implantation With the Melody and from phone calls to the patients and to their TABLE 1 Patient Demographics, Procedural Data, and Post-Procedural Outcomes and Sapien Valves cardiologists and general practitioners. For cases of PPVI With PPVI With IE, every effort was made to obtain Sebastieninformation Hascoet, MD,a Luciaon Mauri, MD,a Caroline Claude, MD,a Emmanuelle Fournier, MD,a Julie Lourtet, MD,b Melody Valve Sapien Valve Standardized c c the Duke criteria, clinical and microbiological Jean-Yves Riou, MD, details, Philippe Brenot, MD, Jérôme Petit, MDa (n ¼ 32) (n ¼ 47) Difference Age (yrs) (73 of19.979;(15.8–28.9) 92.4%). A single stent was sufficient 26.3 (18.9–39.9) 0.58* in all medical and surgical strategies, and outcome. TABLE 1 Continued Weight (kg) Melody56.5 group ! 13.5patients, 65.8 whereas ! 17.6 in the Sapien 0.59* group 4 ABSTRACT STATISTICAL ANALYSIS. Statistical analyses were Male (%) 53.1 66.0 0.26 PPVI With PPVI With patients required 2 to 4 stents. Pre-stenting was not performed using Stata 11.2 software (StataCorp, OBJECTIVES Col- the risk of infective endocarditis (IE) after percutaneous pulmonary valve This study compared Genetic syndrome (%) 18.8 10.6 -0.23 Melody Valve Sapien Valve Standardized implantation (PPVI) with the Sapien and Melody valves. History of severe infectiousperformed 9.4in 6 patients with 8.5 valve-in-valve -0.03 implan- lege Station, Texas). Continuous data(n ¼were 32) described (n ¼ 47) Difference disease (%) History of endocarditis (%) tation. Balloon 6.3 post-dilation 2.1 was performed -0.20 in 19 as of meanInfective ! SD if normally distributed endocarditis during and asThemedian BACKGROUND 25.0 incidence of IE after PPVI is estimated at 3% per year with the Melody valve. The Sapien valve is a 0.0 -0.80* (interquartile range [IQR]) more recently Categorical otherwise. marketed valve used for PPVI. Pacemaker/defibrillator (%)79 patients 6.3 (24.1%) and was 10.6 more common 0.16 in the follow-up (%) variables were described as number (%). METHODS Bivariate We retrospectively included consecutive patients who underwent PPVI at a single center between 2008 and Congenital heart diseases (%) Pulmonary valve replacement 25.0 4.3 -0.59* Melody group (46.9% vs. 6.5%, respectively). Pro- analyses with calculation of standardized differences 2016. IE was diagnosed using the modified DUKE criteria. Conotruncal malformation 81.3 68.1 during follow-up (%) Ross procedure cedure duration, 9.4 21.3 time, and irradiation fluoroscopy were performed to compare variables Percutaneous between the 3.1 PPVI was performed in 79 patients RESULTS 2.1 (Melody valve, 40.5%;-0.06 Sapien valve, 59.5%). Median age was 24.9 years two valve types and between patients (range 18.1 towith 34.6). IEversus occurred in 8 patients (10.1%) at a median of 1.8 years (minimum: 1.0; maximum: 5.6) after TGA were higher 3.1 in the Sapien 0.0 valve group. Surgical 21.9 surgery. 2.1 Causative organisms were methicillin-sensitive Staphylococcus-0.63* aureus (n ¼ 3), Staphylococcus epidermidis (n ¼ 1), PA-IVS/PVS 3.1 4.3 without IE during follow-up. DORV Severe 3.1 procedural complications 6.4 occurred in 2 pa- Kaplan-Meier Death during curves follow-up of (%) the cumulative 3.1 Streptococcus mitis (n ¼ 1), IE inci- Aerococcus 2.1 viridans (n ¼ 1), -0.06 Corynebacterium striatum (n ¼ 1), and Haemophilus influenzae (n ¼ 1). All 8 cases occurred after Melody PPVI (25.0% vs. 0.0%). The incidence of IE was 5.7% (95% confidence interval: RVOT (%) tients (2.5%). One patient died of massive hemo- dence were plotted using the date of PPVI 2.9% asperthe to 11.4%) entry person-year after Melody PPVI. The Kaplan-Meier cumulative incidence of IE with Melody PPVI was Native RVOT 3.1 25.5 Values are time median since [interquartile range] thorax due to perforation date of a distal pulmonary and the PPVI as orthe %. Standardized 24.0%time difference scale. (95% confidence computed The12.2% interval: as the to 43.9%) afterdifference 4 years and in means 30.1% (95%orconfidence interval: 15.8% to 52.5%) Bioprosthesis 9.4 23.4 proportions divided by the SE. *Significant after imbalance. 6 years, compared with 0.0% with the Sapien PPVI after 4 years (p < 0.04 by log-rank test). There was a trend right censor was the date of IE, valve replacement, Homograft branch during 25.0 Sapien valve 31.9PPVI over a Lunderquist toward a higher incidence of IE in the first 20 patients with Melody PPVI (who received prophylactic antibiotics during the DORV ¼ double-outlet right ventricle; PA-IVS ¼ pulmonary atresia with intact ventricular septum; PPVI ¼ Conduits 62.5 19.2 heart transplantation, death, or follow-up percutaneous pulmonary valve implantation; procedure only) andcomple- PVS ¼ pulmonary in patients who had percutaneous interventions, dental care, or noncardiac surgery after PPVI. valve stenosis; RVOT ¼ right ventricle outflow RVOT lesion (%) guidewire. In the other patient, who had a mechanical tion. Differences in incidence were evaluated tract; TGA ¼ transposition of the great arteries. using CONCLUSIONS IE after PPVI may be less common with the Sapien compared with the Melody valve. Stenosis aortic valve, 84.4 a large femoral 50.0 hematoma developed the log-rank test. The Kaplan-Meier method (J Am was Coll Cardiol Intv also © 2017 by the American College of Cardiology Foundation. 2017;10:510–7) Regurgitation 0.0 35.7 used to assess the cumulative incidences of pulmo- Mixed 15.6 14.3 nary valve replacement and of death, with the date of Pre-stenting (%) 1-stage Hascoet PPVIJACC et al. (%) Int. 2017 No. of stents (%) 0 90.6 87.5 93.6 87.2 0.11 0.01 FIGURE 1 Kaplan-Meier Cumulative Incidences of Death and Pulmonary 9.4 6.4 Valve PPVI as the entry date and the time since time scale and with the right censor set Replacement and Kaplan-Meier outflow geryasforthe Cumulative tract valve replacement, heart transplantation, death, (RVOT). PPVI as the P ercutaneous pulmonary valve implantation (PPVI) has emerged as an alternative to sur- certification in 2006 and Food and Drug Administra- tion approval in 2010 for PPVI. The Sapien valve date ofthe right ventricular (Edwards SAPIEN pulmonic transcatheter heart valve, reconstructing Incidences PPVI was firstofdescribed or Infective in Endocarditis Edwards Lifesciences, Irvine, California) was used 2000 (1) and since then many studies have supported initially for transcatheter aortic valve replacement 1 90.6 85.1 end of follow-up. Differences itsinefficacy incidence were (2–13) The Melody valve (Medtronic Inc., and subsequently licensed for PPVI (Europe, 2010;
VALVE(SAPIEN( Hascoet et al. JACC Int. 2017
VALVE(SAPIEN( Edwards SAPIEN XT Transcatheter Heart Valve with the NovaFlex1Deliv- ery System. Vol. 2016. https://www.accessdata.fda. gov/cdrh_docs/pdf13/ p130009s037d.pdf.
(PREVENTION(N(EDUCATION(( PROCEDURE PRE-IMPLANTATION Salle hybride Patient et famille Optimisation gradient Depistage foyer infectieux résiduel Bilan dentaire et ORL Antibioprophylaxie per +/- post procédure POST-IMPLANTATION Education patient, parents, médecin traitant, dentiste Anti-aggrégants au long cours Antibioprophylaxie à vie
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Kociol et al E4ologies(des(myocardites( Recognition and Management of Fulminant Myocarditis CLINICAL STATEMENTS AND GUIDELINES Downloaded from http Kociol et al Figure 5. Causes of lymphocytic myocarditis. Recognition and Management of Fulminant Myocarditis Diagram demonstrating the primary causes and associated subcategories of lymphocytic myocarditis. GCM indicates giant cell myocarditis; IBD, inflammatory bowel disease; RA, rheumatoid arthritis; and SLE, systemic lupus erythematosus. Reprinted from Trachtenberg and Hare.99 Copyright © 2017, American Heart Association, Inc.
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Indication d’une BEM Kociol et al Recognition and Management of Fulminant Myocarditis CLINICAL STATEMENTS AND GUIDELINES Figure 3. Indications for endomyocardial biopsy (EMB). Guideline-based algorithm for whether EMB is indicated. COR indicates Class of Recom- mendation; LOE, Level of Evidence; and MRI, magnetic resonance imaging. *Usually a dilated cardiomyopathy. Fulminant myocarditis may have normal end-diastolic diameter with mildly thickened walls. Exclude ischemic, hemodynam- ic (valvular, hypertensive), metabolic, and toxic causes of cardiomyopathy as indicated clinically. Reprinted from Bozkurt et al.3 Copyright © 2016, American Heart Association, Inc. despite normalization of cardiac enzymes and biomark- EMB, CORONARY ANGIOGRAPHY, ers.78 EMB can be considered the primary diagnostic AND INVASIVE Circ 2020 HEMODYNAMICS strategy76,79 when magnetic resonance imaging is not Kociol et al Recognition and Management of Fulminant Myocarditis In the setting of cardiogenic shock, right-sided heart possible (eg, shock, presence of metal devices) if expe- catheterization and coronary angiography are essential to rienced operators and cardiac pathologists are readily guide management strategies. The decision to perform available. According to guidelines, however, indications S
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Traitement(de(la(myocardite(fulminante( Kociol et al Recognition and Management of Fulminant Myocarditis CLINICAL STATEMENTS AND GUIDELINES Downloaded from h Circ 2020 Figure 4. General approach to initial stabilization of patients in cardiogenic shock. ACS indicates acute coronary syndrome; CABG, coronary artery bypass grafting procedure; ECMO, extracorporeal membrane oxygenation; IABP, intra-aortic bal- loon pump; MCS, mechanical circulatory support; PCI, percutaneous coronary intervention; and VAD, ventricular assist device. Reprinted from van Diepen et al.86
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Immunosuppressive Treatment for Myocarditis in the Pediatric He et al. Immunosuppressive Treatment for Myocarditis in the Pediatric Population: A Meta-Analysis TABLE 1 | Characteristics of studies included in the meta-analysis. Study N Age Study IMSA IMSA dosage, time of Follow-up Observed Inclusion criteria methodology IMSA start variables Bing He* , Xiaoou Li and Dan Li Camargo et al. 50 5 months−15 PNCT P, CyA P & A: 2.5 mg/kg/d, 1 8.4±1.2 months LVEDD, LVEF, Active myocarditis based Department (9)of Pediatrics, Renmin years Hospital of Wuhan University, Wuhan, week; 2.0 mg/kg/d, 3 China PWP, CI, HR on EMB findings weeks; 1.5 mg/kg/d, 4 weeks Cy: 1.5 mg/kg/d, 1 week; The use of immunosuppressants in the treatment of myocarditis in children remains 1.0 mg/kg/d, 7 weeks; 0.5 mg/kg/d, 1 week controversial. Aziz et al. (6) The 68 aim of RCTthis meta-analysis 3.7 ± 2.9 P 2 mg/kg/d, 1 month is to 15.1±9.2 summarize LVEDD, LVESD, the current empirical Duration of symptoms evidence for immunosuppressive years treatment for myocarditis months LVEF in the for
studies of Department arePediatrics, included inRenmin the present study,ofofWuhan Hospital which University, only one Wuhan, treatmentChina in the short term may significantly improve LVEF, is an RCT study; this might result in a lack of statistical reduce LVEDD, and reduce the risk of death and heart transplant power to detect a significant difference in the treatment effect. in pediatric population with myocarditis. Although this meta- Moreover, we were able to ascertain publication bias in only analysis reported beneficial outcomes with immunosuppressive The four use ofstudies, immunosuppressants which means only four of sixin thedata treatment therapy, theof myocarditis in children remains Immunosuppressive Treatment for of six controversial. The aimDueofto this findings of this meta-analysis. studies’ could be merged, which may have impacted the analysis of the meta-analysis the included studies’ lack results have to be interpreted cautiously because one RCT was included in this meta-analysis; more large-scale is to summarize the current empirical RCTs are required in the future. only Myocarditis in the Pediatric evidence for follow-up of long-term immunosuppressive treatment (only two studies had median follow- for myocarditis in the pediatric population. up > 1 year), their inferences can only be applied to short- AUTHOR CONTRIBUTIONS We term searched PubMed, MEDLINE, and Embase for articles to identify studies analyzing Population: A Meta-Analysis outcomes. In this meta-analysis, didn’t report we couldn’t provide data of viral genome and histologic type, because the included the studies efficiency of these immunosuppressive data even if this information exact treatment was BH is responsible for the provision of the overall idea and writing articles. in the data XL collects pediatric and modifiespopulation. Pooled the paper. DL is responsible important to the therapy and prognosis. RCTs in the future for statistical analysis. Bing estimates wereLigenerated and Dan using fixed- or random-effect models. Heterogeneity within • Groupe d’enfants avec immunosuppresseurs He* , Xiaoou Li studies Department was assessed of Pediatrics, Renmin using Hospital Cochran’s of Wuhan University,Q and I2Wuhan, statistics. ChinaFunnel plots and Begg’s rank The were amélioration significative: REFERENCES correlation method were constructed to evaluate use also of immunosuppressants in potential 1. Sagar S, Liu PP, Cooper LT Jr. Myocarditis. Lancet. 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The Newcastle–Ottawa Scale (NOS) for Assessing the Quality of iversity of Naples, Italy decreased studies wasCardiology left assessed ventricular Working Group on using end-diastolic Myocardial Cochran’s dimension and Pericardial Diseases. I (LVEDD) QEurand Nonrandomised statistics. [mean Studies Funnel difference in Meta-Analyses. plots Ottawa, andHospital ON:−0.77 Ottawa mm, rank Begg’s Heart J. (2013) 34:2636–48. doi: 10.1093/eurheartj/eht210 Research Institute (2019). Available online at: http://www.ohri.ca/programs/ Reviewed by: correlation 95%6. CI: method Aziz KU,−1.35 towere Patel N, Sadullah T,−0.20 constructed Tasneem H, mm]Thawerani when toviralevaluate compared H, Talpur S. Acute to the publication conventional clinical_epidemiology/oxford.asp bias. Sensitivity treatment group. analyses Marco Merlo, wereFurthermore, also myocarditis: conducted the20:509–15. Cardiol Young. (2010) riskto doi:evaluate the potential role of immunosuppression: a prospective randomised study. of10.1017/S1047951110000594 death and sources of heterogeneity. Afterwas 15. Okada R, Kawai S, Kasyuya H. Non-specific myocarditis: a statistical and heart transplant clinicopathologicalin study conventional of autopsy cases. Jpn treatment Circ J. (1989) 53:40–8. a detailed niversity of Trieste, Italy Meena Nathan, • MAIS: 1 seule étude RCT, effectifs faibles, screening of 159 studies, six separate studies were identified, with 181 patients in the 7. Drucker significantly NA, Gamma-globulin immunosuppressive Colan higher SD, Lewis treatmentthan AB, Beiser AS, Wessel in thein the of acute myocarditis treatment Circulation. (1994) 89:252–7. DL, Takahashi immunosuppressive M, et pediatric population. group, and 199in in doi: 10.1161/01.CIR.89.1.252 al. doi: 10.1253/jcj.53.40 16. Waller BF, 2007the treatment Catellier MJ, Clark group conventional consecutive MA, Hawley DA, [relative forensic autopsies. Clin treatment risk Pless JE. Cardiac (RR): pathology Cardiol. (1992) 15:760–5. group. The follow-up court 4.74; 95% CI: 2.69, 8.35]. No significant heterogeneity across the studies was observed. rvard Medical School, 8. Bhatt GC, Sankar J, Kushwaha KP. Use of intravenous immunoglobulin doi: 10.1002/clc.4960151014 immunosuppressive compared with standard treatment group therapy is associated with showed improved 17. a significant Klugman D, Berger JT, Sableimprovement CA, He J, Khandelwal SG, Slonim inAD.left ventricular Pediatric EditedUnited by: States Therefraction ejection was no evidence complicated by (LVEF) myocarditis. [mean of publication clinical outcomes in children with acute encephalitis syndrome Pediatr Cardiol. difference bias whenCardiol. 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(1995) 16:61–8. doi: 10.1007/BF00796819 to the conventional management of myocarditis in the 19. Aretz HT, Billingham ME, Immunosuppressive Treatm (2017) 6:e005306. doi: 10.1161/JAHA.116.005306 treatment Edwards WD, Factor SM, Fallon JT, Fenoglio JJ, et al. Myocarditis: a histopathologic definition and classification. Am J group. Furthermore, the risk of death and heart transplant in conventional treatment was Trieste, Italy enaSpecialty Nathan,section: 10. Gagliardi MG, Bevilacqua M, Bassano C, Leonardi B, Boldrini R, Camassei pediatric significantly population. FD, ethigher al. Long term than However, follow up ofinchildren further prospective thewithimmunosuppressive myocarditis treated by Cardiovasc Pathol. (1986) 1:3–14. investigation treatment 20. Cooper LT, Baughman is AM, KL, Feldman warranted group Myocarditis in the Pediatric to [relative Frustaci A, Jessup validate M, Kuhl U, et al.risk (RR): ticle ical was nited 4.74;this submitted to School, States 95% immunosuppression and of children with dilated cardiomyopathy. Heart. finding. CI: (2004) 2.69, 90:1167–71. 8.35]. No significant heterogeneity doi: 10.1136/hrt.2003.026641 disease: a scientificacross statement fromthe Population: A Meta-Analysi The role of endomyocardial biopsy in the management of cardiovascular studies the American wastheobserved. Heart Association, Pediatric Cardiology, There was no evidence of publication bias when assessed by Begg’s test. apondence: section of the journal Keywords: immunosuppressive treatment, myocarditis, pediatric, cardiac function, meta-analysis Bing He*, Xiaoou Li and Dan Li Bing in Frontiers He Conclusions: Pediatrics There may be a possible benefit, in the Frontiers in Pediatrics | www.frontiersin.org 8 short November 2019 | Volume 7 |term, Article 430 to the Department of Pediatrics, Renmin Hospital of Wuhan University, Wuhan, China 1@sina.com addition of immunosuppressive therapy in the management of myocarditis in the ceived: 22 May 2019
Traitement(de(la(myocardite(fulminante( Kociol et al Recognition and Management of Fulminant Myocarditis Table 7. Major Myocarditis Subtypes Resulting in a Fulminant Presentation CLINICAL STATEMENTS Subtype H&E Findings Clinical Manifestations Treatment AND GUIDELINES Fulminant lymphocytic Extensive dense lymphocytic infiltrate Acute heart failure rapidly leading Treatment is primarily supportive; circulatory myocarditis with associated myonecrosis. May have to cardiogenic shock, conduction support as needed to prevent MOSF. Some occasional isolated multinucleated giant abnormalities, or ventricular evidence that in the absence of cardiotropic cells or eosinophils. arrhythmias/SCD. Chest pain. viral genome by PCR, steroids may be helpful GCM Extensive mixed inflammatory infiltrate Acute heart failure caused by systolic Treatments consists of multimodality therapy characterized by the presence of several dysfunction, myocardial restriction, and should be implemented after a tissue multinucleated giant cells (usually or both. Conduction abnormalities, diagnosis has been confirmed. Usual therapy present after 1–2 wk), eosinophils, including CHB and EMD; ventricular includes a combination of a high-dose monocytes, and macrophages in the arrhythmias, including sustained VT/VF steroids, a calcineurin inhibitor (such as absence of noncaseating granulomas. and SCD. Tends to comigrate with other cyclosporine), and an antimetabolite such Edema and extensive myonecrosis often autoimmune diseases. as azathioprine. Cytolytic therapy (purified present. rabbit-derived polyclonal IgG directed at human thymocytes) used for suppression of life-threatening GCM has been reported. Acute NEM Extensive inflammatory infiltration of Acute heart failure/cardiogenic Identify potential precipitant, especially if a the myocardium with mononuclear cells shock. May present with a restrictive drug hypersensitivity (Table 5). High-dose and eosinophils. Associated myonecrosis cardiomyopathy. Prothrombotic steroids. Anticoagulation. Often presents or fibrosis. On EM, may see eosinophil intracardiac state. Peripheral with ST-segment elevations and chest degranulation and deposition of major eosinophilia may or may not be pain mimicking an ST-segment–elevation basic protein. present. Recent viral infection or new myocardial infarction. Rapid angiography, medication. EMB with subsequent circulatory support, and initiation of high-dose intravenous corticosteroids can be lifesaving. ICI myocarditis Newly identified lymphocytic myocarditis Acute heart failure, cardiogenic shock, Treatment includes immediate cessation resulting from the introduction of and atrial fibrillation developing of therapy, high-dose corticosteroids (1 g novel chemotherapeutic agents that soon after ICI therapy is started and solumedrol intravenously daily for 3 d and unleash inhibited antitumor T cells, generally more severe with combination then 2 mg/kg prednisone daily to start, which also may infiltrate and attack ICI therapy. Typically occurs early in followed by a slow wean) and initiation of the myocardium. Histopathology treatment and has a fulminant course. an angiotensin receptor blocker or sacubitril/ consistent with lymphocytic infiltrate valsartan. May initially need MCS. and myocardial necrosis. CHB indicates complete heart block; EM, electron microscopy; EMB, endomyocardial biopsy; EMD, electromechanical dissociation; GCM, giant cell myocarditis; Circ 2020 Downloaded H&E, hematoxylin and eosin; ICI, immune checkpoint inhibitor; IgG, immunoglobulin G; MCS, mechanical circulatory support; MOSF, multiorgan system failure; NEM, necrotizing eosinophilic myocarditis; PCR, polymerase chain reaction; SCD, sudden cardiac death; and VT/VF, ventricular tachyarrhythmia/ventricular fibrillation.
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