EARLY DEGENERATED BIOPROSTHETIC MITRAL VALVE
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1 10 CASE PRESENTATIONS EARLY DEGENERATED BIOPROSTHETIC MITRAL VALVE Irina-Mihaela Ciomaga, Georgiana Russu, Cristina Jitareanu, Violeta Streanga, Aniela Rugina, Nicolai Nistor Sf. Maria Emergency Hospital for Children, Gr. T. Popa University of Medicine and Pharmacy, Iasi ABSTRACT Mitral valve prolapse (MVP) is fairly common in children, often being randomly found in asymptomatic, as well as in symptomatic patients with conjunctive tissue diseases (CTD). The authors report the case of an 11-yearold girl, diagnosed at the age of 6 with MVP and severe mitral regurgitation (MR). She had surgery at the age of seven, when the mitral valve replacement with a biological valve prosthesis was performed. Four years later, the girl was admitted for sudden onset of dyspnoea with orthopnoea, haemoptysis and generalized cyanosis. The diagnosis of acute pulmonary oedema and degenerated biological valvular prosthesis correlated with severe mitral stenosis was evoked by means of clinical and echocardiographic examinations. The evolution was favourable after the replacement of the bioprosthesis with a mechanical prosthesis. Keywords: bioprosthesis, mitral valve, child INTRODUCTION The mitral valve ring is nonplanar and saddleshaped. Usually, the valvular leaflets are shoved towards each other by the papillary muscles contraction and by the chordae tension during ventricular systolic, which leads to the coaptation of the edges of the valve. The valvular prolapse occurs when one valve slides under this coaptation area. The idiopathic mitral valve prolapse (MVP) can occur congenitally, but it is often diagnosed later during adolescence or adulthood. Some of the complications may include arrhythmias, heart failure due to severe mitral regurgitation (MR) or, sometimes, thromboembolic events. Familial cases are autosomally dominant with variable penetrance and expression. Treatment is directed by the presence or the absence of complications. Thus, the asymptomatic cases presenting minimal MR do not require medical treatment, but those with ventricular dysfunction and severe MR require surgical treatment. CASE We present the case of a female child, aged 11 years old, diagnosed at age of 6 with mitral valve prolapse and severe mitral regurgitation. When she was 7, she underwent the replacement of the mitral valve with tissue valve prosthesis which was performed at the Institute for Cardiovascular Diseases and Transplantation from Târgu Mureş. The procedure was followed by chronic treatment with anticoagulants (Sintrom, Aspenter). Four years after inserting the prosthetic valve, the girl presented sudden dyspnea, orthopnea, hemoptysis and generalized cyanosis. She was admitted to the pediatric ward of a county hospital and she was treated with antibiotics (Cefort), mucolytics and cortisone preparations for 7 days. Symptoms initially improved but eventually got worse, so that pulmonary embolism was suspected and the patient was transferred to Acute Care Department of 1-st Pediatrics Clinic from Iaşi. Corresponding author: Georgiana Russu, Sf. Maria Children s Emergency Hospital, 62 Vasile Lupu Street, Iasi g_russu@yahoo.com 276 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN 2014
2 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN On admission, physical examination revealed severe general condition, suffering face, pale skin and mucous membranes, postoperative scar on the mid-sternal line, significant dyspnea and orthopnea, respiratory frequency = 56/min, productive cough, hypoxemia SaO 2 = 85-89% in the atmospheric air. The pulmonary auscultation revealed bilateral crepitation rales, rhythmic heart sounds, tachycardia 130/min, systolic murmur grade III/6 at the apex with posterior radiation, normal liver. The biological exam highlighted neutrophilic leukocytosis, mild hepatocytolisis, elevated creatinphosphokinase level, elongated prothrombin time and decreased prothrombin activity due to the anticoagulant treatment. Chest X-ray showed adjoining macro-opacities occupying almost entirely the both pulmonary areas, bulging cord with right lower arch, normal vascular pedicle. ECG showed sinus tachycardia 140/minute, QRS axis of + 90, PQ = 0.12 sec; ST depression (4 mm) in the PRD, DIII, AVF, V3-V5; biatrial overload; QT = 0.28 sec (normal). Echocardiography performed by emergency (see Fig. 1) showed hyperechoeic prosthesis in dysfunctional mitral position, limited opening, creating severe stenosis and grade III mitral regurgitation, significant dilatation of the pulmonary artery and right heart, grade III tricuspid regurgitation. Positive diagnose was established: acute pulmonary oedema, severe mitral stenosis by degenerated bioprosthesis, pulmonary hypertension. The patient was urgently transferred to the Cardiovascular Surgery Clinic of Iasi, where the replacement of bioprosthesis with a mechanical prosthesis was immediately performed. The postoperative evolution was favourable, overall condition improved, yet a complication occured: an externally popliteal sciatic nerve paresis,which was cured through physiotherapy. DISCUSSIONS Classic MVP is defined as the displacement of one or both leaflets during systole, exceeding the mitral valve annular plane with 2 mm or more under the mitral ring, having as result leaflet thickening. Non-classic prolapse refers to leaflet displacement without valve thickening. The etiology of MVP is not clear and is probably multifactorial. It can result from excessive leaflet tissue (redundancy), myxomatous proliferation of the spongious layer of the valves, and elongation of the chordal apparatus. These alterations are met in the case of individuals with a wide range of congenital heart malformations as well as in acquired heart disease including collagen vascular disease (Marfan syndrome, Loeys-Dietz syndrome), ischemic heart disease, hypertrophic cardiomyopathy, and pectus excavatum, as well as in the case of thin patients (1). Isolated prolapse can be sporadic or familial, with autosomal dominant and x-linked transmission. Prevalence rates are 1-2% in children and 5-15% in adolescents and young adults, twice more frequent in females than in males (2,3). FIGURE 1
3 278 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN 2014 MVP is usually diagnosed on the clinical basis of a mid-systolic click of the mitral valve and a late systolic murmur of mitral regurgitation. Most patients are asymptomatic, and MVP is an incidental auscultatory finding, when a short systolic murmur is discovered in the mitral area. In time, various symptoms can occur: palpitations, fatigability and exertion dyspnea, chest pain, neuropsychiatric symptoms (panic attacks, nervousness, presyncope and syncope). Some patients present skeletal abnormalities that do not fit into any of the recognized connective tissue disorders (height-toweight ratio greater than normal, scoliosis, arachnodactily, pectus excavatum or pectus carinatum) (4). Arrhythmias described at rest or during exercise include premature atrial (23.6%) or ventricular (27.3%) contractions, supraventricular tachycardia, and conduction abnormalities (5). Some studies report a prevalence of ventricular arrhythmias over 30% (6). Also, in 8-16% of the patients with refractory ventricular tachycardia, the only cardiac anomaly was MVP. There is a connection between MVP and sudden death (7,8). If the incidence of sudden death in MVP is not well established, the studies suggest that the risk is 5 or 10 times greater in the cases in which there is also severe mitral regurgitation. It is considered that the relation between MVP and sudden death is due to ventricular arrhythmias (9). In children, the mortality rate is very low. The appearance of mitral regurgitation (MR) and the progression from mild or moderate MR to severe MR are important determinants to morbidity. A study made by Deng showed that the prevalence of MR increased from 29% of patients to 43% of patients during the four years of observation (10). Other possible complications include congestive cardiac failure, rupture of chordae tendineae, infective endocarditis (in cases per 100 patient years), thromboembolic phenomena including cerebrovascular accidents, and sudden death. Cardiac arrhythmias such as ventricular tachycardia and ventricular fibrillation are more common in MVP (2). In childhood, MVP is not progressive, and the majority of patients do not require specific therapy, but only periodic observation. Asymptomatic patients with isolated mitral systolic clicks need only counseling and reassurance. They are recommended to avoid excessive use of caffeine, cigarettes, alcohol, and prescription or over-the-counter drugs that contain stimulants such as epinephrine or ephedrine to minimize catecholamine and cyclic adenosine monophosphate (AMP) stimulation. The most recent recommendations have limited the indications of subacute bacterial endocarditis antibiotic prophylaxis only to patients with the highest risk, undergoing the highest risk procedures. In this category one can include: patients with a prosthetic valve or a prosthetic material used for cardiac valve repair, patients with previous endocarditis, patients with cyanotic congenital heart disease without surgical repair or with residual defects, palliative shunts or conduits, patients with congenital heart disease with complete repair with prosthetic material whether placed by surgery or by percutaneous technique, up to 6 months after the procedure and patients with a residual defect at the site of implantation of a prosthetic material or device by cardiac surgery or percutaneous technique. The antibiotic prophylaxis is no longer recommended for other valvular diseases or congenital heart diseases (11) The surgical treatment (plastic surgery of mitral valve or replacement with prosthesis) has precise indications established by the American and European guidelines: patients with moderate-severe MR, symptomatic patients with acute severe MR, symptomatic patients with severe chronic MR with cardiac failure New York Heart Association (NYHA) functional class II-IV symptoms, asymptomatic patients with chronic severe MR and mildto-moderate LV dysfunction or with preserved LV function, new onset atrial fibrillation, or pulmonary artery hypertension. In the case of children, surgery is indicated only when the medical treatment or the mitral valve repair have failed. In the case of patients younger than one year, the mitral valve replacement must be delayed as much as possible because it is associated with substantially increased risk of morbidity and mortality. The mitral valve replacement has as a result the highest mortality from all the other pediatric valve procedures (10-30%) and it has the worst long-term prognosis between 5 and10 years the survival is between 50-80% (13). Bioprosthetic xenografts have been found to have limited durability at the mitral position in the case of children, with a mortality between 79%, 75% and 74% at 1, 5 and 10 years respectively. This suggests the idea that the most part of the cases of mortality occur in the immediate postoperative period. (14) Comparing with mechanic prosthetic valves, bioprosthetic valves have the distinct advantage of not needing lifelong anticoagulation, but only three months after the surgery. The tissue of origin is generally porcine with the exception of a bovine pericardial valve manufactured from fixed bovine
4 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN pericardium. Xenografted valves calcify when placed into the human circulation, ultimately leading to their failure. This calcification process appears to occur more rapidly in the case of younger patients. Structural deterioration of bioprosthetic valves is an inevitable consequence of their utilization in the humans. This incidence is nonlinear with deterioration and subsequent failure increasing at a greater rate after a certain period of time. In the case of children this time frame is often very short (14). Actual data show that the medium life of a bioprosthesis in the case of adult in15 years (15). The given case follows the general trend described in literature, that of premature deterioration of the mitral bioprosthesis, in the first four years. The replacement by a mechanical valve saved the life of the patient, with a slow favorable evolution after surgery. Anticoagulant treatment was recommended, with regular INR follow-up, which must be maintained at an optimal value of Another recommendation was the endocarditis antibiotic prophylaxis. A peculiarity of the case is the external sciatic nerve paresis as a postoperative complication, alleviated through physiotherapy. CONCLUSIONS The cases with MVP with severe MR, like the presented case, require surgery for mitral repair or replacement. The bioprosthesis offer the advantage of a short course of anticoagulant treatment, but has the major disadvantage of deterioration, as early as the patient is younger. REFERENCES 1. Tissot C., Cherian S., Buckvold S., Kalangos A. Aquired mitral valve stenosis and regurgitation, in Da Cruz E, Ivy D, Jaggers J (eds): Pediatric and Congenital Cardiology,Cardiac Surgery and Intensive Care, Springer-Verlag London 2014: Venugopalan P. Pediatric Mitral Valve Prolapse, febr Sattur S., Bates S., Movahed M.R. Prevalence of mitral valve prolapse and associated valvular regurgitations in healthy teenagers undergoing screening echocardiography. Exp Clin Cardiol 2010; 15:e Séguélaa P.E., Houyelb L., Acara P. Congenital malformations of the mitral valve. Archives of Cardiovascular Disease 2011, 104: Zuppiroli A., Mori F., Favilli S., Barchielli A., Corti G., Montereggi A., Dolara A. Arrhythmias in mitral valve prolapse: relation to anterior mitral leafl et thickening, clinical variables, and color Doppler echocardiographic parameters. Am Heart J 1994; 128: Turker Y., Ozaydin M., Acar G., et al. Predictors of ventricular arrhythmias in patients with mitral valve prolapse. Int J Cardiovasc Imaging. 2010:26: Maron B.J., Epstein S.E., Roberts W.C. Causes of sudden death in competitive athletes. J Am CollCardiol. 1989; 7: Boudoulas H., Schaal S.F., Stang J.M., Fontana M.E., Kolibash A.J., Wooley C.F. Mitral valve prolapse: cardiac arrest with long-term survival. Int J Cardiol 1990; 26: Kligfield P., Levy D., Devereux R.B., Savage D.D. Arrhythmias and sudden death in mitral valve prolapse. Am Heart J 1987; 113: Deng Y.B., Takenaka K., Sakamoto T. et al. Follow-up in mitral valve prolapse by phonocardiography, M-mode and two-dimensional echocardiography and Doppler echocardiography, Am J Cardio 1990, 65 (5): Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009), The Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC), Eur Heart J (2009) 30, Vahanian A., Alfieri O., Andreotti F., Antunes M.J., Barón- Esquivias G., Baumgartner H., et al. Guidelines on the management of valvular heart disease (version 2012): The Joint Task Force on the Management of Valvular Heart Disease of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS), Eur Heart J. Oct 2012; 33 (19): Wearden P.D. Prosthetic valves, in Da Cruz E, Ivy D, Jaggers J (eds): Pediatric and Congenital Cardiology,Cardiac Surgery and Intensive Care, Springer-Verlag London 2014: Caldarone C.A., Raghuveer G., Hills C.B. et al. Long-term survival after mitral valve replacement in children aged < 5 years: a multiinstitutional study. Circulation 2001, 104(12 Suppl 1):I143 I Suri R.M., Aviernos J.F., Dearani J.A. et al. Management of less-than-severe mitral regurgitation: should guidelines recommend earlier surgical intervention. Eur J Cardiothoracic Surg. 2011, 40 (2):
5 10 PREZENTĂRI DE CAZ BIOPROTEZĂ VALVULARĂ MITRALĂ DEGENERATĂ PRECOCE Irina-Mihaela Ciomaga 1, Georgiana Russu 2, Cristina Jităreanu 2, Violeta Ştreangă 1, Aniela Rugină 1, Nicolai Nistor 1 1 Universitatea de Medicină şi Farmacie Gr. T. Popa, Iaşi 2 Spitalul de Urgenţă pentru Copii Sf. Maria, Iaşi REZUMAT Prolapsul de valvă mitrală (PVM) este destul de frecvent întâlnit la copil, fi ind deseori o descoperire întâmplătoare la un copil asimptomatic, dar şi la copii simptomatici, cu boli ale ţesutului conjunctiv. Autorii raportează cazul unei fetiţe de 11 ani, diagnosticată la vârsta de 6 ani cu insufi cienţă mitrală severă prin prolaps de valvă mitrală şi operată la vârsta de 7 ani, când s-a practicat înlocuirea valvei mitrale cu o proteză valvulară biologică. La 4 ani de la protezarea valvulară, fetiţa se prezintă în urgenţă pentru instalarea bruscă a dispneei cu ortopnee, hemoptiziei şi cianozei generalizate. Examenul clinic corelat cu ecocardiografia au stabilit diagnosticul de edem pulmonar acut şi proteză biologică valvulară degenerată, cu stenoză mitrală severă. Evoluţia a fost favorabilă după înlocuirea în urgenţă a bioprotezei cu o proteză mecanică. Cuvinte cheie: bioproteză, valvă mitrală, copil INTRODUCERE Inelul valvei mitrale este nonplanar, având formă de şa. În mod normal, foiţele valvulare sunt împinse una spre cealaltă în timpul sistolei ventriculare prin contracţia muşchilor papilari şi tensionarea cordajelor, ceea ce determină coaptarea mar ginilor valvulare. Prolapsul valvular apare când una dintre valve alunecă sub această zonă de coaptare. PVM idiopatic poate fi congenital, dar diagnosticat târziu, în adolescenţă sau la vârsta adultă. Complicaţiile includ aritmia, insuficienţa cardiacă secundară regurgitării mitrale severe şi, uneori, evenimente tromboembolice. Cazurile familiale au transmitere autozomal dominantă cu penetranţă şi expresie variabilă. Tratamentul este condus de prezenţa sau absenţa complicaţiilor. Astfel, cazurile asimptomatice, cu refluare mitrală minimă nu necesită tratament medicamentos, însă prezenţa disfuncţiei ventriculare şi a refluării mitrale severe impun tratamentul chirurgical. PREZENTARE DE CAZ Prezentăm cazul unui copil de sex feminin, în vârstă de 11 ani, diagnosticat la vârsta de 6 ani cu insuficienţă mitrală severă prin PVM, căruia, la vârsta de 7 ani, i s-a practicat înlocuirea valvei mitrale cu o proteză valvulară tisulară la Institutul de Boli Cardiovasculare şi Transplant din Târgu-Mureş, procedură urmată de tratament cronic cu anti coagulante (Sintrom, Aspenter). La 4 ani de la protezarea valvulară fetiţa prezintă brusc dispnee cu ortopnee, hemoptizie şi cianoză generalizată; este internată în secţia de pediatrie a unui spital judeţean unde urmează tratament cu antibiotice (Cefort), mucolitice şi preparate cortizonice timp de 7 zile. Simptomele s-au ameliorat iniţial, pentru ca apoi să se reacutizeze, suspicionându-se diagnosticul de embolie pulmonară, pentru care a fost transferată în departamentul de Terapie Acută al Clinicii I Pediatrie Iaşi. Adresa de corespondenţă: Georgiana Russu, Spitalul Clinic de Urgenţă pentru Copii Sf. Maria, Str. Vasile Lupu nr. 62, Iaşi g_russu@yahoo.com 336 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN 2014
6 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN La internare, examenul clinic a relevat stare generală gravă, facies suferind, tegumente şi mucoase palide, cicatrice postoperatorie pe linia medio-sternală, dispnee importantă cu ortopnee, polipnee = 56/min, torace normal conformat, excursii costale si metrice, tuse productivă, hipoxemie SaO 2 = 85-89% în aerul atmosferic, ascultaţia pulmonară relevă raluri subcrepitante bilateral, zgomote cardiac ritmice, tahicardie 130/min, suflu sistolic grad III/6 la nivelul apexului cu iradiere interscapulovertebral, ficat în limite normale. Biologic s-a evidenţiat leucocitoză cu neutrofilie, hepatocitoliză uşoară, CPK cu valori crecute, timp de protrombină alungit şi activitatea protrombinică scăzută secundar tratamentului cu anticoagulante. Radiografia cardio-toracică descrie macroopacităţi confluate care ocupă aproape în totalitate ambele arii pulmonare, cord cu bombarea arcului inferior drept, pedicul vascular normal. ECG: tahicardie sinusală 140/minut, axa QRS +90º, PQ = 0,12 sec; sub denivelare S-T (4 mm) în DII, DIII, AVF, V3-V5; suprasolicitare biatrială; QT = 0,28 sec (normal). Ecocardiografia efectuată de urgenţă (vezi Fig. 1) a evidenţiat proteză hiperecogenă în po ziţie mitrală disfuncţională, cu deschidere limitată, realizând stenoză severă şi refluare grad III, dila tarea importantă a arterei pulmonare şi cordului drept, cu refluare tricuspidiană grad III. S-a stabilit diagnosticul pozitiv de edem pul monar acut, stenoză mitrală severă prin bioproteză degenerată, hipertensiune arterială pulmonară şi a fost transferată în urgenţă la Secţia Clinică de Chirurgie Cardiovasculară Iaşi, unde i s-a înlocuit imediat bioproteza cu o proteză mecanică. Evoluţia postoperatorie a fost favorabilă, starea generală s-a ameliorat, dar a apărut ca şi complicaţie pareză de nerv sciatic popliteu extern, remisă sub fizioterapie. DISCUŢII Clasic, PVM este definit ca deplasarea în timpul sistolei ventriculare a uneia sau ambelor foiţe ale valvei mitrale cu 2 mm sau mai mult sub inelul mitral, cu îngroşarea valvelor. Prolapsul atipic constă în deplasarea valvelor, dar acestea au grosime normală. Etiologia PVM este neclară şi probabil multifactorială. Prolabarea poate fi determinată de excesul de ţesut valvular (valve redundante), proli ferarea mixomatoasă a stratului spongios al valvelor şi elon garea cordajelor. Aceste modificări apar la pacienţi cu o mare varietate de malformaţii congenitale cardiace sau boli ale ţesutului conjunctiv (sindrom Marfan, Loeys-Dietz, Ehler-Danlos), cardiopatie ischemică, cardiomiopatie hipertrofică sau pectus excavatum, ca şi la pacienţi cu constituţie astenică (1). Prolapsul izolat poate fi sporadic sau familial, cu transmitere autozomal dominantă şi x-linkată. Incidenţa prolapsului de valvă mitrală creşte cu vârsta, fiind de aproximativ 1-2% la copilul mic şi 5-15% la adolescent şi adultul tânăr, fiind de două ori mai frecvent la fete decât la băieţi (2,3). Diagnosticul clinic se stabileşte pe prezenţa unui clic mezosistolic de închidere a valvei mitrale şi a unui suflu telesistolic de regurgitare mitrală. Majoritatea pacienţilor sunt asimptomatici, fiind descoperiţi cu ocazia unui examen medical de ru- FIGURA 1
7 338 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN 2014 tină, când se decelează un suflu sistolic scurt în focarul mitral. În timp, pot să apară simptome ca: palpitaţii, oboseală, dispnee la efort, dureri toracice, simptome neuropsihiatrice (atac de panică, nervozitate, sincopă). Unii pacienţi prezintă modificări scheletice care nu pot fi incluse în nicio boală a ţesutului conjunctiv (talie înaltă, scolioză, arahnodac tilie, pectus excavatum sau carinatum) (4). Aritmiile care apar cel mai frecvent în repaus sau la efort sunt extrasistole atriale (23,6%) sau ventriculare (27,3%), tahicardie supraventriculară sau tulburări de conducere (5). Unele studii raportează o prevalenţă a aritmiilor ventriculare în PVM de peste 30% (6). De asemenea, la 8-16% dintre pacienţii cu tahicardie ventriculară refractară singura anomalie cardiacă găsită a fost PVM. S-a constatat o asociere între PVM şi moartea subită (7,8). Dacă incidenţa morţii subite în PVM nu este bine stabilită, literatura de specialitate sugerează că riscul este de 5-10 ori mai mare în cazul în care există şi o regurgitare mitrală semnificativă concomitentă. Se consideră că relaţia dintre PVM şi moartea subită se datorează aritmiilor ventriculare (9). Totuşi, la copil, mortalitatea este foarte scăzută. Apariţia regurgitării mitrale şi progresia de la forma uşoară spre cea severă sunt determinanţi importanţi ai morbidităţii. Deng şi colaboratorii au observat că incidenţa regurgitării mitrale a crescut de la 29% la 43% dintre pacienţi în timpul celor 4 ani de urmărire (10). Alte complicaţii sunt insu ficienţa cardiacă, ruptura cordajelor tendinoase, endocardita infecţioasă (0,1-0,3 la 100 pacienţi pe an), fenomene tromboembolice, inclusiv accidente vasculare cerebrale şi moartea subită. Aritmiile cardiace, cum ar fi tahicardia ventriculara şi fibri laţia ventriculară, sunt mai frecvente la pacienţi cu prolaps de valvă mitrală (2). La copil, prolapsul de valvă mitrală nu este progresiv şi majoritatea pacienţilor sunt asimpto matici, necesitând doar urmărire periodică. Se re comandă evitarea cafeinei, fumatului, alcoolului şi medicamen telor care conţin stimulante, cum ar fi epinefrina sau efedrina, pentru a minimaliza descărcarea catecolaminelor şi stimularea AMPc. Profi laxia endocarditei infecţioase are indicaţii foarte precise. Conform ultimului ghid publicat de Socie tatea Euro peană de Cardiologie în 2009, se reco mandă profilaxie cu antibiotic doar în cazul pa cienţilor cu risc major de endocardită: cei cu proteză valvulară sau la care s-a folosit material protetic pentru repararea valvei; pacienţi cu istoric de endo cardită; pacienţi cu malformaţie cardiacă cianogenă neoperată, sau cu shunturi reziduale postoperator, sau cu shunturi paleative; pacienţi cu malformaţii cianogene corectate cu material protetic plasat prin intervenţie clasică sau prin cateterism, pe o durată de 6 luni postoperator; pacienţi cu defect rezidual la locul implantării protezei sau device implantat prin cateterism. Profilaxia antibiotică nu se mai reco mandă în prezent la alte forme de valvulopatii sau malformaţii cardiace (11). Tratamentul chirurgical (plastia valvei mitrale sau înlocuire cu proteză) are indicaţii precise, stabilite de ghidurile americane şi europene (12): pacienţi cu refluare mitrală moderată-severă, pa cienţi simptomatici cu refluare mitrală acută severă, pacienţi simptomatici cu refluare severă cronică (insu ficienţă cardiacă clasa NYHA II-IV), pacienţi asimptomatici cu refluare cronică severă şi dis funcţie ventriculară sau cu funcţie normală dar cu hipertensiune pulmonară. La copil, protezarea mitrală este indicată doar la cazurile la care a eşuat tratamentul medicamentos sau plastia mitrală. În cazul pacienţilor cu vârsta sub 1 an, protezarea mitrală trebuie amânată cât mai mult din cauza morbidităţii şi mortalităţii deosebite asociate cu această procedură. Înlocuirea valvei mitrale are cea mai mare mortalitate perioperatorie dintre toate celelalte proteze valvulare (10-30%) şi cel mai rău pronostic pe termen lung supravieţuire la 5-10 ani între 50-80% (13). S-a observat că bioprotezele cu xenogrefă în poziţie mitrală au cea mai limitată durabilitate la copil, mortalitatea fiind de 79%, 75% şi 74% la 1, 5 şi respectiv 10 ani, sugerând faptul că majoritatea de ceselor au loc în perioada imediat postoperatorie (14). Faţă de protezele mecanice, care necesită tratament anticoagulant toată viaţa, avantajul protezelor biologice constă în faptul că pacientul necesită doar trei luni de tratament anticoagulant postoperator, după care acesta se poate întrerupe. Aceste proteze sunt realizate din ţesut porcin sau din pericard bovin, însă inconvenientul principal al protezelor biologice este calcifierea, care apare mai rapid la pacienţi mai tineri. Deteriorarea structurală a biopro tezelor valvulare este o consecinţă inevitabilă a utilizării lor la om. Acest incident este nonlinear, cu deteriorare şi insuficienţă funcţională şi apare cu frecvenţă crescută după o anumită perioadă de timp care, la copil, este deseori foarte scurtă (14). Datele actuale arată că durata medie de viaţă a unei bioproteze la adult este de 15 ani (15). Cazul prezentat se înscrie în tendinţa generală descrisă în literatură, de degenerare precoce a bioprotezei mitrale, în 4 ani de la instalarea ei. Înlocuirea cu o proteză mecanică a salvat viaţa pacientei, evoluţia postoperatorie a fost lent favorabilă.
8 REVISTA ROMÂNÅ DE PEDIATRIE VOLUMUL LXIII, NR. 3, AN A fost recomandat tratament cronic anticoagulant, cu control periodic al INR care trebuie menţinut op tim între 3,5-4,5 şi profilaxia cu antibiotice a endocarditei bacteriene înaintea oricărei manevre chirurgicale sau stomatologice sângerânde. O particularitate a cazului este apariţia, ca şi complicaţie postoperatorie, a unei pareze de nerv sciatic popliteu extern, care a evoluat ulterior favorabil sub fizioterapie. CONCLUZII Cazurile de PVM cu regurgitare mitrală severă (cum a fost şi cazul prezentat) necesită intervenţie chirurgicală, constând fie în repararea valvei, fie în înlocuirea ei. Valvele biologice oferă pacientului avantajul de a urma, postoperator, doar trei luni de tratament anticoagulant; au însă dezavantajul că se deteriorează cu atât mai repede cu cât vârsta pacientului este mai mică.
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