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Cardiomyopathie du péripartum Staff d’Anesthésie du Lundi 20 Avril 2015 CHI Poissy St-Germain Sarah Féray – Interne Cas clinique Madame TK, 36 ans, origine africaine • Antécédents médicaux : – Obésité IMC = 33 – Aucun FdR cardiovasculaire • Antécédents obstétricaux : – G3P3 : – AVB en 2007 (4250g) – AVB en 2009 (4950g) – AVB en 2011 (5120g) • Antécédents chirurgicaux : aucun • Allergie : non connue Histoire de la maladie • Hospitalisé à 10 mois de sa dernière grossesse pour décompensation cardiaque globale • Se plaint depuis 2 mois d’une dyspnée d’effort Examen clinique initial : • Etat général conservé, apyrétique, TA 120/70, FC 90/min • Dyspnée NYHA III • Bruit du Coeur régulier, souffle systolique de 3/6ème mitral • Signes d’insuffisance cardiaque gauche : crépitants aux bases pulmonaires • Signes d’insuffisance cardiaque droite : OMI, hepatomegalie, reflux hépato-jugulaire Examens complémentaires • ECG : ryhtme sinusal à 90/min, trouble de la repolarisation non spécifique • Radio thorax : cardiomégalie, syndrome interstitiel accentué au hile • Biologie : normale sauf NTproBNP 2000 pg/ml, troponine négative • ETT : VG dilaté - parois normotrophiques avec hypokinésie globale FEVG = 33% OG dilatée Cavités droites non dilatés, pas d’HTAP Fuite mitrale modérée Diagnostic et PEC • Insuffisance cardiaque globale sur cardiomyopathie dilatée, hypokinétique, non connue auparavant chez une patiente de 36 ans • Hypothèse : cardiomyopathie dilatée liée à la grossesse à Coroscanner : normal à IRM cardiaque : cardiomyopathie dilatée non ischémique, VG dilaté, FE à 33%. Pas d’étiologie spécifique retrouvée = élimination diagnostic différentiel • Traitement médical débuté : Triatec, Bisoprolol, Lasilix, Kardégic Evolution • Suivi régulier, tous les 6 mois : – Persistance d’une fonction VG altérée (FEVG = 40%) à 2 ans de l’épisode initial mais stabilité – Asymptomatique dans la vie quotidienne, pas de dyspnée au repos ou à l’effort modérée • Discussion de la mise en place d’une DAI • CAT en cas de nouvelle grossesse? Nouvelle grossesse • Se présente en février 2015, enceinte à 7 SA +2 jour • Staff pluridisciplinaire DAN : demande d’ITG d’indication maternelle • Consultation d’anesthésie : insuffisance cardiaque à Aspiration sous AL potentialisée plutôt qu’AG • Réalisation de l’Aspiration le 27/02/15 sous AL + Propofol en titration (total = 80 mg). Stabilité tensionnelle per et post opératoire Définition CMP-PP • Cardiomyopathie idiopathique : – signes cliniques d’IC secondaire à dysfonction VG au 3ème trimestre ou dans les mois suivant l’accouchement à pic dans le premier mois post accouchement – Absence de cause identifiable à l’insuffisance cardiaque = dg d’élimination – Absence de cardiopathie pré-existante – Altération Echocardiographique de la fonction systolique du VG, FEVG < 45% (+/- dilatation ventriculaire) Pic de fréquence des cardiomyopathie au cours du péri-­‐partum Epidémiologie • Incidence très variable de 1/1000 à 1/4000 naissances • Facteurs de risque : – Age maternel > 30 ans – Multiparité – Grossesses gémellaires – Origine Africaine – Obésité – Pré-eclempsie et HTA gravidique – Tocolyse prolongée (> 4 semaines) Physiopathologie G Vanzetto, A Martin, H Bouvaist, S Marlière, M Durand, O Chavanon Figure 1 Ensemble des mécanismes physiopathologiques supposés ou démontrés contribuant à la survenue d’une cardiomyopathie du Changements physiologiques • 50% d’augmentation du volume intravasculaire : pic au début/milieu du 3ème trimestre • Diminution progressive des résistances vasculaires systémiques et Augmentation DC (30-40%) à PAM conservée, augmentation 15% FC • Variations importantes DC durant le travail avec tachycardie et augmentation ~ 500 ml de volume sanguin dans la circulation à chaque contraction • Etat d’hypercoagulabilité • Diminution de la CRF Physiopathologie • Hypothèse inflammatoire : – Biopsies myocardique : lésion « myocardite aigue » – Perturbation réponse inflammatoire au cours de la grossesse – Facteur infectieux initiant/aggravant cette réaction inflammatoire inappropriée : virus • Hypothèse Auto-immune : – Ac anti actine, anti myosine utérins libérés – Modification immunitaire de fin de grossesse (perte de la tolérance immunologique du fœtus / persistance Ag fœtaux circulant) • Hypothèse Hormonale : élévation stress oxydatif à activation cathepsine D à clivage en la prolactine en 16kDAProlactine à dysfonction cardiomyocytes, endothéliales Diagnostic différentiel • Eliminer une cardiopathie préalable à la grossesse (interrogatoire) : – Cardiomyopathie dilatée familiale – Antécédents de cardiopathies hypertrophiques – Prise anthracyclines • Eliminer une cause aigue de dysfonction systolique ventriculaire gauche : – Infarctus du myocarde ( ECG +++ et coronarographie si besoin) – Myopéricardite (Fièvre, syndrome inflammatoire +/- douleurs thoraciques, ETT, IRM si diagnostic très suspect) – Valvulopathies (ETT) Diagnostic différentiel • Atteinte cardiaque de la pré-éclampsie – dysfonction diastolique – Pression remplissage élevée MAIS fonction systolique normale • Pré-eclampsie et CMP-PP partagent certains mécanismes physiopathologiques (lésions endothélium) • Plusieurs cohortes de patiente avec CMP PP : grande prévalence d’HTA/pré-éclampsie à pré-éclempsie prédispose à CMP-PP ? • Résolution rapide après l’accouchement Versus traitement et suivi de plusieurs mois Diagnostic • Clinique : – Typique d’insuffisance cardiaque : • DYSPNEE (superficielle à l’effort puis d’aggrave rapidement) • OAP inaugurale, toux nocturne, majorée par décubitus • Signes Insuffisance cardiaque gauche et droite – Signes non spécifiques : • Douleur thoracique, palpitations • Embolies systémiques ou pulmonaires Diagnostic • Paraclinique : – ECG : non spécifique, tachycardie, trouble du rythme, trouble repolarisation à type ondes T négatives – Radio de Thorax : cardiomégalie – ETT : examen clé = dysfonction systolique ventriculaire gauche et dilatation ventriculaire +/- sévère Diagnostic IRM cardiaque: éliminer diagnostic différentiel • Fibroses myocardique : hypersignal, rehaussement tardif = absente à élimine myocardite • Eliminer ischémie (dissection coronaire au cours effort acchmt) • Estimation fonction VG, volume • Détection thrombi PAS DE REHAUSSEMENT TARDIF APRES GADOLINIUM ICI SUR VG MODEREMENT DILATE Pronostic • Favorable dans 50% des cas : récupération complète de la fonction systolique VG • Amélioration partielle de la fonction systolique dans la majeur partie autres cas Rare cas de défaillance myocardique sévère pouvant aboutir à la nécessité d’un support HD (ECMO) voir d’une greffe (<10%) à Mortalité : 1 à 2% • • Facteur de mauvais pronostic : – Gravité de la défaillance HD initiale et sa réponse au ttt – Complications emboliques – Existence d’une cardiopathie séquellaire au delà du 6ème mois après diagnostic Prise en charge initiale • Traitement conventionnel : – – – – – Restriction hydro-sodée Diurétique de l’anse, dérivés nitrés si signes congestifs IEC dans le post partum (Teratogène + IRA) ß bloquant cardiosélectif +/- antialdostérone • Traitement anticoagulant : Héparinothérapie dose curative phase aigue – thrombus à l’écho – passage en ACFA • Si HD instable : inotrope positif (dobutamine) • • Assistance circulatoire Transplantation cardiaque Prise en charge obstétricale (CMP 3ème trimestre) • Collaboration multidisciplinaire (GO,AR,Cardio,Néonat) • Planifier un déclenchement ou une extraction Pas de recommandations • Césarienne = risque hémorragique, thrombo-embolique, infectieux si FEVG < 35% ? VERSUS • Voie basse = augmentation du débit cardiaque Eviter épreuve d’effort, travail long, douloureux Abréger l’expulsion : forceps Possible si état cardiaque stable (FEVG > 35% ?) Prise en charge anesthésique Pas de consensus : idem insuffisant cardiaque Voie basse Analgésie péridurale – Titration des AL pour éviter modification HD – Association AL faible dose/concentration + morphinique = Bloc d’installation très progressive – Traitement de l’hypotension artérielle : phényléphrine ou ephédrine-phényléphrine à éviter tachycardie maternelle / maintien perfusion utérine – Proclive latéralisée à gauche Prise en charge anesthésique Pas de consensus : idem insuffisant cardiaque Césarienne APD seule /APD-Rachi / Rachianesthésie continue AG : à éviter • IOT séquence rapide : etomidate, celocurine, morphinique • Stabilité hémodynamique (monitorage ++) – Induction lente, dosage réduit – Pré-charge : monitorer le remplissage, peu de préchargedépendance. – Post-charge : maintenir basse à pression perfusion coronnaire – Correction HD avec vasoconstricteurs, inotropes, sans modifier profondeur anesthésie – Halogénés : Sevoflurane Prise en charge anesthésique Abaisser la postcharge Favoriser la contractilité Apport d’oxygène Monitorage fonction cardiaque remplissage Ocytocine CI relative Nalador Normothermie Analgésie ✔Surveillance post op continue USI Rappels • Péridurale lombaire : – VasodilataJon veineuse, baisse du retour veineux, bradycardie • Rachianesthésie : sympathicolyse brutale • AG : – VenJlaJon mécanique en pression posiJve : diminuJon pré-­‐charge, augmentaJon post charge – Agents anesthésiques Prise en charge au long cours IEC B bloquant Diurétique si nécessaire (Pression remplissage élevées) Aldactone si NYHA ≥ II - III Surveillance régulière : clinique + ETT Si persistance FEVG ≤ 35% : discussion DAI en prévention primaire de TdR ventriculaire +/stimulation multi-sites si présence BBG complet • Transplantation cardiaque • • • • • • Traitements spécifiques sans preuves : Immunoglobuline IV , Immunosupresseur Bromocriptine (en cours d’étude) Prise en charge obstétricale C-I de la contraception oestro-progestative Récidive grossesse ultérieure : 25 à 100% - - - - Contre indiqué si FEVG < 50% Déconseiller même si récupération complète (info patiente ++) IMG en cas dégradation de FEVG au cours 1 ou 2ème trimestre Cardiomyopathie du péripartum Journées européennes de la Société française de Intérêt ETT dépistage ? Tableau I Perspectives thérapeutiques Évolution en cas de nouvelle grossesse (d’après [23]) D’autres approches, telles que l’administration globulines IV, seraient à évaluer de manière [26]. De même, l’ajout d’un traitement anti-TN pentoxifylline) au traitement conventionnel semb les chances de normalisation de la fonction systoli manière plus récente, l’équipe de Hilfiker-Kleiner dant sur les données de leur modèle expérim impliquant un produit issu de la dégradation de dans la dysfonction systolique ventriculaire au cou (cf chapitre Physiopathologie), a testé l’intérêt po traitement par bromocriptine dans un essai de randomisé sur 12 patientes gravides ayant des ant CPP. Les 6 patientes traitées par bromocriptine pronostic favorable et sont demeurées asymptoma que 3 des 6 patientes non traitées par bromoc Fonction Persistance systolique d’une dysfonction normalisée systolique Risque d’insuffisance cardiaque 26 % 50 % Dégradation de la FEVG > 20 % 17 % 33 % Risque d’accouchement prématuré 13 % 50 % Risque de décès de la patiente 0% 25 % Retour à la fonction systolique initiale (avant la seconde grossesse) 90 % 60 % (FEVG : fraction d’éjection ventriculaire gauche). Conclusion • • • • • • • • Cause rare d’insuffisance cardiaque Physiopathologie incertaine Pas de traitement spécifique pour l’instant Evolution favorable dans majorité des cas sous traitement médical simple Rare cas de défaillance cardiaque sévère = transplantation, décès Suivi au long cours si récupération incomplète Risque lors nouvelle grossesse ++ PEC Multidisciplinaire Can J Anesth/J Can Anesth (2015) 62:278–288 DOI 10.1007/s12630-014-0290-y CASE REPORTS / CASE SERIES Anesthetic management and outcomes of parturients with dilated cardiomyopathy in an academic centre Gestion anesthésique et évolution de parturientes atteintes de cardiomyopathie dilatée dans un centre universitaire Unyime S. Ituk, MBBS • Ashraf S. Habib, MBBCh Carrie M. Polin, MD • Terrence K. Allen, MBBS • Received: 22 January 2014 / Accepted: 2 December 2014 / Published online: 11 December 2014 ! Canadian Anesthesiologists’ Society 2014 Abstract Purpose This study examines the peripartum anesthetic management and outcomes of women with dilated cardiomyopathy in a large university medical centre over a seven-year period. Principal findings Twenty-five women were included in this series, 18 with a new diagnosis of cardiomyopathy and seven with a history of cardiomyopathy. Sixteen patients (64%) identified themselves as African American, seven and 15 operative deliveries. One patient had fetal loss at 19 weeks gestation. Twelve women had labour induced with an intravenous infusion of oxytocin at a rate of 0.0010.02 IU!min-1. An oxytocin infusion at a variable rate with a maximum dose of 0.05 IU!min-1 was administered after vaginal delivery to maintain uterine tone. Epidural analgesia was initiated prior to induction of labour or in the latent phase of labour. Seven Cesarean deliveries were performed under combined spinal-epidural anesthesia, five Cardiomyopathy in pregnancy 281 Table 1 Patient characteristics Patient Age (yr) BMI (kg!m-2) Gravidity/ Parity Gestational age at diagnosis (weeks) LVEF (%) Interval between LVEF measurement and delivery (weeks) NYHA class Other Medical history 1 43 28 G1P0 31 35 \1 III HTN 2 26 38 G1P0 28 15 2 IV GDM 3 4 34 37 50 42 G6P4 G6P2 29 19 30 15 7 \1 II II HTN, GDM HTN 5 34 37 G11P0 30 35 1 II HTN, DM 6 30 36 G4P1 29 35 3 II AICD 7 32 27 G4P1 25 40 7 I - 8 30 28 G5P4 Pre-existing 30 3 II Congenital endocardiofibroelastosis 9 39 40 G12P8 31 25 \1 II HTN 10 28 26 G7P2 38 35 \1 II - 11 40 28 G1P0 35 35 \1 III DM, HTN, CAD 12 29 40 G1P0 34 15 \1 IV DM, HTN 13 32 50 G4P2 18 40 4 III Sleep apnea 14 15 29 28 43 29 G3P2 G4P2 36 24 35 20 \1 2 III III Preeclampsia - 16 27 44 G5P3 Pre-existing 40 4 I HTN 17 33 27 G1P0 Pre-existing 35 7 I A-V block, pacemaker 18 29 28 G2P1 7 40 9 II - 19 36 60 G6P3 Pre-existing 45 6 II HTN, Preeclampsia 20 37 48 G3P2 Pre-existing 20 2 III DM 21 34 48 G11P0 29 35 5 II HTN, DM 22 24 28 G2P1 Pre-existing 40 2 II - 23 25 50 G8P4 22 35 4 II HTN, DM 24 32 38 G4P3 8 40 8 II ASD 25 31 43 G4P2 Pre-existing 40 2 II Atrial fibrillation BMI = body mass index; A-V block = atrioventricular block; LVEF = left ventricular ejection fraction; NYHA = New York Heart Association; HTN = hypertension; GDM = gestational diabetes mellitus; DM = diabetes mellitus; AICD = automatic implantable cardioverter–defibrillator; CAD = coronary artery disease; ASD = atrial septal defect induction of labour or in the latent phase of labour. The Seven Cesarean deliveries were performed under Patient Gestation (weeks) at delivery Mode of delivery Urgency of delivery Indication for Cesarean delivery Type of Anesthesia Invasive Monitoring Neonatal weight (grams)/APGAR score Peripartum Complications 1 31 Cesarean Scheduled Breech presentation CSE ABP 1,860/6,1 - 2 31 Cesarean Scheduled Breech presentation CSE ABP, PAC 1,865/8,9 Cardiogenic shock, LV clot 3 4 36 19 Cesarean D & E (IUFD) Scheduled - Breech presentation - CSE CSE ABP ABP 3,875/9,9 - - 5 32 Cesarean Scheduled Breech presentation CSE ABP 1,560/9,9 Wound sepsis 6 32 FAVD - - Epidural ABP 1,420/3,6 - 7 37 FAVD - - Epidural ABP 2,480/8,9 - 8 31 FAVD - - Epidural ABP 1,780/4,8 - 9 31 SVD - - None None 1,820/8,9 1,730/4,8 Precipitous labour 10 38 Cesarean Emergent NRFHT* Epidural ABP, CVC 3,645/9,9 Uterine atony 11 35 Cesarean Urgent Deteriorating cardiac function Epidural ABP 2,250/7,8 - 12 34 Cesarean Urgent Deteriorating cardiac function General ABP, PAC 2,080/9,9 SVT requiring cardioversion 13 39 FAVD - - Epidural None 3,070/8,9 - 14 36 Cesarean Urgent Deteriorating cardiac function ABP, CVC 2,800/5,8 Pulmonary edema 15 34 FAVD - General (Failed epidural) Epidural ABP, CVC 2,620/8,9 - 16 33 Cesarean Urgent Placenta previa CSE CVC 2,030/6,7 - 17 40 Cesarean Scheduled Breech presentation CSE None 3,905/8,9 - 18 38 FAVD - - Epidural None 3,150/9,9 - 19 38 Cesarean Emergent Severe Preeclampsia* General (Failed epidural) ABP, CVC 3,120/1,5 Cardiac Arrest 20 32 Cesarean Emergent NRFHT* Epidural ABP, CVC 1,890/8,9 PVC, atrial fibrillation 21 32 Cesarean Emergent NRFHT* Epidural None 1,560/9,9 Wound sepsis 22 33 Cesarean Urgent Deteriorating cardiac function Epidural None 2,080/9,9 - 23 32 Cesarean Urgent Previous Cesarean x3 CSE None 1,760/6,7 - 24 39 FAVD - - Epidural None 3,070/8,9 - 25 30 FAVD - - Epidural None 3,785/8,9 SVT Cardiomyopathy in pregnancy Table 3 Mode of delivery and anesthetic management 283 123 CSE = combined spinal-epidural; ABP = intra-arterial blood pressure; PAC = pulmonary artery catheter; LV = left ventricle; D & E = dilatation and evacuation; IUFD = intrauterine fetal demise; FAVD = forceps-assisted vaginal delivery; SVD = spontaneous vaginal delivery; NRFHT = non-reassuring fetal heart tone; CVC = central venous catheter; SVT = supraventricular tachycardia; PVC = premature ventricular contraction. APGAR scores were measured at one and five minutes. *Labouring prior to Cesarean delivery Bibliographie • Mise au point 2012 - Journées Européennes de la SFC Cardiomyopathie du péripartum - Gérald Vanzetto, Alix Martin, Hélène Bouvaist, Stéphanie Marlière, Michel Durand, Olivier Chavanon • Cardiopathies et grossesse – SFAR – Vincent Laudenbach • Précis d’anesthésie cardiaque – Chapitre 13 Anesthésie et cardiomyopathie • Pregnancy and non-valvular heart disease--anesthetic considerations – Annals of cardiac anesthesia 2010 • Peripartum cardiomyopathy : current management and future perspectives – European Heart Journal, 2015 Remerciement • Docteur David Berville, Cardiologue, CHI de Poissy Merci de votre attention oughout pregnancy and postpartum (Table 1). So n unspecific marker for pregnancy complications sia as well as for heart failure and other diseases, ed in most PPCM patients with little overlap to m women (Table 1).23,39,40 MiR-146a is specifically erum of PPCM patients compared with healthy n and patients with DCM (Table 1).23,38 sFlt1, a clampsia that is supposed to clear rapidly after dey increased in PPCM patients as are asymmetric nd Cathepsin D activity (Table 1).23,33 Failure to marker profile including NT-proBNP, oxLDL, prolactin is associated with adverse outcome in In turn, creatine-kinase and C-reactive protein elivery stress in healthy postpartum women and rker for cardiac injury, is often within normal tients (Table 1) and therefore less suited as bio.11 currently NT-proBNP is the only commercially or efficient screening of peripartum heart failure r, it is not specific for PPCM and may be elevated s such as preeclampsia and pulmonary embolism. ase specific potential candidate, but overall there or better diagnostic and prognostic biomarkers Table 1 Overview of biomarkers analysed in peripartum cardiomyopathy patients Biomarker Relevance for PPCM NT-proBNP Not specific for PPCM, but good sensitivity for heart failure.23,39 16-kDa Prolactin Pathophysiological factor of PPCM, high technical effort for measurement, diagnostic accuracy needs to be evaluated.37,42 Elevated plasma levels in PPCM patients, diagnostic accuracy needs to be evaluated.39,49 ................................................................................ Interferon-g Asymmetric Dimethylarginine (ADMA) Cathepsin D Marker for endothelial dysfunction and cardiovascular risk, diagnostic accuracy needs to be evaluated.23 Activity elevated in plasma of PPCM patients, diagnostic accuracy needs to be further evaluated.23,37 Soluble fms-like tyrosine kinase-1 (sFlt-1) Elevated plasma levels in PPCM patients, diagnostic accuracy needs to be further evaluated.33 Pathophysiological factor of PPCM, high technical effort for measurement, diagnostic accuracy needs to be further evaluated.23,38 microRNA-146a PPCM, peripartum cardiomyopathy. protein and tumour necrosis factor-a, TNF-a) after treatment with pentoxifylline on top of conventional heart failure therapy sug- Downloaded from by guest on Ap tic concepts and ment for peripartum opathy D. Hilfiker-Kleiner et al. A.T. Dennis, J.M. Castro Table 1 263 Comparison of heart failure in peripartum cardiomyopathy and heart failure in preeclampsia Pathological mechanism Additional features Hypertension Proteinuria Associated features Haemolysis Abnormal liver function Thrombocytopenia Seizures Renal dysfunction Vascular thrombus Arrhythmia Mitral regurgitation Echocardiography features Cardiac volumes and structure Left atrium volume Left ventricular volume Right ventricular volume Pericardial effusions Left ventricular hypertrophy Cardiac function Left ventricular systolic function Contractility Cardiac output Myocardial tissue Doppler systolic velocities Ejection fraction Right ventricular systolic function Diastolic function Initial pharmacological treatment Inotropic agents Systemic anticoagulation Antihypertensive agents Parenteral magnesium sulphate Peripartum cardiomyopathy Preeclampsia Systolic dysfunction Diastolic dysfunction No No Yes Often No No No No No Yes* Yes^ Yes Yes Yes Yes Yes Yes (proteinuria) Not reported Not reported Not reported Dilated Dilated Dilated Infrequent and small No! Normal Normal Normal Frequent and larger Frequent Reduced Reduced Reduced Reduced Reduced Reduced Normal! Preserved– Preserved Preserved/increased Normal range– Preserved– Not affected Abnormal/reduced Commonly used Yes No No Uncommonly used Uncommonly used Yes Yes Reported with severe ventricular dysfunction; ^Atrial fibrillation, ventricular tachycardia and ectopics reported; !Unless hypertension present before pregnancy; –Systolic function may be reduced in the presence of malignant hypertension. * The New England Journal of Medicine Co py r ight © 2 001 by t he Massachus et t s Medic al S o ciet y VOLUME 344 MAY 24, 2001 NUMBER 21 MATERNAL AND FETAL OUTCOMES OF SUBSEQUENT PREGNANCIES IN WOMEN WITH PERIPARTUM CARDIOMYOPATHY URI ELKAYAM, M.D., PADMINI P. TUMMALA, M.D., KALPANA RAO, M.D., MOHAMMED W. AKHTER, M.D., ILYAS S. KARAALP, M.D., OMAR R. WANI, M.D., AFSHAN HAMEED, M.D., ISRAEL GVIAZDA, B.S., AND AVRAHAM SHOTAN, M.D. ABSTRACT Background Peripartum cardiomyopathy is a rare but sometimes fatal form of heart failure. Little is known about the outcomes of subsequent pregnancies in women who have had the disorder. Methods Through a survey of members of the American College of Cardiology, we identified 44 women who had had peripartum cardiomyopathy and had a total of 60 subsequent pregnancies. We then reviewed the medical records of these women and interviewed the women or their physicians. Results Among the first subsequent pregnancies in the 44 women, 28 occurred in women in whom left ventricular function had returned to normal (group 1) and 16 occurred in women with persistent left ventricular dysfunction (group 2). The pregnancies were associated with a reduction in the mean (±SD) left ventricular ejection fraction both in the total cohort (from 49±12 percent to 42±13 percent, P<0.001) and in each group separately (from 56±7 percent to 49±10 P ERIPARTUM cardiomyopathy is a rare form of heart failure of unknown cause that occurs during pregnancy or during the postpartum period.1-3 Although approximately 20 percent of women with the disorder either die or survive only because they receive cardiac transplants, the majority recover partially or completely. Although the women who recover may desire to become pregnant again, there is a concern that such pregnancies may be associated with an increased risk of recurrence of cardiomyopathy.1-4 Information about the outcome of additional pregnancies, however, is limited.4-8 There is therefore no consensus regarding recommendations for future pregnancies in women who have had peripartum cardiomyopathy.3 We undertook a study to determine maternal and fetal outcomes of subsequent pregnancy among women with a history of peripartum cardiomyopathy. METHODS T H E O U TC O M E S O F S U B S EQ U E N T P R EG N A N C I E S I N WO M E N W I T H P E R I PA R T U M C A R D I O M YO PAT H Y 60 All women! Group 1! Group 2 50 56±7 52±9 49±10 49±12 Percentage of Women 45±13 42±13 40 32±11 30 36±9 34±11 36±13 32±11 28±12 20 10 0 IndexŁ Pregnancy PostpartumŁ Follow-up SubsequentŁ Pregnancy LastŁ Follow-up Figure 1. Mean (±SD) Left Ventricular Ejection Fraction in 44 Women at the Time of the Diagnosis of Peripartum Cardiomyopathy (Index Pregnancy), at Postpartum Follow-up, during the First Subsequent Pregnancy, and at the Last Follow-up a Mean of 72 Months after the First Subsequent Pregnancy. Group 1 included all the women with a left ventricular ejection fraction of 50 percent or higher before subsequent pregnancies, and group 2 included all those with a left ventricular ejection fraction of less than 50 percent before subsequent pregnancies. For the total cohort (all women), P<0.001 for the comparison between postpartum follow-up and the index pregnancy, P<0.001 for the comparison between subsequent pregnancy and postpartum follow up, and P=0.06 for the comparison between last follow-up and subsequent pregnancy. For group 1, P<0.001 for the comparison between postpartum follow-up and the index pregnancy, P=0.002 for the comparison between subsequent pregnancy and postpartum follow-up, and P=0.06 for the comparison between last followup and subsequent pregnancy. For group 2, P=0.05 for the comparison between postpartum follow-up and the index pregnancy and P=0.08 for the comparison between subsequent pregnancy and postpartum follow-up. Fetal Outcome Among the 35 women who had a subsequent pregnancy and did not have an abortion, 21 had a normal vaginal delivery, and 14 delivered by cesarean section. Premature delivery (defined as delivery at less than 37 weeks’ gestation) occurred in three women (13 percent of the subgroup) in group 1 (at 30, 32, and 36 weeks) and in six women (50 percent of the subgroup) TABLE 1. INCIDENCE OF MATERNAL COMPLICATIONS DURING THE FIRST SUBSEQUENT PREGNANCY IN WOMEN WHO HAD HAD PERIPARTUM CARDIOMYOPATHY.* GROUP NO. OF WOMEN SYMPTOMS OF HEART FAILURE >20% DECREASED DECREASE LVEF AT FOLLOW-UP IN LVEF no. of women (%) DEATH son between subsequent pregnancy and postpartum follow-up. n who had a subsequent pregan abortion, 21 had a normal delivered by cesarean section. ined as delivery at less than 37 rred in three women (13 pern group 1 (at 30, 32, and 36 n (50 percent of the subgroup) at 30 weeks, one at 34 weeks, wo at 36 weeks). There was no the nine abortions, five were se occurred in group 1 (4 peruent pregnancies) and the othpercent of the first subsequent n had 16 additional pregnangroup 1, five women had one ach and four women had two each; of those in group 2, one TABLE 1. INCIDENCE OF MATERNAL COMPLICATIONS DURING THE FIRST SUBSEQUENT PREGNANCY IN WOMEN WHO HAD HAD PERIPARTUM CARDIOMYOPATHY.* GROUP NO. OF WOMEN SYMPTOMS OF HEART FAILURE >20% DECREASED DECREASE LVEF AT FOLLOW-UP IN LVEF DEATH no. of women (%) All women Group 1 Group 2 Women who did not have abortions Group 1 Group 2 44 28 16 35 6 (21) 7 (44) 6 (21) 4 (25) 4 (14) 5 (31) 0 3 (19)† 23 12 6 (26) 6 (50) 4 (17) 4 (33) 2 (9) 5 (42) 0 3 (25)‡ *Group 1 consisted of women with recovered left ventricular function, defined as a left ventricular ejection fraction (LVEF) of 50 percent or higher, before the subsequent pregnancy; group 2 consisted of women with persistent left ventricular dysfunction (an LVEF of less than 50 percent). †P=0.06 for the comparison with group 1. ‡P=0.05 for the comparison with group 1. N Engl J Med, Vol. 344, No. 21 · May 24, 2001 · www.nejm.org · 1569 The New England Journal of Medicine wnloaded from nejm.org at INSERM DISC DOC on April 11, 2015. For personal use only. No other uses without permission. Copyright © 2001 Massachusetts Medical Society. All rights reserved. nector showing the arch in the midline on the nt flap and then slightly pulled the catheter . Finally thinking that there is a blood ther sort of blockade we pulled out the rprise, it was clear. We rechecked the t the catheter tip connecter (click and ] once placed and clicked for fixing, nd if loosely fixed the drug spilled by ched another connector over the same ned well after clicking. gs through malfunctioning epidural ported,[1,2] but blockade caused by and ready connector has not been The connector (click and ready) has base (Lemon yellow) through which the other is the flap (Transparent) on licks and holds the catheter in place. paratus is an easy and convenient way atheter to the syringe prior to the filter ncreased grip strength and providing Department of Anaesthesiology, Lady Hardinge Medical College, New Delhi, India Address for correspondence: Dr. Devalina Goswami, Type V, Block 3, Quarter No 17, Lodhi Road Complex Govt Quarters, New Delhi-110 003, India. E-mail: [email protected] Case Report References Importance of transesophageal echocardiography in peripartum Gupta S, Singh B, Kachru N. "Blocked" epidural catheter: Another cause. Anesth Analg 2001;92:1617-8. cardiomyopathy undergoing lower section cesarean section 2. Arnaoutoglou HM, Tzimas PG, Papadopoulos GS. Knotting of an epidural catheter: A rare complication. Acta Anaesthesiol Belg under regional anesthesia 2007;58:55-7. 1. Access this article online Goyal, Kalpana Irpachi, Barya Smita1 Poonam Malhotra Kapoor, Sameer Quick of Response Department Cardiac Code: Anaesthesia, CTC, AIIMS, 1Department of Obstetrics and Gynaecology, Pt. Madam Mohan Malviya Hospital, New Delhi, India Website: www.joacp.org Journal of Anaesthesiology Clinical Pharmacology | July-­‐September 2014 Abstract DOI: 10.4103/0970-9185.86614 Peripartum cardiomyopathy is a relatively rare but life threatening disease. The etiology and pathogenesis of peripartum cardiomyopathy is generally centered upon viral and autoimmune mechanism. This case report describes the anesthetic management of a patient with term pregnancy suffering from dilated peripartum cardiomyopathy planned for cesarean section , successfully managed with epidural anesthesia after precipitate labour. Key words: Epidural anesthesia, peripartum dilated cardiomyopathy, precipitate labor Low dose spinal anesthesia for peripartum A workshop organized by the National Heart, Lung, and Blood Introduction cardiomyopathy Institute and the Office of Rare Diseases Research in 1997 Journal of cardiomyopathy Anaesthesiology Clinical Pharmacology ctober-­‐December an additional criterion proposed by Hibbard et al.[2] Peripartum (PPC) is a relatively rare form | Oadded Sir, of left ventricular (LV) systolic dysfunction demonstrated by 2011 Vol 2failure 7 | Issue of acute|heart (HF)4 associated with pregnancy. The [1] Peripartumpresents cardiomyopathy is many a dilated cardiomyopathy diagnosis a challenge as full term parturients associated with cardiac failure in the last month of pregnancy experience dyspnea, fatigue, and peripheral edema. Pearson or within five monthsdata of delivery. is nowith identifiable cause et al.[1] published on 27There patients pregnancyof cardiac failure, no heart disease prior to the last month of associated cardiomyopathy who presented in the peripartum pregnancy, and left ventricular systolic dysfunction. It has period. These investigators coined the term “PPC” and defined diagnostic criteria on the basis of their patient’s 567 Clinical Pharmacology | October-December 2011 | Vol 27 | Issue 4 characteristics and available diagnostic tools at the time. These criteria included: 1. The development of HF in the last month of pregnancy or within 5 months of delivery; 2. The absence of a determinable etiology for HF; and 3. The absence of demonstrable heart disease before the last month of pregnancy. echocardiography with LV ejection fraction (LVEF) 45%, fractional shortening 30%, or both. As there is paucity in literature to emphasize, the role of transesophageal echocardiography (TEE) being a mandatory diagnostic tool in such cases under regional anesthesia, we report a case of PPC in which TEE was used judiciously to optimize the fetal and maternal outcome. Case Report A 22-year-old woman, presented as gravida 1, para 0, at 37 weeks of gestation, with pregnancy induced hypertension and symptoms of cardiac failure. At 36th week of pregnancy, the patient had developed shortness of breath on mild exertion, Journal of the American College of Cardiology ! 2014 by the American College of Cardiology Foundation Published by Elsevier Inc. Vol. 63, No. 25, 2014 ISSN 0735-1097/$36.00 http://dx.doi.org/10.1016/j.jacc.2014.04.014 Peripartum Cardiomyopathy Predictors of Recovery and Current State of Implantable Cardioverter-Defibrillator Use Jayasree Pillarisetti, MD, MSC,* Ashok Kondur, MD,y Anas Alani, MD,y Madhu Reddy, MD,* Madhuri Reddy, MD,z James Vacek, MD, MSC,* Carl P. Weiner, MD,z Edward Ellerbeck, MD, MPH,x Theodore Schreiber, MD,y Dhanunjaya Lakkireddy, MD* Kansas City, Kansas; and Detroit, Michigan Objectives The purpose of this study was to identify the predictors of left ventricular (LV) recovery in patients with peripartum cardiomyopathy (PPCM) and to record rates of implantable cardioverter-defibrillator (ICD) use. Background PPCM is a rare, life-threatening disease. The use of ICDs has not been clearly understood in this patient group. Identification of the predictors of persistent LV dysfunction can help select patients at risk for sudden cardiac death. Methods A retrospective study was conducted at 2 academic centers between January 1, 1999, and December 31, 2012. Clinical and demographic variables and delivery records of patients with a diagnosis of PPCM (International Classification of Diseases, 9th Revision code 674.5) were reviewed. Improvement in LV function was noted from echocardiography reports. Results The total sample comprised 100 patients, of whom 55% were African Americans, 39% were Caucasians, and 6% were Hispanic, with a mean age of 30 ! 6 years. Mean left ventricular ejection fraction (LVEF) at diagnosis was 28 ! 9%. Forty-two percent of patients showed improvement in LVEF over a mean duration of 33 ! 21 months. Postpartum diagnosis (hazard ratio: 3.0; p ¼ 0.01) and Caucasian/Hispanic race (hazard ratio: 2.2; p ¼ 0.01) were predictors of improvement in LVEF. Only 7 of the 58 patients (12%) who did not have improvement in their LVEF had an ICD implanted. There were 11 deaths, with a trend toward higher mortality in those who did not display improved LV function (15% vs. 5%; p ¼ 0.1). Conclusions More than one-third of women with PPCM improve LV function with delayed recovery noted in the majority of these patients. Caucasians and those diagnosed in the postpartum period appear to be the most likely to recover. The rate of ICD implantation for primary prevention of sudden cardiac death in this patient group is low. (J Am Coll Cardiol 2014;63:2831–9) ª 2014 by the American College of Cardiology Foundation Peripartum cardiomyopathy (PPCM) is a rare, idiopathic cardiomyopathy characterized by the development of systolic heart failure toward the end of pregnancy or in the months after delivery (1,2). The reported incidence shows significant geodemographic variation, from 1 in 500 live births in Haiti to 1 in 4000 live births in the United States (3–6). Identified risk factors for PPCM include multiparity, advanced maternal age, twins, preeclampsia, gestational hypertension, and African-American race (1,2,7–9). Despite the recognition of this disease as a separate entity in 1937, the mortality rates are not yet well characterized (8–19), ranging from 4% to 50% (2,8–19). At least one-fourth of deaths in PPCM are sudden cardiac deaths presumed to be caused by ventricular tachyarrhythmias (16). Sudden cardiac
