TAKOTSUBO KARDIOMIOPATIJA - DOSADASNJA SAZNANJA I PRIKAZ PRVE SERIJE BOLESNIKA OTKRIVENIH V SRBIJI
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1 Med Pregl 2010; LXIII (1-2): Novi Sad: januar-februar. 75 Klinicko bolnicki centar Zemun Kardiolosko odeljenje Pregledni clanak Review article UDK : IO.2298/MPNS I002075P TAKOTSUBO KARDIOMIOPATIJA - DOSADASNJA SAZNANJA I PRIKAZ PRVE SERIJE BOLESNIKA OTKRIVENIH V SRBIJI TAKOTSUBO CARDIOMYOPATHY: REPORT OF THE FIRST CASE SERIES IN SERBIA AND REVIEW OF THE LITERATURE Biljana PUTNIKOVIC, Vojkan CVOROVIC, Milos PANIC, Predrag MILICEVIC, Gordana VOJINOVIC-MAGLIC i Aleksandar N. NESKOVIC Sazeta~ - Ta~otsllbo kardiomiopatija predstavlja relativno nov kardioloski cntitet koji se karakterisc tranzitornom asinergijom apikalnog I medijalnog dela levc kornore koja nastaje u odsustvu signifikantnc stenozc koronarnih arterija, a prcthodi ioj snazan emocionalni iii fizicki stres. Sindrom se najcesce javlja kod starijih zena, a prczentuje se bolovima u grudirna, elektrokardiografskim promenama na nivou ST segmenta i T-talasa i minimalno povisenim vrednostirna biomarkera nekroze miokarda. Predlozeno ie nekoliko mogucih mehanizarna nastanka bolesti: spazam koronarnih arterija, dinamicka opstrukciju leve komore, disfunkcija koronarne mikrocirkulacije i direktna kateholaminska povreda. U vecini slucajcva, nakon dramaticne prezentacije, cesto kornplikovane akutnom srcanorn slaboscu. sledi potpuni oporavak. Terapija jc empirijska i usmerena na suportivne mere. Intrahospitalni mortalitet je manji od I%, ali se malo zna 0 dugorocnoj prognozi ovih bolesnika. Pored pregleda dosadasnjih saznanja 0 takotsubo kardiomiopatiji dostupnih u literaturi, prikazana je i prva serija bolesnika koji su dijagnostikovani i leceni LI nasoj zernlji. Kljucne reci: Takotsubo kardiomiopatija; Zena; Znaci i sirnptomi; Dijagnoza; Tcrapija Uvod rasprave, hirurske procedure, trauma, teska pogorsanja hronicnih bolesti itd.). Tipicna klinicka slika Takotsubo kardiomiopatija (sindrom apikalnog podrazumeva iznenadnu pojavu bola u grudirna kao baloniranja, stres kardiomiopatija, "ampula" kardio- vodeceg simptoma (prisutan 1I % slucajeva), mioptija, "amfora" kardiorniopatija, sindrom slom- ali isto tako bolesnici se mogu zaliti samo na disp- Ijenog srca) predstavlja relativno nov kardioloski neju, odnosno na kratkotrajne gubitke svesti [5-10, entitet, koji su originalno opisali Sato i saradnici 13J4J 6-18]. Veliki broj bolesnika u ranom kli- [1], u cijoj osnovi se nalazi tranzitorna apikalna nickom toku pokazuje znake manifestne srcane asinergija leve komore koja nastaje u odsustvu sig- slabosti koja je ponekad 'leoma izrazena, tako da zanifikantne stenoze epikardijalnih koronarnih arte- hteva primenu inotropnih lekova i/ili intraaortne barija, a prezentuje se bolovima u grudima, elektrokar- Ion pumpe: Posle ovako drarnaticne prezentacije, diografskim promenama i minimalnim porastom kod vecine bolesnika nakon nekoliko dana dolazi do kardiospecificnih enzima. Zahvaljujuci karakteris- popravljanja hemcdinarnickog stanja i postepenog ticnorn izgledu leve komore, sindrom je originalno oporavka. Srnrtni ishodi su retki «1 % bolesnika), nazvan takotsubo kardiomiopatija zbog slicnosti sa ali Sll do sada ipak opisani slucajevi fatalnih ruptura japanskom spravom za hvatanje hobotnica (cup sa zida leve komore [19], pojave malignih porernecaja uzanim vratom i sirokorn bazom). Tokom devede- ritma 1I vidu perzistentnih ventri- kularnih fibristih godina vee ina izvestaja 0 ovoj bolesti dolazila lacija, kao i akutne srcane insuficijencije rezistentne je od japanskih autora [2-7], da bi nesto kasnije bile na SVll primenjenu terapiju [20]. opisane i prve serije u SAD i Evropi [8-11]. Elektrokardiografske karakteristike Epidemioloske i klinicke karakteristike Ukupna ucestalost sindroma apikalnog baloniranja ne moze se sa sigurnoscu utvrditi, ali je retrospektivnim analizama podataka utvrdeno da 1,5 do 2,5% bolesnika primljenih u bolnicu pod dijagnozom akutnog koronarnog sindroma ispunjava kriterijume za dijagnozu takotsubo kardiomiopatije [12-15]. Iakoje najmladi opisani bolesnik imao svega deset godina [6], sindrom se daleko cesce javlja kod starije populacije, narocito kod osoba u sedmoj i osmoj deceniji zivota [5-8,12-15]. Takode, prisutna je izrazita polna zastupljenost tako da se sindrom priblizno 9 puta cesee javlja kod zena. Za sindrom je karakteristicno da kod preko 60% bolesnika nastanku simptoma prethodi snazan emocionalni iii fizicki stres (smrt bliske osobe, zucne Elektrokardiografske (EKG) promene kod bolesnika sa sindromom apikalnog baloniranja u mnogo cernu podsecaju na one koje se vidaju kod bolesnika sa akutnim infarktom miokarda. Vecina ovih bolesnika se prezentuje sa promenama na nivou ST segmenta i/ili T-talasa, pri cernu su promene najizrazenije u prekordijalnim odvodima. Pored toga, opisani su i retki slucajevi novonastalog bloka leve, odnosno desne grane Hisovog snopa, ali i bolesnici sa potpuno normalnim EKG nalazom (vecina bolesnika tokom evolucije bolesti ipak razvija elektrokardiografske promene) [6,9-11,21]. Tipicna dinamika elektrokardiografskih promena podrazumeva pojavu elevacije ST segmenta u odvodima V2- V6, koja je obicno kratkotrajna (ponekad svega nekoliko casova), a smenjuje je formiranje dubokih negativnih Adresa autora: Prof. dr Biljana Putnikovic, Klinicko-bolnicki ccntar Zcmun Zemun, V~lkova 9. putnikovicbeidive.co.uk
2 76 Putnikovic B, i sar. Takotsubo kardiomiopatija.skracenice EKG - clcktrokardiograrn CPK - kreatin-fosfokinaza CK-MB - kreatin-fosfokinaza MB izoenzim BNP - mozdani natriuretski peptid AIM - akutni infarkt miokarda LK - leva komora EF - ejekciona frakcija CFVR - rezerva brzine koronarnog protoka DDT - deceleraciono vrerne dijastolne brzine protoka camp - ciklicni adenozin monofosfat ACEi - inhibitori angiotenzin konvertujuceg enzima ASA - acetilsalisicilna kiselina BB - beta blokatori LMWH - niskornolekulami heparin OMI - prva marginalna grana cirkumfleksne arterije PDA - zadnja descendentna arterija UFH - nefrakcionisani heparin VF - ventrikularna fibrilacija T-talasa uz znatno produzavanje QTc intervala; nezativni T-talasi dostizu maksimum treceg dana, a zatim postepeno postaju plici, da vbi u periodu izmedu druge i trece nedelje doslo do njihovog ponovnog produblj ivanja, nakon ~.oje sledi postepena, cesto usporena, norrnalizacija [~1,22]. Potpuno povlacenje ele~trokardlogr~fskl~v promena moze da traje 1 nekoliko meseci I obicno znatno zaostaje za oporavkorn.funkcije leve komore. Na osnovu iznetog, jasno Je da razlikovanje akutnog prednjeg infarkta miokarda i sindroma api~aln<?g baloniranja na osnov.u EKG. promena moz.~ biti veoma tesko, Ogura I saradnici [22].su serijskim pracenjern EKG promena kod bolesmka sa takotsubo kardiomiopatijom i prednjim infarktom rmokarda dosli do zakljucka da odnos zbira ~T elevacija u V4-V6 i ST elevacija u VI-V3 veer od 1 (LSTe V4:-V6/L~Te VI-V3>1) uzistovremeno.odsustvo reciprocnih promena u inferiornim odvodima sa velikom sigurnoscu ukazuje na sindrom apikalnog baloniranja (specificnost 100%). Ipak, neophodno je naglasiti da je ovaj zakljucak izveden na osnovu relativno malog broja bolesnika (13 bolesnika sa takotsubo kardiomiopatijom i 13 bolesnika sa akutnim prednj im infarktom.miokarda) i da nijedan bolesnik sa sindromom apikalnog baloniranja ukljucen u analizu nije imao reciprocne pro1?ene u inferiornim odvodima, dok su postojanje tih promena kod bolesnika sa sindromom apikalnog baloniranja ipak opisali drugi autori. Laboratorijske analize Povisene vrednosti kreatin-fosfokinaze (CPK), MB-izoenzima (CK-MB) i troponina nadene su kod vecine bolesnika sa sindromom apikalnog baloniranja (56-100%) [6,8,10, 13,14,23]. Prerna do sada objavljenim radovima, dinamika kardiospecificnih markera se razlikuje od one koja se vida kod akutnog infarkta miokarda. Nairne, kod vecine bolesnika sa takotsubo kardiomiopatijom maksimalne vrednosti CPK, CK-MB i troponina registrovane su prvog dana hospitalizacije, za razliku ~d infarkta miokarda zde se maksimalne vrednosti ocekuju h nakon pocetka bolova u grudima. Isto tako, maksimalne vrednosti biomarkera nekroze miokarda kod bolesnika sa sindrornom apikalnog baloniranja obicno ne dostizu "infarktne" vrednosti, uprkos velikoj zoni asinergije leve kornore. Nekoliko istrazivaca [11,13,24] je pratilo vrednosti mozdanog natriuretskog peptida (brain natriuretic peptide BNP) kod bolesnika sa takotsubo kardiorniopatijom i kod vecine su ustanovljene znatno povisene vrednosti, ali opet za razliku od akutnog infarkta miokarda i drugih kardi~losk}h oboljenja,.~~ivo ~NP kod ovih bolesmka mje bio u korelacij I sa ishodorn bolesti. Jedno od mogucih objasnjenja ove diskrepanee bilo bi da je razlog izrazitog povisenja vrednosti BNP kod bolesmka sa sindromorn apikalnog baloniranja u povecanorn zidnorn stresu nastalorn usled hiperkontraktilnosti bazalnih segmenata koj I dovode do opterecenja pritiskom distalnog dela leve komore, slicno kao kod bolesnika sa hipertoficnom opstruktivnom kardiomiopatijom [18]. Irnajuci 1I vidu da emocionalni, odnosno fizicki stres ima veliku ulogu u nastanku ovog sindroma, do sada je sprovedeno vise istrazivanja tokom kojih Sll kod ovih bolesnika odredivane koncentracije kateholamina u plazmi [6,11-13,18]. Wittstein i saradniei [11] su serijskim pracenjem i poredenjem vrednosti kateholamina i BNP kod bolesnika sa takotsubo kardiomiopatijom i bolesnika sa Killip III akutnim infarktom miokarda (AIM) dosli do zakljucka da je nivo kateholamina 2-3 puta veci kod bolesnika sa sindromom apikalnog baloniranja, sto ukazuje na to da je uloga kateholamina u nastanku ove bolesti od velikog znacaja i da povisene vrednosti kateholamina u krvi nisu rezultat sarno akutno nastale srcane slabosti i reakcije organizma na stres. Vazno je napomenuti i da su se ovako visoke vrednosti kateholamina odrzavale u krvi bolesnika i 7-9 dana nakon pocetka bolesti, a da je, s druge strane, nivo BNP, iako znacajno povisen u perakutnoj fazi, nakon osam dana bio nizi nego kod bolesnika sa Killip III AIM sto ukazuje na brzi oporavak funkcije leve komore. Morfoloske i angiografske karakteristike Ehokardiografske i ventrikulografske studije [5 11,14,16-18] kod bolesnika ~a takotsubo k.::rdiomiopatijom u akutnoj fazi bolesti pokazuju tlpl.can pore: rnecaj kontraktilnosti, sa akmezllom apikalnog I medijalnog dela leve komore uz ocuvanu kontraktilnost (iii cak ~ipe:~o~~ra.ktilnost).ba~almh. segm~nata, sto na taj nacm cim karakteristicnu sliku aprkalnog baloniranja. Globalna sistolna funkcija le- ve komore (LK) je u akutnoj fazi bolesti znacajno snizena i prema do sada objavljenim radovima [6, 10,11,13:15,21,23], prosecna vrednost ejekcione frakcije (EF) se kretala ~0-49~o..Pored.toga, kod manjeg broja bolesnika opisano je I postojanje tranzitorne opstrukcije u izlaznom traktu leve komore [6,8,10,14,25,26]. Angiografska ispitivanja su poka-
3 Med Preg12010; LXIII (1-2): Novi Sad: januar-februar. 77 zala da kod ovih bolesnika iii ne postoji koronarna bolest iii su nadene sarno neopstruktivne aterosklerotske lezije epikardijalnih koronarnih arterija (luminala stenoze < 50%) [5,6,8,11,13-15,17,21,22]. Oporavak funkcije LK je relativno brz i obicno potpun, tako da u periodu od sedam dana do nekoliko nedelja dolazi do drasticnog poboljsanja sistolne funkcije, sa prosecnorn EF 60-76% [5,6,10,11,13 15,19,21]. Patohistoloske analize Irnajuci u vidu nisku smrtnost, vecina patohistoloskih podataka kod bolesnika sa takotsubo kardiomiopatijom dobijena je putem endomiokardne biopsije. Patohistoloski nalaz je nespecifican i najcesce se sastoji od blage do umerene intersticijalne infiltracije mononuklearnim limfocitima i makrofagima, uz slabo izrazenu intersticijalnu fibrozu i contraction band nekrozu kardiomiocita [5,7,16,22,27]. Patofizioloski mehanizmi lako je sindrom prvi put opisan pre vise od petnaest godina, patofizioloski mehanizam njegovog nastanka jos uvek nije razjasnjen. Na osnovu klinicke slike kojom dominiraju intenzivan ernocionalni, odnosno fizicki stres koji neposredno prethode bolesti, bolovi u grudima kao tipicna prezentacija bolesnika, prisustva EKG promena koje imitiraju akutni koronarni sindrom, kao i brojnih sprovedenih ispitivanja postavljeno je nekoliko mogucih objasnjenja. Ovde cerno razmotriti cetiri najcesce pominjane hipoteze. 1) Spazam epikardnih koronarnih arterija Spazam epikardnih koronarnih arterija nastao usled ekscesivnog lucenja kateholamina pod uticajem stresa jedna je od prvih teorija 0 patofizio-. loskom mehanizmu nastanka takotsubo kardiomiopatije [2,5,28]. Osnovni nedostaci ove teorije su sledeci: a) regionalni poremecaji kontraktilnosti po svojoj opseznosti i regiji miokarda koji zahvataju (citav srednji i apikalni deo leve komore) prevazilaze irigaciono podrucje sarno jedne koronarne arterije, tako da bi eventualni spazam morae zahvatiti prakticno sve epikardne arterije u isto vreme i to na priblizno istom nivou, b) angiografska ispitivanja ne podrzavaju ovu teoriju; prema raspolozivirn podacima, procenat bolesnika kod kojih Je intrakoronarnim davanjem acetilholina, odnosno ergonovma, bilo moguce izazvati spazam koronarnih arterija kretao se 0-43%, dok se procenat spontanih spazarna uocenih prilikom koronarne angiografije kretao 0-11% [5-8,16,17], c) kod bolesnika kod ~ojihje spazam uspesno isprovociran l1isu zabelezene IS: tovremene elektrokardiografske 'prom~ne. koje bi odgovarale onim koje su bolesnici irnali pn pnje!ti~i. S obzirom na iznesene cinjenicc, spaza.m velikih krvnih sudova najverovatnije ne predstavlja.osno~nl mehanizam nastanka takotsubo kardiomiopatiic, iako je moguce da ucestvuje u patofiziologiji u pojedinim slucajevima, 2) Dinamicka opstrukcija leve komore Relativno novi predlozeni mehanizam nastanka takotsubo kardiorniopatije je prisustvo dinamicke intrakavitarne opstrukcije leve komore. Teorija je nastala kao rezultat ehokardiografski uocenog gradijenta pritiska u supljini leve komore kod bolesnika sa takotsubo kardiomiopatijom. Kao posebna karakteristika ovih bolesnika opisuje se postojanje sigmoidnog septuma i "Iabavog mitralnog aparata" [26], odnosno postojanje hipertofije miokarda u sredisnjern delu septuma [29]. Ova "poremecena" arhitektonika leve komore bi bila preduslov nastanku sindroma. Po Merli i saradnicima [29], sam mehanizam nastanka bolesti bi bio sledeci: ekscesivno lucenje kateholamina dovelo bi, s jedne strane, do smanjenja subendokardne perfuzije usled spazma koronarne mikrocirkulacije, a s druge strane, usled inotropnog dejstva na miokard i sledstvene hiperkontraktilnosti bazalnih delova leve komore nastala bi intrakavitarna opstrukcija u levoj komori koja bi je prakticno podelila na dva dela - donji deo koji bi radio pod normalnim pritiskom i gornji deo u kome bi vladao izrazito visok pritisak. Jako povisen telesistolni pritisak u apikalnom delu leve komore bi povecanjem zidnog stresa povecao potrosnju kiseonika. Oba ova mehanizma bi posledicno dovela do ishemijske lezije i poremecaja kontraktilnosti. Usled gubitka kontraktilnosti kardiorniocita gubi se mogucnost daljeg generisanja intrakavitarnog gradijenta tako da pritisak u "apikalnoj komori" postepeno opada, sto dovodi do oporavka miokardne perfuzije i sprecavanja trajnog ostecenja - miokardne nekroze. Kako se kardiomiociti oporavljaju, tako dolazi do ponovnog generisanja gradijenta pritiska i zapocinjanja novog ciklusa, pri cernu ciklusi traju sve dok su u krvi prisutne poviscne vrednosti kateholamina. U prilog postojanju opisanog sleda dogadaja ukazuje cinjenica da je po oporavku funkcije leve komore moguce izazvati intrakavitarnu opstrukciju tokom niskodoznog dobutaminskog stres-ehokardiografskog testa, dok apikalni deo miokarda istovremeno pokazuje tipicnu sliku osarnucenog miokarda. Medutim, iako na prvi pogled veoma primam Ijiva, teorija dinamicke opstrukcije kao glavnog patofizioloskog mehanizma nastanka sindroma apikalnog baloniranja ima nekoliko bitnih mana. Kao prvo, conditio sine qua non nastanka bolesti bi bilo prethodno postojanje porernecene arhitektonike leve komore - osobe koje imaju normalnu levu komoru, prema tome, nikada ne bi mogle oboleti. S druge strane, iako je velika veeina ovih bolesnika podvrgnuta ehokardiografskom pregledu, procenat bolesnika kod kojih je opisano postojanje intakavitarnog wadijenta, odnosno gradijenta u izlaznom traktu ieve komore krece se 0-18% [6,8,10,11,14]. 3) Disfunkcija koronarne mikrocirkulacije Dusfunkciju koronarne mikrocirkulacije kod bolesnika sa takotsubo kardiomiopatijom opisalo je vise autora. Kurisu i saradnicima [19] su medu prvima, koristeci TIMI frame count metodu [30] (metoda podrazumeva brojanje frejmova potrebnih da intrakoronarno dat kontrast prede rastojanje
4 78 Putnikovic B, i sar. Takotsubo kardiomiopatija izrnedu dye prethodno odredene tacke duz magistralne koronarne arterije), utvrdili znacajno sporij i protok kontrasta u epikardnim koronarnim arterijama u odsustvu hemodinarnicki znacajne stenoze, a njihovi nalazi su potvrdeni i od drugih [14]. Nishikawa i saradnici [31] su 99lTITc-tetrafosmin SPECT analizom kod jednog bolesnika takode nasli perfuzione defekte miokarda nastale na nivou mikrocirkulacije, da bi konacno Kume i saradnici [32], mereci rezervu brzine koronamog protoka (coronary flow velocity reserve, CFVR) I deceleraciono vreme dijastolne brzine protoka (DDT) kod 7 bolesnika sa sindromom apikalog baloniranja u toku prva 24 h i tri nedelje nakon pocetka simptoma, utvrdili smanjenje i CFVR i DDT u toku akutne faze bolesti u sve tri magistralne koronarne arterije, uz normalizaciju ovih parametara nakon tri nedelje. Cinjenicama koje govore u prilog spazmu mikrocirkulacije moze se dodati i akutno srnanjivanje ST elevacije intrakoronarnim ubrizgavanjem nikorandila kod bolesnika sa sindromom apikalnog baloniranja [33]. S druge strane, Abe i saradnici [22] su, mereci CFVR i DDT u prednjoj descendentnoj arteriji kod 4 bolesnika sa takotsubo kardiomiopatijom, dobili potpuno suprotne rezultate, pri cemu je neophodno napornenuti da su merenja kod ovih bolesnika vrsena sarno jednom i to u rasponu 1-32 dana od pocetka simptoma. Iako mnoge cinjenice ukazuju na postojanje mikrovaskularnog spazma kao mehanizma nastanka takotsubo kardiomiopatije, nadene promene ne moraju da ukazuju na uzrocno-posledicnu vezu. Nairne, smanjenje protoka kroz mikrocirkulaciju moze biti posledica kako intramiokardnih poremecaja (edem tkiva, celularna infiltracija) tako i porasta teledijastolnog pritiska u levoj komori, nastalog usled opsezne asinergije, uz spoljasnju kornpresiju manjih krvnih sudova. Pored toga, svakako ostaje otvoreno i pitanje same ctiologije mikrovaskulamog spazma. 1) Direktna kateholaminska povreda Cetrvrti predlozeni patogenetski mehanizam nastanka takotsubo kardiomiopatije je direktna kateholaminska povreda kardiorniocita. Nairne, na osnovu do sada objavljenih radova [34-36], poznato je da kateholamini mogu posredstvom ciklicnog adenozin monofosfata (camp) kao i povecanjem koncentracije slobodnih radikala da dovedu do znacajnog porasta intracelulame koncentracije jona Ca++, koji zatim dovodi do aktivacije proteolitickih enzima i degradacije miofibrila. Histoloskorn analizom utvrdeno je da se kod ovakve vrste ostecenja miokarda moze uociti dosta specificna slika: hiperkontraktilne sarkomere sa gustim poprecno postavljenim eozinofilnim trakama uz mononuklearni intersticijalni celijski infiltrat (tzv. contraction-band nekroza) slika veoma slicna patohistoloskim promenama opisanim i kod bolesnika sa sindromom apikalnog baloniranja. Trebalo bi imati u vidu da je tkivo miokarda u vecini slucajeva dobijeno biopsijom; uraden jevrlo mali broj autopsija koje ornogucavaju detaljn!jl patohistoloski pregled. Razlog zahvatanja sarno distalne dye trecine leve komore ovim promenama Tabela 1. Predlozeni kriterijumi klinike Mayo za postavljanjc dijagnoze takotsubo kardiomiopatije Table 1. Criteria for diagnozing Takotsubo cardiomyopathy suggested bv Mayo clinic 1. Tranzitoma akinezija iii diskinezija apikalnog i medijalnog dela leve komore sa regionalnim poremecajima kontraktilnosti koji se sire van irigacionog podrucja jedne epikardne koroname arterije/transitoly akinesia or dyskinesia ofthe lej; ventricular apical spreading and medial pari with regional contractility disorders outside the irrigauonal region ol(1i1epicardial coronary artery 2. Odsustvo opstruktivne koroname bolcsti ili angiografski dokazane akutne rupture plaka/7he absence ofan obstructive coronary disease or angiographicallv proved acute plaque rupture 3. Novonastale elektrokardiografske promene (ST elevacija iii inverzija T tajasa)/newly developed elcctrocardiographu: changes (.'IT-elevation or I~ wave tnverston 4. Odsustvo/Znc absence of - skorasnje znacajne povrede glave/a recent significant head injury - intrakranijalne hemoragije/1i1tracramal haemorrhage - feohromocitoma/phaeochromocytoma - opstruktivne epikardijalne koroname bolesti/an obstructive epicardial coronary disease - miokarditisa/myocarditis - hipertroficne kardiomiopatije/hypertrophlc cardiomvopthv o~asnjava se cinjenicom da je zbog veceg broja u i p-receptora vrh srca prirodno osetljiviji na dejstvo kateholamina, dok je reverzibilnost promena posledica cinjenice da do prave nekroze miocita nije doslo i da je za potpum funkcionalni oporavak potrebna sarno ponovna sinteza ostecenih proteina. Glavni nedostatak ove teorije lezi u cinjenici da su kod priblizno 25% bolesnika sa takotsubo kardiomiopatijom koncentracije kateholamina u serumu tokom akutne faze u fizioloskim granicama. Dijagnoza i diferencijalna dijagnoza Zasad ne postoje jedinstveno prihvaceni kriterijumi za postavljanje dijagnoze tq~otsubo kadiomiopatije. U literaturi se mogu naci dye predlozene grupe kriterijuma: kriterijumi klinike Mayo (Tabela 1) r371 i kriterijumi iapanskih autora (Tabela 2) Tabela 2. Predlozeni kriterijumi japanskih autora za postavljanje dijagnoze takotsubo kardiomiopatije Table 2. Criteria for diagnozing Takotsubo cardiomyopathy suggested bv Japanese authors Major kriterijumilma/or criteria: - reverzibilno apikalno baloniranje sa hiperkontraktilnoscu bazalnih segmenata/reversible apical ballooning with hypercontractility ofthe basal segments - elektrokardiografske promene na nivou ST segementa i T-talasa koje podsecaju na akutni infarkt miokarda/electrocardiographic changes at the level of Sl segments and T waves resembling an acute myocardial infarction Minor kriterijumi/minor criteria: - prethodi fizicki iii psihicki stres kao precipirajuci faktor/previous physical or mental stress as a precipitatingfactor - blago povisene vrednosti biomarkera nekroze miokarda/slightly tncreased values ofmyocardial necrosis biomarkers - bolu grudima/ore«pam Kriterijumi za iskljucivanje/erduding criteria: - ishemijska "osamucenost" miokarda/iscltaemic mvocardial failure _subarahnoidalna hemoragija/suharachnoir./ haemorrhage feohromocitomska kriza/phaeochro/l/ocytomlc crisis _akutni miokarditis/acute myocarditis - tahikardijom indukovana kardiomiopatija/tachycardw'lilduced cardlllmyopatity
5 Med Pregl 2010; LXIII (1-2): Novi Sad: januar-februar, 79 Tabela 3. Karakteristike bolcsnika sa dijagnostikovanom takotsubo kardiomiopatijom lecenih II KBC Zcrnun u periodu od avgusta do novembra god inc Table 3. Characteristics ofpatients diagnozed to have takotsubo cardiomyopathy and treated at the Clinical Hospital Centre Zemun in the period from August 2004 to November 2006 Redni broj Starost Pol Stresor Simptomi EKG (akutna faza) EF% (aku EKG tokom EF~'o (Iaza Koronarourafija Terapija bolesnika Age Sex Stressor Symptoms I:'(OIj (acute phase) Ina faza evolucije oporavka ( 'orollrirogrol'hy Thcrap; l'attcnt acute phase) U'C; durins; number 4 34 Z luena Srcani zastoj VF, negativni T-talasi 25 rasprava u V2-V5 64 l Epistaksa, Sol u grudima, Negativni T-talasi u 25 efedrin gusenje DJ. avl, V2-V4 56 Z Ginekoloska Sol u grudima Elevacija ST segrnenta 50 operacija u VI-V6 44 Z Svada Sol u grudima Elevacija 5T segmenta 30 u V2-V5 40 i. Svada Sol u grudima Elevacija 5T segmenta 40 DJ. avl, V3-V6 [38]. Osnovna dilema koja se moze javiti u svakodnevnoj klinickoj praksi proistice iz slicnosti klinicke prezentacije takotsubo kardiomiopatije i akutnog infarkta miokarda - treba imati na umu da je relativna incidencija takotsubo kardiomiopatije 22 bolesnika na 800 do 1000 bolesnika sa akutnim infarktom miokarda [39]. Buduci da se sindrom cesto prezentuje bolom u grudima i elevacijama ST seg- evolution Ncgativni T-talasi II V2-V5 Negativni T-talasi u V2-V4 Negativni T-talasi u V2-V6 Plitko ncgativni T-talasi u V2-V4 Plitko ncgativni T-talasi u VI-V3 recovery phase) 60 Urcdan nalaz A5A, UFS. SS. ACEi 50 Stenoza OMI 40% ASA, LMWH. SS, ACEi, furosernid 60 Stcnoza 90% PDA A5A, LMWH. SB, ACEi 60 Uredan nalaz ASALMWH, SS 60 Uredan nalaz A5A, UFH, B13, ACEi menta u prekordijalnim odvodima, a da je stres poznati faktor rizika i za koronarnu bolest [40], primena (odnosno odluka 0 nedavanju) trornboliticke terapije namece se kao krucijalno pitanje. Iako zasad, nazalost, ne postoje jasni klinicki kriterijumi koji bi ornogucili rano razlikovanje ove dye bolesti, ipak je na osnovu anamnestickog podatka 0 prethodom stresu i karakteristicnog ehokardiografskog nalaza asinergije koja zahvata citav medijalni i apikalni deo leve komore (teritorija koja prevazilazi irigaciono podrucje jedne koronarne arterije!) moguce posumnjati da se radi 0 takotsubo kardiomiopatiji i bolesnika uputiti na urgentnu koronarnu angiografiju. Terapija Terapijske mere kod bolesnika sa takotsubo kardiomiopatijom su u osnovi suportivne sa posebnom paznjorn usmerenom na rano detektovanje manifestne srcane slabosti, kardiogenog soka i malignih aritmija. S obzirom na pretpostavljenu ulogu kateholamina u nastanku sindroma, neki autori u slucaju Slika 1. Apikalni presek 4 supljine 64-godiSnje bolesnice koja je primljena u koronarnu jedinicu zbog bola 1I grudima pracenog gusenjern, nastalog neposredno nakon epizode epistakse tretirane prednjorn tamponadom uz upotrebu efedrina. Na snirnku se moze jasno videti akinezija medijalnog i apikalnog dcla Ieve kornore u akutnoj fazi boiesti (B), kao i potpuni oporavak nakon cetiri dana (D) Legenda: A: dijastola - akutna faza; B: sistola - akutna faza: C: dijastola - nakon cetiri dana: D: sistola - nakon cetiri dana. Fig. I. The apical cross-section of 4 cavities in a 64-year-old female patient presented with a chest pain followed by suffocation, which developed immediately after an epistaxis episode treated by the anterior tamponade together with ephedrine. The photo clearly shows akinesis of the medial and apical part of the left ventricle in the acute phase (B) as we!! as the complete recovery after 4 days (D) Legend: A: diastole - the acute phase: B: systole - the acute phase: C: diastole - after 4 days: D: systole - after 4 days. Stika 2. Koronarni angiogram bolesniee prikazane na Slici 1. Strelieorn je pokazano suzenje prvc marginalne grane eirkumfleksne koronarnc arterije od 40%. Bcz drugih promena na epikardijalnim koronamirn arterijama Fig. 2. Coronary angiogram ofthe patient presented in Fig. 1. The arrow shows the 40% constriction of the first marginal branch ofthe circumflex coronary artery. There are no other changes in the epicardial coronary arteries
6 80 Putnikovic B, i sar. Takotsubo kardiomiopatija kardiogenog soka preporucuju primenu intraaortne balon pumpe umesto standardnog medikamenoznog tretmana simpatikomimeticima. Kod bolesnika sa izrazenorn opstrukcijom u izlaznom traktu leve komore primena beta blokatora uz nadoknadu teenosti moze imati povoljan terapijski ucinak. Iskustvo Klinieko-bolnickog centra Zemun Prvi slucaj takotsubo kardiomiopatije u nasoj ustanovi otkriven je u avgustu godine. Nakon toga do novembra godine otkriveno je jos cetin slucaja. U istom periodu u KBC Zemun su Ieeena 823 bolesnika sa akutnim infarktom miokarda. Prema tome, takotsubo kardiomiopatija je dijagnostikovana kod 0,6% bolesnika koji su se prezentovali pod slikom akutnog infarkta miokarda. Karakteristike ovih bolesnika prikazane su u Tabeli 3, a tipicni ehokardiogram i koronarni angiogram jedne bolesnice na shkama 1 i 2. Prema nasirn saznanjima, ovo je prva serija bolesnika sa takotsubo kardiomio- patijom koji su dijagnostikovani zemlji. Zakljucak leceni u nasoj Takotsubo kardiomiopatija predstavlja relativno novi kardioloski entitet koji klinickirn, elektrokardiografskim i laboratorijskim karakteristikama u mnogo cemu podseca na akutni infarkt miokarda. Patogeneza sindroma je jos uvek nedovoljno razjasnjena, a na osnovu do sada sprovedenih istrazivanja moguce je da zapravo i ne postoji jedinstveni etioloski faktor. Upadljiva predorninacija zena, neosporni uticaj stresa na nastanak bolesti, karakteristicno zahvatanje apikalnog i medijalnog dela leve komore, kao i tipicni potpuni oporavak u relativno kratkom periodu sarno su neke od karakteristika ovog sindroma za koje zasad nema potpunog objasnjenja. Formiranje nacionalnog registra za takotsubo kardiomiopatiju omogucilo bi sagledavanje prave ucestalosti i olaksalo istrazivanje ovog sindroma u nasoj zemlji. Literatura I. Sato H, Tateishi H. Uchida T. Takotsubo-type cardiomyopathy due to multivessel spasm. In: Kodama K, Haze K, Hon I\1, eds. Clinical aspect of myocardial injury: from ischemia to heart failure. Tokyo: Kagakuhyouronsha; p Dote K, Sato H, Tateishi H, Uchida T, Ishihara M. Myocardial stunning due to simultaneous multivessel coronary spasms: a review of 5 cases. J Cardiol 1991; 21: Dote K, Mitsuda H, Ninomiya M, et al. Tako-tsubo cardiomyopathy (acute reversible catecholamine cardiomyopathy). In: Okada R, editor. Syndrome of cardiovascular disease. Ill. Tokyo: Nihon Rinsyoh Co.: p Ishihara M, Satoh H, Tateishi H. Tako-tsubo type cardiomyopathy. Kokyu-to-Junkan 1997;45: Kawai S, Suzuki H, Yamaguchi H. Tanaka K, Sawada H, Aizawa T, et al. Ampulla cardiomyopathy (Takotsubo cardiomyopathy): reversible left ventricular dysfunction with ST segment elevation. Jpn Circ J 2000;64: Tsuchihashi K, Ueshima K, Uchida T, Oh-Mura N, Kimura K, Owa M, et al. Transient left ventricular apical ballooning without coronary artery stenosis: a novel heart syndrome mimicking acute myocardial infarction. 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N Engl J Med 2005;352: Ito K, Sugihara H, Katoh S, Azuma A. Nagakawa M. Assessment of Takotsubo (ampulla) cardiomyopathy using 99mTc-tetrofosmin myocardial SPECT - comparison with acute coronary syndrome. Ann Nucl Med 2003; 17: Akashi YJ, Nakazawa K, Sakakibara M, Miyake F, Musha H, Sasaka K. 123 I-MIBG myocardial scintigraphy in patients with Takotsubo cardiomyopathy. J Nucl Med 2004;45: Bybee KA, Prasad A, Barsness GW, Lerman A..~affe AS, Murphy JG, et al. Clinical characteristics and thrombolysis in myocardial infarction frame counts in women with transient left ventricular apical ballooning syndrome. Am J Cardiol 2004: 94: Matsuoka K, Okubo S, Fujii E, Uchida F, Kassai A. Aoki T, et al. Evaluation of the arrhythmogenicity of stressinduced Takotsubo cardiomyopathy from the time course of the 12-lead surface electrocardiogram. Am J Cardiol 2003;92: Akashi YJ, Nakazawa K, Sakakibara M. Miyake F. Koike H. Sasaka K. The clinical features of Takotsubo cardiomyopathy. 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Med Pregl 2008;61 (5-6): Introduction intracavitary obstruction, coronary microvascular dysfunction Takotsubo cardiomyopathy is a relatively novel cardiac syn- and direct catecholamine-mediated cardiomyocite injury. drome that is characterized by transient left ventricular asyn- Therapy andprognosis ergy involving apical and mid-ventricular segments. Complete recovery usually occurs after dramatic presentation, Epidemiology andpathophisiology frequently complicated with acute heart failure. Therapy is em- It occurs predominantly in elderly women in the absence ofob- piric and directed towards supportive measures against cardiostructive coronary artery disease and is usually associated with genic shock, acute heart failure, dysrhythmias. In-hospital severe emotional or physical stress. This syndrome is mani- mortality rate is less than I%, but long-term prognosis is still fested with chest pain, electrocardiographic changes that mimic unknown. acute myocardial infarction, and minimal myocardial enzy- In addition to the review ofthe literature on takotsubo cardiomatic release. Several different mechanisms have been pro- myopathy, we present the first series ofpatients with this synposed: coronary artery spasm, dynamic left ventricular outflow/ drome detected in Clinical Hospital Center Zemun. Key words: Takotsubo Cardiomyopathy: Female; Signs and Symptoms: Diagnosis; Therapeutics Rad je primljen Prihvacen za starnpu 15. III BIBLID :(2009):LXII: 1-2:75-81.
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