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SESELJ VOJISLAV

KARDIOLOSKA EVALUACIJA

Oktobar 2009.

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Postovani,

Evaluacija je uradjena na osnovu elementarnog kardioloskog pregleda koji je izvrsen u julu 2009 godine i dostupnih medicinskih dokumenata.

Svi dodatni pregledi koji su zahtevani u nalazu od jula 2009 godine, trazeni su na osnovu anamnestickih podataka dobijenih od pacijenta, uvida u tok ranijeg lecenja ili osnovanih hipoteza autora ove evaluacije, prema principima „Evidence Based Cardiology“ i „Dobre lekarske prakse“.

Drugim recima, autor se pridrzavao principa naucnog metoda rada i epistemologije prema kojima potvrdjivanje ili iskljucivanje bolesti, a posebno procena rizika u buducnosti, moraju biti iskljucivo zasnovane na do sada poznatim i merljivim dokazima (u ovom slucaju medicinskim pregledima i podacima iz strucno-naucne literature).

Ovo je posebno vazno kada se zna da kod ovog bolesnika postoje znacajni rizici, a da je moguce postojanje tzv. „silent“formi bolesti ili predklinickih stadijuma bolesti.

Autor je odgovoran za rezultate svog pregleda u pritvorskoj jedinici Tribunala u Hagu, ali nije odgovoran za tacnost ostalih dobijenih dokumenata.

Autor ne moze biti odgovoran za menjanje niti proizvoljno tumacenje bilo kog dela teksta bez prethodne konsultacije.

16. Oktobar 2009. U Beogradu, Serbia

Zdravko M. Mijailovic, MD, PhD, Cardiologyst Head of the Clinic for Cardiology Military Medical Academy – Belgrade, Serbia American Registred for Diagnostic Cardiac Sonography Associate Professor of Internal medicine / Cardiology/ Fellow of European Society of Cardiology Fellow of American Colledge of Cardiology Member of American Heart Association Member of American Society of Echocardiography

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SADRZAJ KARDIOLOSKA EVALUACIJA..........................................................................................1

SADRZAJ..................................................................................................................................3

REZIME................................................................................................................................6

NAJVAZNIJI KARDIOVASKULARNI PODACI OD ZNACAJA ZA EKSPERTIZU: ...................................................................................................................15

FAKTORI RIZIKA............................................................................................................16

Zivotna dob .....................................................................................................................16

PODATAK (CINJENICA) ........................................................................................16

Dokaz o tacnosti podatka:..........................................................................................16

RIZICI (OPASNOSTI): .........................................................................................16

DOKAZI:.....................................................................................................................16

ZAKLJUCAK:........................................................................................................................ 17

Literatura:...................................................................................................................17

Muski pol .........................................................................................................................19

RIZICI (OPASNOSTI): .........................................................................................19

ZAKLJUCAK:........................................................................................................................ 21

Literatura:...................................................................................................................21

Gojaznost – “Body mass index” ....................................................................................22

PODATAK (CINJENICA): .......................................................................................22

Dokaz o tacnosti podatka:..........................................................................................22

RIZICI (OPASNOSTI): .........................................................................................22

DOKAZI:.....................................................................................................................23

ZAKLJUCAK:........................................................................................................................ 25

Literatura:...................................................................................................................26

Hiperholesterolemia .......................................................................................................26

PODATAK (CINJENICA): .......................................................................................26

Dokaz o tacnosti podatka:..........................................................................................26

RIZICI (OPASNOSTI): .........................................................................................26

DOKAZI:.....................................................................................................................27

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ZAKLJUCAK:........................................................................................................................ 30

Literatura:...................................................................................................................30

Arterijska hipertenzija...................................................................................................31

PODATAK (CINJENICA): .......................................................................................31

Dokaz o tacnosti podatka:..........................................................................................31

RIZICI (OPASNOSTI): .........................................................................................31

DOKAZI:.....................................................................................................................33

ZAKLJUCAK:........................................................................................................................ 37

Literatura:...................................................................................................................37

Stresovi ............................................................................................................................38

PODATAK (CINJENICA): .......................................................................................38

Dokaz o tacnosti podatka:..........................................................................................38

RIZICI (OPASNOSTI): .........................................................................................38

DOKAZI:.....................................................................................................................38

ZAKLJUCAK:........................................................................................................................ 44

Literatura:...................................................................................................................44

Porodicno opterecenje....................................................................................................46

PODATAK (CINJENICA): .......................................................................................46

Dokaz o tacnosti podatka:..........................................................................................46

RIZICI (OPASNOSTI): .........................................................................................46

DOKAZI:.....................................................................................................................47

ZAKLJUCAK:........................................................................................................................ 48

Literatura:...................................................................................................................48

EKG promene:....................................................................................................................49

PODATAK (CINJENICA): .......................................................................................49

Dokaz o tacnosti podatka:..........................................................................................49

RIZICI (OPASNOSTI): .........................................................................................49

DOKAZI:.....................................................................................................................49

ZAKLJUCAK:........................................................................................................................ 52

Literatura:...................................................................................................................53

EHOKARDIOGRAFSKE promene: ...............................................................................54

PODATAK (CINJENICA): .......................................................................................54

Dokaz o tacnosti podatka:..........................................................................................55

RIZICI (OPASNOSTI): .........................................................................................55

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DOKAZI:.....................................................................................................................55

ZAKLJUCAK:........................................................................................................................ 56

Literatura:...................................................................................................................56

PAROKSIZAM ATRIJALNE FIBRILACIJE: .................. ............................................57

PODATAK (CINJENICA): .......................................................................................57

Dokaz o tacnosti podatka:..........................................................................................57

RIZICI (OPASNOSTI): .........................................................................................57

DOKAZI:.....................................................................................................................57

ZAKLJUCAK:........................................................................................................................ 59

Literatura:...................................................................................................................59

ZAKLJUCAK .........................................................................................................................61

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REZIME

Faktori rizika za kardiovaskularne bolesti:

• Zivotna dob (bolesnik zivotne dobi 55 godina). • Muski pol • Gojaznost (telesna tezina oko 120 kg, telesna visina oko 1,97 m, BMI oko 30,9

kg/m2 – racunato po formuli BMI=tezina u kg/visina u m2) • Hypercholesterolemia ( holesterol 5,4 mmol/l, trigliceridi 2,0 mmol/l, HDL

holesterol 1,0 mmol/l, LDL holesterol 3,4 mmol/l ) • Arterijska hipertenzija (misli da od ranije, a sigurno od 1995. godine ima

povisene vrednosti arterijskog krvnog pritiska. 1995. godine mu je izmeren krvni pritisak 190/120 mmHg i tada je dobio sledecu terapiju: Prilazid plus 5 mg ujutru i 5 mg uvece.Navodi da je ovu terapiju uzimao oko 10 godina.Do sada najvece vrednosti izmerenog krvnog pritiska bile su pre nekoliko meseci, ovde u Hagu, i to maksimalno 170/120 mmHg.Najcesce vrednosti krvnog pritiska su: za sistolni 120-140 mmHg, a za dijastolni 80-100 mmHg.Ovo su srednje vrednosti u poslednjih nekoliko godina od kada uzima sledecu terapiju: Ascal cardio 1x 100 mg, Cilazapril 2x 5 mg, Hydrochloorthiazide 1x 25 mg, Lercanidipinehydrochloride 2x 10 mg,

• Porodicno opterecenje za koronarne bolesti, i to: otac je umro od iznenadne srcane smrti u svojoj 54. godini. Majka je bila srcani bolesnik i umrla je u 84. godini zivota.

• Izrazeni hronicni stresni sindrom ( boravak u pritvorskim uslovima itd.)

Dosadasnje bolesti:

Kao dete lecen od rahitisa. U osnovnoj skoli lecen od upale pluca. 1980 g. imao je ponovnu upalu pluca / recidiv/. Tih godina imao je gnojnu upalu krajnika. 1986 g. lecen od upale mokracne besike. Tokom ispitivanja navodno mu je receno da je imao pocetnu tuberkulozu bubrega. 1986 g. lecen od prostatitisa. 1986 g. dijagnostikovana polenska alergija. Od tada je poceo da dobija Flosteron / kortikosteroid / u prevenciji alergijske kijavice. Daje podatak da se od tada pocinje gojiti. 1987 g. je operisao krajnike. Nakon toga u jos jednom navratu imao upalu pluca. 1992 g. operisao diskus herniju. Nakon toga je isao u ambulantu alternativne medicine gde je tretiran akupunkturom 1977 g. nosi naocare / kratkovidost dioptrija oko 2.5/.

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1997 g. u Klinickom centru Srbije dijagnostikovana mu je bronhijalna astma. Iako je i ranije dobijao terapiju od tada je na redovnoj inhalacionoj terapiji uz Seretide 250 mg. i Flosteron amp. Po potrebi. U sezonama kada se ocekuje ekspozicija alergenu dobija preventivnu terapiju za alergije. 2003 g. je operisao obostrano preponske kile. I dalje ima povremenu nelagodnost i povremene bolove u predelu testisa. 2005 g. ispitivan je u vezi sa rektalnim krvarenjem. 2006 g. Poceo da uzima Diflucan zbog oralne gljivicne infekcije. 2006 g. dijagnostikovan hemangiom jetre. 2006 g. Radjena magnetna rezonanca kicmenog stuba. Dijagnostikovan prolabiran diskus C5/ C6. Takodje vidjene degenerativne promene na kostano zglobnim sistemima. 2006 g. Ispitivan je kod gastroenterologa zbog sumnje na pozitivnost helikobacter pilori. 2006 g. Radjena gastroskopija. Nadjen refluks ezofagitis stepena C. 2006 g. Radjena kolonoskopija. Test je opisan kao normalan. 2007 g. Radjen CT skener abdomena i pri tome nije bilo sigurnih znakova ingvinalne hernije. Marta 2007 g. Radjeno je ultrazvucno snimanje abdominalnih organa. U desnom reznju jetre su uocljive tri ehogene promene jedna od 3 cm i dve od 1,5 cm, sto je odgovaralo hemangiomima. 2007 g. Nakon toga radjena magnetna rezonanca abdomena i prem a opisu potvrdjeno je da se radi o hemangiomima u jetri. Tokom 2008 g. Prema podacima iz medicinske dokumentacije dolazilo je do cestog variranja krvnog pritiska, cak do 190/120 mmHg. Avgusta i septembra 2008 g. Se zalio na bolove u desnoj nozi nezavisno od fizickog napora. Od avgusta 2008 g. zna za povecane vrednosti transaminaza, posebno AST, ALT ali i bilirubina. Februara 2009 g. Ponavljan je ultrazvuk abdomena ukljucujuci i jetri i pri tome nisu nadjene nove patoloske promene. Maja 2009 g. U jednom navratu izmerena je glukoza do 10.6. Juna 2009 g. Radjen je pregled uha, grla i nosa i dokazana infekcija uha.

Dosadasnje srcane bolesti

Nije redovno kontrolisao krvni pritisak , ali misli da verovatno duze vreme ima hipertenziju. Krajem jula 2009. godine ( na osnovu E-maila od 04. Avgusta 2009. godine), bolesnik je imao epizodu atrijalne fibrilacije koja je konvertovana u sinusni ritam odgovarajucim lekovima. Od tada uzima sledece lekove:Ascal cardio 1xdd 100 mg, Cilazapril 2xdd 5 mg, Hydrochloorthiazide 1xdd 25 mg, Lercanidipinehydrochloride 2xdd 10 mg, Pantaprazol 1xdd 40 mg, Montelukast 1xdd 10 mg, Seretide discus 250/50 2xdd 1 inhalation, Salbutamol 100 mcg po potrebi.

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Povremeno imao atipicne nelagodnosti u grudima , a povremeno i u abdomenu, ali je to pripisivao strajku gladju.

Sadasnje glavne tegobe

Uobicajeni fizicki napor dobro podnosi , ali pri intenzivnijim naporima / fudbal itd./ cesto oseti veliki nedostatak vazduha. Negira anginozne tegobe. Nije uzimao Nitroglicerin. Navodi da se nelagodno oseca i ne moze da lezi na levoj strani. Ima osecaj nepravilnog srcanog rada , uglavnom posle fizickih napora. Lezi na normalnom uzglavlju . Nema nocnih gusenja. Primecuje otoke nogu , posebno tokom dana i posle duzeg stajanja. Povremeno ima vrtoglavice ali nije gubio svest. U predelu leve polovine cela ima ceste bolove tipa probada. Zali se na potiljacne glavobolje ,zujanje u usima. Negira febrilnosti. Druge tegobe ne navodi. Objektivni kardioloski nalaz (fizickim pregledom):

Opste stanje: svestan, orijentisan, eupnoican , afebrilan, gojazan po opstem tipu. Glava: uobicajene konfiguracije , bez bolne osetljivosti na sukusiju. Vene vrata nisu napete i ne cujem sumove. Nad arerijama vrata ne cujem sumove. Fizickim pregledom ima se utisak da je stitasta zlezda u granicama normale. Grlo lako hiperemicno nije edematoxno, gnojne naslage se ne vide. Limfne zlezde: nije uocena patoloska periferna limfadenopatija. Grudni kos uobicajene konfiguracije. Na plucima lako oslabljeno vezikularno disanje. Povremeno polifoni zvizduci. Nema znakova zastojnih promena. Srcana akcija ritmicna oko 70/min. povremene ekstrasistole , tonovi nesto tisi/ verovatno zbog konfiguracije grudnog kosa/, patoloske sumove ne cujem. Arterijski krvni pritisak na levoj ruci 150/100 mmHg. U svim standardnim polozajima. Arterijski krvni pritisak na desnoj ruci 145/95 mmHg. U svim standardnim polozajima. Abdomen mek, palpatorno bolno neosetljiv, fizickim pregledom nema znakova prisustva slobodne tecnosti. Jetra na rebarnom luku /verovatno spustena/ Slezina se ne palpira. Fizickim pregledom nema slobodne tecnosti u abdomenu.

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Na potkolenicama nema kardijalnih edema , pulzacije perifernih arterija lako oslabljene. EKG: (opis EKG-a dajem po secanju iz jula 2009. godine, jer nisam dobio originalne EKG zapise). Sinusni ritam oko 70/min., registrovane dve komorske ekstrasistole (PVC).

REZULTATI OSNOVNIH LABORATORIJSKIH ANALIZA (datum 3 0. juli 2009. godine): ALT 51 U/l (povecan), totalni bilirubin 29 umol/l (povecan), konjugovani bilirubin 5 umol/l (povecan), T3 2,6 nmol/l (na gornjoj granici normale), holesterol 5,4 mmol/l, trigliceridi 2,0 mmol/l, HDL holesterol 1,0 mmol/l, LDL holesterol 3,4 mmol/l,. Ostale laboratorijske vrednosti opisane su kao normalne.

MERENJE KRVNOG PRITISKA TOKOM 24 CASA (datum 29. ju li 2009. godine): (U prevodu koji sam dobio napisane su samo sledece reci: tabela, aktivnosti, simptomi, lekovi). Dakle, nema izmerenih vrednosti krvnog pritiska, niti lekarskog opisa ovog nalaza, pa se o ovom pregledu ne mogu izjasnjavati.

ERGOMETRIJA (datum 29. juni 2009. godine): (U prevodu sam dobio samo tekst koji sadrzi opise parametara ergometrijskog testa, ali nisam dobio originalni EKG zapis). Postignuto je opterecenje od 187 W, sto iznosi 86% ciljnog opterecenja. Tom prilikom, srcana frekvenca je maksimalno bila 150 u minuti, sto iznosi 90% ocekivane frekvence. Maksimalne vrednosti krvnog pritiska su bile 210/95 mmHg. Navodi se da bolesnik nije imao anginoznih bolova, te da su razlozi za prestanak testa zamor. U prevodu nije jasno da li je prilikom opterecenja bilo poremecaja srcanog ritma, niti drugih promena. Na osnovu opisa koji sam dobio, zakljucujem sledece: ergometrijski test je pokazao ocuvanu koronarnu rezervu, ali postoji tendencija hipertenzivnog reagovanja u opterecenju.

PREGLED FUNDUSA OKA (datum 5. avgust 2009. godine): na ocnom dnu nisu vidjene patoloske promene. Preporucena kontrola za godinu dana.

RADIOLOSKI PREGLED GRUDNOG KOSA (datum 5. avgust 2009. godine): RTG snimak grudnog kosa ne pokazuje patoloske promene.

FUNKCIJA RESPIRATORNOG SISTEMA (datum 5. avgust 2009. godine): saturacija 97%, puls 88/min.

ZAKLJUCAK PULMOLOGA (datum 5. avgust 2009. godine): bolesnik boluje od astme, ali se stanje moze smatrati zadovoljavajucim. Trenutno nema pogorsanja stanja. Preporucuje se nastavak dosadasnje terapije. Ukoliko je potrebno, cesce koristiti ventolin. Bilo bi pozeljno uzimati Singulair 10 mg.

U anamnezi nema nikakvih indikacija za sindrom opstruktivne apneje u snu. Za pacijenta bi bilo korisno da se izvrsi nocno merenje saturacije, kako bi se iskljucio Pikvikov sindrom ili OSAS (sindrom opstruktivne apneje u snu).

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MAGNETNA REZONANCA SRCA SA DOBUTAMINSKIM OPTERECE NJEM ( 11.09.2009. godine ): maksimalna doza Dobutamina bila 40 mcg. Srcana frekvenca povecana od 68/min. do 185 /min. a krvni pritisak od 130/85 do 185/90 mmHg. Nije imao tegoba tokom testa. Nisu registrovani poremecaji kontraktilnosti. Takodje nisu registrovani defekti perfuzije.

PREGLED ENDOKRINOLOGA (datum 5. avgust 2009. godine): secer 4,9 mmol/l, ASAT 27 U/l, ALAT 52 U/l, bilirubin total 29 umol/l, konjugovan 5mmol/l, CRP 5 mg/l, TSH 0,7 mU/l, FT4 17,2 pmol/l, holesterol 5,4 mmol/l, trigliceridi 2,0 mmol/l, HDL holesterol 1,0 mmol/l, LDL holesterol 3,4 mmol/l, holesterol HDL holesterol odnos 5,4. Zakljuceno je da nema znakova secerne bolesti, niti poremecaja funkcije stitaste zlezde. Postoji prevelika telesna tezina (BMI 40). Takodje, postoji poviseni LDL holesterol (3,4 mmol/l). Blago povisena transaminaza, verovatno uzrokovana steatozom. Poviseni nekonjugovani bilirubin, verovatno zbog Gilbertove konjugovane anomalije.

PREGLED NEUROLOGA (datum 6. avgust 2009. godine): Uradjen je carotid duplex test. Nisu nadjene hemodinamski znacajne stenoze na karotidnim arterijama. Bolesnik ima radikulopatiju koju povremeno suzbija nesteroidnim antiinflamatornim lekovima. U ovom trenutku nema znakova radikulitisa.

EHO PREGLED DONJIH EKSTREMITETA (datum 6. avgust 2009. godine): Pregled pokazuje ocuvanu cirkulaciju kroz arterije i vene femoralis, kao i vene poplitea. Nema znakova tromboze unutrasnjih vena.

KOMPJUTERSKO-TOMOGRAFSKA ANGIOGRAFIJA (CTA) TORAKSA (datum 21. mart 2006. godine): Nalaz je opisan kao normalan. Ukupan kalcijumski skor je 0.

PREGLED HIRURGA (datum 4. avgust 2009. godine): Operisao bruh, levo ingvinalno, 2003. godine. Fizickim pregledom (na dodir) nisu nadjeni znaci recidiva. Preporucen ehogram.

DIJAGNOZE:

Hypertensio arterialis Fibrilatio atriorum parosmalis ( na osnovu E-maila od 04. avgusta 2009. godine) Hypercholesterolemia Obesitas Hemangioma hepatis Asthma bronchiale Discopathia C5/C6 Status post operationem hearnie ingvinalis lat. sin.

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RIZICI I OPASNOSTI: � Zbog znacaja zivotne dobi od 55 godina kao faktora rizika, moguc je nastanak

koronarne arterijske bolesti u skorijem vremenskom intervalu, bez obzira sto su ostali testovi na ishemiju za sada uglavnom normalni.

� Samo na osnovu pola, muskarci , koji uz to jos imaju i arterijsku hipertenziju, imaju relativni rizik oko 2 za razvoj srcanih bolesti, cak i kada su im svi drugi zdravstveni parametri normalni.

� Najveci broj muskaraca zivotne dobi od 50 do 59 godina, u desetogodisnjem period, ima rizik od nastanka kardiovaskularnih bolesti od 6% do preko 20%.

� Osobe muskog pola, sa povecanom telesnom masom ( gojaznost BMI ≥ 30,9 kg/m2

), imaju i do 30 procenata veci rizik za razvoj kardiovaskularnih obolenja u odnosu na normalno uhranjene osobe.

� Ukoliko ove osobe imaju i hipertenziju, tada je relativni rizik za razvoj

kardiovaskularnih bolesti veci od 3.

� Obesity is associated with an increased risk of morbidity and mortality as well as reduced life expectancy. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system.

� Ovaj bolesnik ima povisene vrednosti LDL holesterola i blago povisene vrednosti ukupnog holesterola te prema tome ima znacajan rizik za razvoj ateroskleroze i svih drugih kardiovaskularnih komplikacija.

� Prediktivna verovatnoca razvoja nepovoljnih kardiovaskularnih dogadjaja kada se uzme u obzir ovaj faktor rizika je oko 30 %.

� Uzimajuci u obzir vrednosti pritiska koje su se kretale i preko 175/105 mmHg., ovaj bolesnik ima i do osam puta /8x/ veci rizik za kardiovaskularnu smrt u odnosu na kontrolnu grupu /videti grafikone/.

� Kako pacijent ima i druge faktore rizika koji su udruzeni sa arterijskom hipertenzijom to znaci da je verovatnoca nastanka nepovoljnih kardiovaskularnih dogadjaja opisana eksponencijalnom krivuljom u funkciji vremena.

� U slucajevima izenadnog besa ili ljutnje relativni rizik od nastanka infarkta srca je izmedju 2 i 4.

� Ukoliko bi doslo do razvoja infarkta srca dalje depresivne reakcije bi za 24% pogorsale tok te bolesti u odnosu na 17.6% koliko bi se desavalo u kontrolnoj grupi ovih bolesnika.

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� Zbog socijalne izolacije stopa mortaliteta kod ovih bolesnika je znacajno

povecana u odnosu na grupe koje nisu u uslovima socijalne izolacije / pritvora/.

� Iznenadna srcana srcana smrt oca predstavlja snazan factor rizika za nastanak iznenadne srcane smrti cak i bez obzira na postojanje ili ne postojanje strukturnih ostecenja miokarda.

� Znajuci da bolesnik ima povremeno sistolni pritisak veci od 155 mmHg, relativni rizik od razvoja iznenadne smrti se krece oko 1.4 na 1000 tokom jedne godine.

� Registrovane ventrikularne ekstrasistolne aritmije u mirovanju /PVC/ u odredjenom procentu smanjuju verovatnocu prezivljavanja ovih bolesnika u periodu od 80 meseci.

� Uocene ventrikularne ekstrasistole u mirovanju ukazuju da ovaj bolesnik moze imati sklonost poremecajima srcanog ritma, a sto je i detektovano epizodom atrijalne fibrilacije /prema podacima iz Vaseg E-maila iz avgusta 2009 g./

� Blago povecana leva pretkomora ukazuje na pocetno strukturno ostecenje miokarda. Slicno patofiziolosko znacenje ima i blaga aortna regurgitacija.

� U daljem toku je moguca progresija ovih poremecaja, pojava dodatnih strukturnih ostecenja srca i pojava novih kardiovaskularnih dogadjaja kao sto su poremecaji srcanog ritma tipa atrijalne fibrilacije itd.

� Arterijska hipertenzija je najcesci uzrok atrijalne fibrilacije ili drugih oblika supraventrikularnih poremecaja srcanog ritma u bolesnika koji nemaju reumatsku manu.

� U bolesnika zivotne dobi 50-59 godina atrijalna fibrilacija ima verovatnocu razvoja mozdanog udara od oko 3% na godisnjem nivou.

� Takodje atrijalna fibrilacija dodatno dovodi do str ukturnih ostecenja miokarda i razvoja novih nepovoljnih kardiovaskularnih dogadjaja.

� Zbog uzimanja bronhodilatatora /lekovi za astmu/ povecana je verovatnoca nastanka srcanih aritmija koje u odredjenim stanjima mogu biti potencijalno veoma opasne.

� Iz istih razloga otezana je medikamentozna kontrola krvnog pritiska i srcanog ritma /Beta adrenergicka stimulacija/.

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KARDIOLOSKA TERAPIJA:

Cilazapril 2x 5 mg, uz povremnu kontrolu krvnog pritiska i srcane frekvence kada se doza moze korigovati. Hydrochloorthiazide 1x 25 mg, uz povremenu kontrolu krvnog pritiska i elektrolita u krvi kada se doza moze korigovati. Lercanidipinehydrochloride 2x 10 mg, uz povremnu kontrolu krvnog pritiska i srcane frekvence kada se doza moze korigovati. Pravacor 20 mg uvece uz dijetu za snizavanje holesterola u krvi, uz redukciju telesne mase, a obavezna i kontrola transeminaza za oko 3-4 nedelje Ascal cardio 1x 100 mg, posle dorucka Pantaprazol 1x 40 mg, uz kontrolu i savete gastroenterologa Montelukast 1x 10 mg, po preporuci i savetima pulmologa i alergologa Seretide discus 250/50 2x 1 inhalacija, po preporuci i savetima pulmologa i alergologa Salbutamol 100 mcg po potrebi, po preporuci i savetima pulmologa i alergologa.

PREPORUKE: 1. Redovno uzimanje odgovarajuce terapije

2. Neophodna je redukcija telesne mase ( gojaznosti ) koja moze pomoci znacajnom

smanjenju krvnog pritiska, a time i smanjenju sveukupnih kardiovaskularnih rizika ovog bolesnika.

3. Neophodno sprovesti sve mere prevencije / lecenja/ poremecaja lipida u krvi /

holesterola i LDL/ kako primenom higijensko –dijetetskog rezima, tako i kontrolisanim i razumnim koriscenjem hipolipemika /statina/.

4. Izuzetno je vazno, kako ne medikamentoznim tako i medikamentoznim

nacinima lecenja krvni pritisak drzati u granicama normale / manje slana ishrana itd/.

5. Preduzeti sve razumne, a realno moguce mere, radi sprecavanja iznenadnih

mentalnih stresnih situacija kod ovog bolesnika /ukoliko je potrebno i medikamentoznim tretmanom/.

6. Neophodno je pratiti bolesnika i povremeno monitorirati /24 casovni holter EKG

itd./ mogucu pojavu kompleksnih poremecaja srcanog ritma i po potrebi sprovoditi sve neophodne dijagnosticke i terapijske procedure.

7. Neophodno je povremeno ehokardiografsko pracenje ovog bolesnika, povremena kontrola srcanog ritma, stroga kontrola krvnog prit iska /jer je poznato da je arterijska hipertenzija jedan od najvaznijih faktor a koji dovode do nastanka atrijalne fibrilacije u bolesnika koji nemaju znacajna ostecenja srcanih zalistaka, a imaju verifikovane povecane dimenzije leve srcane pretkomore/.

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8. Neophodno je preduzeti sve mere sprecavanja nastanka ventrikularnih

ekstrasistola /PVC/ , mogucih epizoda atrijalne fibrilacije, drugih fatalnih poremecaja srcanog ritma, kao i sprecavanja nastanka emoblijskih dogadjaja, a posebno infarkta mozga.

9. Potrebne su redovne kontrole kod kardiologa, pulmologa, alergologa, gastroenterologa, neurologa, hirurga, hepatologa, a po potrebi i drugih specijalnosti.

10. Savetuje se i izvrsiti ultrazvucni pregled stomaka / kako je preporuceno od strane hirurga, ali prema meni dostupnoj dokumentaciji to do sada nije ucinjeno/.

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NAJVAZNIJI KARDIOVASKULARNI PODACI OD ZNACAJA ZA EKSPERTIZU:

1. Faktori rizika za kardiovaskularne bolesti: • Zivotna dob 55 godina. • Muski pol • Gojaznost, TT = 120 kg, TV = 1,97m, BMI = 30,9 kg/m2 • Hypercholesterolemia ( holesterol 5,4 mmol/l, LDL holesterol 3,4 mmol/l ) • Arterijska hipertenzija ( max 190/120 mmHg, najcesce za sistolni 120-140 mmHg,

a za dijastolni 80-100 mmHg ) • Stresovi • Porodicno opterecenje - sklonost (otac je umro od iznenadne srcane smrti u svojoj

54. godini)

2. Dosadasnja nesrcana obolenja • Asthma bronchiale • Hemangioma hepatis • Discopathia C5/C6 • Status post operationem hearnie ingvinalis lat. sin. • Reflux oesophagitis

3. Dosadasnja srcana obolenja it ok bolesti

• Arterijska hipertenzija • Paroksizam atrijalne fibrilacije (Krajem jula 2009. godine, na osnovu E-maila od

04. Avgusta 2009. godine, bolesnik je imao epizodu atrijalne fibrilacije koja je konvertovana u sinusni ritam odgovarajucim lekovima).

4. Sadasnje glavne tegobe • Nedostatak vazduha pri intenzivnijim naporima / fudbal itd. / • Osecaj nepravilnog srcanog rada , uglavnom posle fizickih napora

5. Objektivni nalaz:

• Srce i. EKG: Ventrikularne ekstrasistole u mirovanju

ii. Transtorakalna ehokardiografija: � Blago povecane dimenzije leve pretkomore � Blaga aortna regurgitacija

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FAKTORI RIZIKA

Zivotna dob

PODATAK (CINJENICA) 55 godina

Dokaz o tacnosti podatka: Podaci iz dokumentacije

RIZICI (OPASNOSTI):

• U dobi od 55 godine, kod muskarca, verovatnoca nastanka koronarne bolesti je oko 51%, cesto i bez drugih znacajnih provokativnih faktora.

• Prema Framingamskoj studiji, ali i u ostalim novijim studijama, zivotna dob je nezavistan faktor rizika, a absolutni rizik od koronarne bolesti se progresivno povecava sa povecavanjem starosne dobi.

DOKAZI: Prevalence of cardiovascular disease in American adults

Verovatnoca postojanja KAB je oko 51%

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(Adapted from the American Heart Association)

Preuzeto iz J Am Coll Cardiol 1999;34:1348 –59

ZAKLJUCAK:

• Zbog znacaja zivotne dobi od 55 godina kao faktora rizika, moguc je nastanak koronarne arterijske bolesti u skorijem vremenskom intervalu, bez obzira sto su ostali testovi na ishemiju za sada uglavnom normalni.

Literatura: 1. Rossouw JE: Hormones, genetic factors, and gender differences in cardiovascular

disease. Cardiovasc Res 2002, 53: 550–557.

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2. Am J Cardiol. 1989 Sep 15;64(10):555-9. 3. J Am Coll Cardiol 1999;34:1348 –59.

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Muski pol

PODATAK (CINJENICA):

Muski

RIZICI (OPASNOSTI):

� Samo na osnovu pola, muskarci , koji uz to jos imaju i arterijsku hipertenziju, imaju relativni rizik oko 2 za razvoj srcanih bolesti, cak i kada su im svi drugi zdravstveni parametri normalni.

� Najveci broj muskaraca zivotne dobi od 50 do 59 godina, u desetogodisnjem period, ima rizik od nastanka kardiovaskularnih bolesti od 6% do preko 20%.

DOKAZI:

Relative coronary heart disease risk in men

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Relativni rizik za KAB samo po osnovu pola dobi je oko 2

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Estimated 10-year hard CHD risk: Framingham Heart Study offspring and cohort men

Estimated 10-year hard coronary heart disease (CHD) risk: Framingham Heart Study offspring and cohort men. The risk of hard CHD (myocardial infarction, CHD death) according to age decile is shown for Framingham men according to several categories of CHD risk (< 6%, 6%-10%, 10%-20%, and > 20% over 10 years). Most men are at very low risk up to age 40 years. After age 50 years the majority of men are at intermediate risk, and high risk (> 20%/10 years) is an important contributor only after 60 years of age. (Adapted from Pasternak et al. )

ZAKLJUCAK: • Kod ovog bolesnika, relativni rizik za nastanak kardiovaskularnih bolesti je oko

2, a desetogodisnja verovatnoca je od 6% do preko 20% .

Literatura:

1. D'Agostino RB, Grundy S, Sullivan LM, Wilson P: Validation of the Framingham coronary heart disease prediction scores: results of a multiple ethnic groups investigation. JAMA 2001, 286: 180–187.

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2. Pasternak RC, Abrams J, Greenland P, et al.: 34th Bethesda Conference: task force #1. Identification of coronary heart disease risk: is there a detection gap? J Am Coll Cardiol 2003, 41: 1863–1874.

Gojaznost – “Body mass index”

PODATAK (CINJENICA):

Visina = 1,97 m

Telesna masa = 120 kg

BMI = 30,9 kg/m2

Dokaz o tacnosti podatka:

Podaci iz medicinske dokumentacije

RIZICI (OPASNOSTI):

� Osobe muskog pola, sa povecanom telesnom masom ( gojaznost BMI ≥ 30,9 kg/m2 ), imaju i do 30 procenata veci rizik za razvoj kardiovaskularnih obolenja u odnosu na normalno uhranjene osobe.

� Ukoliko ove osobe imaju i hipertenziju, tada je relativni rizik za razvoj kardiovaskularnih bolesti veci od 3.

� Obesity is associated with an increased risk of morbidity and mortality as well

as reduced life expectancy. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system.

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DOKAZI:

Yusuf S et al, Lancet 2005

Population attributable risk percent for overweight and obesity in relation to

cardiovascular disease risk factors and outcome in men

Ovaj bolesnik ima znacajan rizik od razvoja svih kardiovaskularnih obolenja i to samo po osnovu gojaznosti.

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The population attributable risk percent for overweight (body mass index [BMI] 25-30 kg/m2) and obesity (BMI > 30 kg/m2) in relation to a variety of cardiovascular disease (CVD) risk factors and CVD outcomes is shown for men. In general, approximately 25% of CVD outcomes can be attributed to excess adiposity and the effects of overweight are generally greater that what is observed for frank obesity. CHD—coronary heart disease

Women

0

1

2

3

4

5

6

<21 22 23 24 25 26 27 28 29 30

Body Mass Index (kg/m )

Rela

tive

risk

Men

0

1

2

3

4

5

6

<21 22 23 24 25 26 27 28 29 30

Body Mass Index (kg/m )

Type 2 diabetes

Cholelithiasis

Hypertension

Coronary heart disease

2 2

Relatiom between body mass index (BMI) and comorbidities. Two large-scale studies, the Nurses Health Study and Health Professionals Follow-Up Study, followed large groups of subjects for several years. Among these subjects, the risk of various diseases was closeley related to BMI. Cholelithiasis, hypertension, and coronary heart disease all increased at comparable rates-a person with a BMI of 30 had approximatley three to four times the risk of a person with a BMI of 21. The risk of type 2 diabetes, however, increased much more sharply.

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0

50

100

150

200

250

300

Mor

talit

y ra

tio

Low risk

Moderate risk

High risk

15 20 25 30 35 40

BMI (kg/m )2

a

b

c

a b c

Relationship between body mass index (BMI) and mortality ratio

Lifestyle Modification

Modification Approximate SBP reduction

(range)

Weight reduction 5–20 mmHg/10 kg weight loss

Adopt DASH eating plan 8–14 mmHg

Dietary sodium reduction 2–8 mmHg

Physical activity 4–9 mmHg

Moderation of alcohol

consumption

2–4 mmHg

ZAKLJUCAK:

• Gojaznosti je vazan faktor rizika koji se ne sme zanemarivati, jer uz druge nepovoljne cinioce, moze dovesti do kriticnog narusavanja zdravlja ovog bolesnika.

• Prema istrazivanjima, samo zbog velikog BMI koji je veci od 30, postoji znacajna verovatnoca razvoja koronarne smrti ali i drugih nepovoljnih kardiovaskularnih dogadjaja.

• Redukcija telesne mase ( gojaznosti ) moze pomoci znacajnom smanjenju krvnog pritiska, a time i smanjenju sveukupnih kardiovaskularnih rizika ovog bolesnika.

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Literatura: 1. Wilson PW, D’Agostino RB, Sullivan L, et al.: Overweight and obesity as

determinants of cardiovascular risk: the Framingham experience. Arch Intern Med 2002, 162: 1867–1872.

2. Willet WC, Dietz WH, Colditz GA. Guidelines for healthy weight. N Engl J Med 1999;341:427-434.

3. Paul Poirier, Thomas D. Giles, George A. Bray, Yuling Hong, Judith S. Stern, F. Xavier Pi-Sunyer and Robert H. Eckel. Statement on Obesity and Heart Disease From the Obesity Committee of the Weight Loss: An Update of the 1997 American Heart Association Scientific Obesity and Cardiovascular Disease: Pathophysiology, Evaluation, and Effect of Council on Nutrition, Physical Activity, and Metabolism. Circulation 2006;113;898-918; originally published online Dec 27, 2005; DOI: 10.1161/CIRCULATIONAHA.106.171016.

4. Express—Succinct evidence-based recommendations. Published in JAMA May 21, 2003.

5. Bray GA. Ann Inter Med 1985;103:1052-1062.)

Hiperholesterolemia

PODATAK (CINJENICA):

( holesterol 5,4 mmol/l, LDL holesterol 3,4 mmol/l

Dokaz o tacnosti podatka:

Podaci iz medicinske dokumentacije

RIZICI (OPASNOSTI):

� Oksidirani LDL je znacajniji 26redictor kardiovasku larnih obolenja u odnosu na ukupni holesterol, a povisene vrednosti LDL su marker ubrzane ateroskleroze.

� In patients 30-74 years of age with HTN (BP ≥140/90 mm Hg [130/80 mm Hg if diabetes mellitus, DM] or medication for HTN) from the NHANES 2001-2002 (N=676), this analysis assessed the CHD events that could be prevented from combined control of BP, LDL-C, and HDL-C (Patients with CVD were excluded from the analysis since the Framingham risk algorithms used were not applicable for these persons.).Using Framingham risk algorithms, 10-year risk of CHD (and corresponding number of CHD events) were projected based on both current (“uncontrolled”) risk factor levels an d “controlled” risk factor levels, using nominal treatment goals. The difference in CHD events predicted represented the events “prevented”. SUDAAN software utilized sample weights for projecting to the US population.

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Control of BP, LDL-C, and HDL-C was defined as Nominal control of BP: <140/90 mm Hg (or <130/80 mm Hg if DM was present). Nominal control of lipids: LDL-C <130 mg/dL (or <100 mg/dL if DM was present) and HDL-C >45 mg/dL.In the overall group of patients with HTN, 38% of CHD events could potentially be prevented by nominal control of BP and lipids.

DOKAZI:

Factors Contributing to Cardiometabolic Risk

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PROCAM StudyMI-Incidence according to LDL-cholesterol and triglycerides

The incidence of myocardial infarction (MI) increases with increasing TG levels and with increasing LDL-cholesterol levels

Blood Pressure, lipids and coronary artery disease

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ZAKLJUCAK: � Ovaj bolesnik ima povisene vrednosti LDL holesterola i blago povisene

vrednosti ukupnog holesterola te prema tome ima znacajan rizik za razvoj ateroskleroze i svih drugih kardiovaskularnih komplikacija.

� Prediktivna verovatnoca razvoja nepovoljnih kardiovaskularnih dogadjaja kada se uzme u obzir ovaj faktor rizika je oko 30 %.

� Zato je neophodno sprovesti sve mere prevencije / lecenja/ kako primenom higijensko –dijetetskog rezima, tako i kontrolisanim i razumnim koriscenjem hipolipemika /statina/.

Literatura:

1. Cui Y et al. Non high density lipoprotein cholesterol level as a predictor of cardiovascular disease mortality. Arch Intern Med 2001; 161: 1413-19.

2. Amaki T, et al. Cirulatin malondyaldehide modified LDL is a biochemical risk marker for coronary artery disease. Heart 2004: 90: 1211-13.

3. John D. Brunzell, Michael Davidson, Curt D. Furberg, Ronald B. Goldberg,

Barbara, V. Howard, James H. Stein, and Joseph L. Witztum. Lipoprotein Management in Patients With Cardiometabolic Risk: Consensus Conference Report From the American Diabetes Association and the American College of Cardiology Foundation. J. Am. Coll. Cardiol. 2008;51;1512-1524; originally published online Mar 27, 2008; doi:10.1016/j.jacc.2008.02.034.

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Arterijska hipertenzija

PODATAK (CINJENICA):

• Arterijska hipertenzija ( max 190/120 mmHg, najcesce za sistolni 120-140 mmHg, a za dijastolni 80-100 mmHg )

Dokaz o tacnosti podatka:

Podaci iz medicinske dokumentacije

RIZICI (OPASNOSTI):

� Blaga sistolna hipertenzija od 140-159mmHg je udruzena sa 50-60% vecom incidencijom kardiovaskularne smrti

� Izolovana sistolna hipertenzija je znacajniji 31actor rizika od dijastolne kod osoba starijih od 50 godina, prema JNC VII preporukama.

� High-normal blood pressure is associated with an increased risk of major cardiovascular events, which are defined as death due to cardiovascular disease or as having recognized myocardial infarction, stroke, or congestive heart failure. In a study by Vasan et al. (2001), patients with a high-normal blood pressure (i.e., a systolic blood pressure of 130–139 mm Hg and a diastolic blood pressure of 85–89 mm Hg) at baseline were tracked for 10 years to determine the incidence of cardiovascular events at follow-up. Initially, the 6,859 patients in the study were free of both hypertension and clinical cardiovascular disease. Over the course of the study, however, a high-normal blood pressure was found to be associated with an increased risk of cardiovascular events; the 10-year incidence of such events was 8% in men between the ages of 35 and 64 years and 25% in men between the ages of 65 and 90 years. When compared with optimal blood pressure, having a high-normal blood pressure was associated with a risk factor-adjusted hazard ratio for cardiovascular disease of 1.6.

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� Lewington et al. (2002) evaluated data from approximately 1 million adults who participated in 61 prospective observational studies on blood pressure and mortality. In adults between the ages of 40 and 69 years, each 20/10-mm Hg increase in blood pressure doubled the risk of mortality from stroke, ischemic heart disease, and other vascular causes. This finding was the same for men and women. It is included as a key message in the 2003 JNC 7 report on high blood pressure.

� The importance of SBP elevation as a cause of cardiovascular disease (CVD) mortality is emphasized by the Prospective Studies Collaboration, a meta-analysis of 120,000 deaths among 1 million participants in 61 cohorts, which is among the largest meta-analyses of its kind. Individuals with preexisting vascular disease were excluded from the meta-analyses.

� During 12.7 million person-years at risk, there were about 56,000

vascular deaths (12,000 stroke, 34,000 ischemic heart disease [IHD], 10,000 other vascular) from ages 40 to 89 years. This slide shows the stroke and IHD mortality rates in each decade of age versus usual BP at the start of that decade. Throughout middle age, each difference of 20 mm Hg usual (long-term average) SBP is associated with a more than 2-fold difference in the stroke death rate. Because stroke is more common in old age than in middle age, the absolute annual differences in stroke death associated with a given BP difference are greater in old age. Similarly, each 20–mm Hg difference in usual SBP was associated with 2-fold differences in the death rate from IHD. The proportional differences found in vascular mortality were reduced substantially in the 80- to 89-year group. The data from this large study indicate that usual BP is directly and significantly related to vascular mortality, with no threshold evident down to 115/75 mm Hg. The long-term average BP is positively related to the risks of death from vascular disease not only among individuals who are considered hypertensive, but also among those who would usually be considered normotensive.

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DOKAZI:

Slide SourceHypertension Online

www.hypertensiononline.org

*Defined as death due to cardiovascular disease or as having recognizedmyocardial infarction, stroke, or congestive heart failure.

Cumulative Incidence of Major

Cardiovascular Events (%) 16

12

10

8

6

4

2

0

14

0 2 4 6 8 10 12

Time (Years)

Optimal<120/80 mm Hg

Normal120–129/80–84 mm Hg

High-Normal130–139/85–89 mm Hg

Impact of High-Normal Blood Pressure on Risk of Major Cardiovascular Events* in Men

Vasan RS. N Engl J Med. 2001;345:1291-1297.

Blood Pressure:

Impact of High-Normal Blood Pressure on Risk of Major Cardiovascular Events in Men

Slide SourceHypertension Online

www.hypertensiononline.org

Lewington S, et al. Lancet. 2002;360:1903-1913;Chobanian AV, et al. JAMA. 2003;289:2560-2572.

Cardiovascular Mortality RiskIncreases as Blood Pressure Rises*

Cardiovascular

Mortality Risk

Systolic/Diastolic Blood Pressure (mm Hg)

0

1

2

3

4

5

6

7

8

115/75 135/85 155/95 175/105

2x

4x

8x

*Measurements taken in individuals aged 40–69 years, beginning with a bloodpressure of 115/75 mm Hg.

Cardiovascular Mortality Risk Increases as Blood Pressure Rises

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Stratification of CV Risk in four categories. SBP: systolic blood pressure; DBP: diastolic blood pressure; CV: cardiovascular; HT: hypertension. Low, moderate, high and very high risk refer to 10 year risk of a CV fatal or non-fatal event. The term ‘added’ indicates that in all categories risk is greater than average. OD: subclinical organ damage; MS: metabolic syndrome. The dashed line indicates how definition of hypertension may be variable, depending on the level of total CV risk.

The National Health Nutrition Examination Survey (NHANES)

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The importance of SBP elevation as a cause of cardiovascular disease

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ZAKLJUCAK: � Uzimajuci u obzir vrednosti pritiska koje su se kretale i preko 175/105 mmHg.,

ovaj bolesnik ima i do osam puta /8x/ veci rizik za kardiovaskularnu smrt u odnosu na kontrolnu grupu /videti grafikone/.

� Kako pacijent ima i druge faktore rizika koji su udruzeni sa arterijskom hipertenzijom to znaci da je verovatnoca nastanka nepovoljnih kardiovaskularnih dogadjaja opisana eksponencijalnom krivuljom u funkciji vremena.

� Zbog toga je izuzetno vazno kako ne medikamentoznim tako i medikamentoznim nacinima lecenja krvni pritisak drzati u granicama normale.

Literatura:

1. Odonnell CJ.et al. Hypertension and borderline isolated systolic hypertension increase risks of cardiovascular disease and mortality in male physicians. Circulation 1997; 95:1132-7.

2. 2007 Guidelines for the Management of Arterial Hypertension The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC). European Heart Journal doi:10.1093/eurheartj/ehm236.

3. Conroy RM, Pyorala K, Fitzgerald AP, Sans S, Menotti A, De Backer G, De

Bacquer D, Ducimetiere P, Jousilahti P, Keil U, Njolstad I, Oganov RG, Thomsen T, Tunstall-Pedoe H, Tverdal A, Wedel H, Whincup P, Wilhelmsen L, Graham IM. Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project. Eur Heart J 2003;24:987–1003.

4. World Health Organization/International Society of Hypertension. 2003. World

Health Organization (WHO)/International Society of Hypertension (ISH) statement on management of hypertension. J Hypertens 2003;21:1983–1992.

5. Vasan RS, Larson MG, Leip EP, et al. Impact of high-normal blood pressure

on the risk of cardiovascular disease. N Engl J Med. 2001;345:1291-1297.

6. Lewington S, Clarke R, Qizilbash N, Peto R, Collins R, for the Prospective Studies Collaboration. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002;360:1903-1913.

7. Chobanian AV, Bakris GL, Black HR, et al, for the National High Blood

Pressure Education Program Coordinating Committee. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA. 2003;289:2560-2572.

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8.

Stresovi

PODATAK (CINJENICA): Brige zbog aktuelnih nepovoljnih zivotnih dogadjaja, razmisljanja o buducnosti, socijalna izolacija, promenjivo raspolozenje.

Dokaz o tacnosti podatka: Podaci iz medicinske dokumentacije, razgovor sa bolesnikom.

RIZICI (OPASNOSTI):

� Stresovi povecavaju rizik od infarkta srca oko tri puta � Mentalni stres je jedan od najznacajnijih provokativnih cinilaca razvoja

nepovoljnih pa i smrtnih vaskularnih dogadjaja. � Ovo je dokazano u velikom broju kardioloskih istrazivanja. � Zbog nedostatka slobode i svi druge vrste stresova su izrazene kod ovakvih

bolesnika.

DOKAZI: Intense anger as a trigger for MI

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Intense anger is a trigger for myocardial infarction (MI) over a 2-hour hazard period , potentially useful information for individuals who are chronically angry.

INTERHEART study: depression in MI cases

The INTERHEART study reported increased depression in myocardial infarction cases compared with control subjects in all areas of the world and in all ethnic groups. Overall, depression occurred in 24% of cases versus 17.6% of control subjects; odds ratio = 1.55 [1.42-1.69]).

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Mortality rate according to level of social isolation

A study by House et al. reported on more than 37,000 people in five prospective studies in the United States and Europe observed for 8 to 13 years; categories of social ties included marriage, contact with extended family and friends, church membership, and other formal and informal affiliations. All-cause mortality was increased up to fourfold in initially healthy persons with the lowest versus the highest levels of social integration, with relative risk (RR) ratios higher for men than for women.

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Recurrent MI in socially isolated people

Case et al. observed 1234 patients for 1 to 4 (mean 2.7) years after acute myocardial infarction. At 6 months post myocardial infarction, the rate of recurrent events (another nonfatal myocardial infarction or cardiac death) was 79% greater in those living alone compared with those living with others. This was independent of marital disruption (divorce, separation, or widowhood). Similarly, Williams et al. observed 1368 consecutive patients undergoing cardiac catheterization and reported 3.34 times risk of death within 5 years in unmarried patients without a close confidant compared with those married or unmarried with a close confidant.

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High cardiac mortality correlates with social isolation

More recently, Brummet et al. reported that the most isolated coronary artery disease patients, those with three or fewer individuals in their social network, had the highest cardiac mortality over an approximately 4-year period after cardiac catheterization showing significant coronary artery disease (relative risk [RR] = 2.43). Socially isolated patients had less than half the number of social visits reported by the other patients, with more than one third averaging less than one network contact every 3 days. Isolated patients were less likely to be married or have a confidant, and they were pleased with a smaller proportion of the relationships that they did have. Once patients had social networks more than three individuals, there was no additional benefit for having larger networks. Apparently, once past a threshold, the adverse effect of social isolation is no longer a significant risk factor for cardiac death.

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Relationship between anger levels and MI and CHD mortality (view part: A • B)

In 2000, Williams et al. reported on 12,986 Americans without known coronary heart disease at baseline, aged 45-64 at entry, who were observed for a median of 53 months in the Atherosclerosis Risk in Communities (ARIC) Study. Anger was assessed by the Spielberger Trait Anger Scale. There was a strong graded relationship between increasing "trait anger" and subsequent myocardial infarction (MI) and coronary heart disease mortality. The increased multivariate-adjusted hazard ratio (HR) of "hard events," (nonfatal and fatal MI) was 2.69 (95% CI, 1.48-4.90) for high versus low anger and 1.35 (95% CI, 0.87-2.10) for moderate versus low anger (A). Results were significant for only normotensive individuals, approximately two thirds of the population. A similar relationship between scores on the Spielberger Trait Anger Scale and increased risk of hemorrhagic and ischemic stroke was found in a sample of 13,851 men and women followed for a median of 77.3 months in the same study. After multivariate adjustment, results were significant for only those <60 years of age [high trait anger vs low trait anger relative risk = 2.82 (95% CI, 1.65-4.80)].

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ZAKLJUCAK: � U slucajevima izenadnog besa ili ljutnje relativni rizik od nastanka infarkta srca

je izmedju 2 i 4. � Ukoliko bi doslo do razvoja infarkta srca dalje depresivne reakcije bi za 24%

pogorsale tok te bolesti u odnosu na 17.6% koliko bi se desavalo u kontrolnoj grupi ovih bolesnika.

� Zbog socijalne izolacije stopa mortaliteta kod ovih bolesnika je znacajno povecana u odnosu na grupe koje nisu u uslovima socijalne izolacije / pritvora/.

Literatura:

1. Mittleman MA, Maclure M, Tofler GH, et al.: Triggering of acute myocardial infarction by heavy physical exertion. N Engl J Med 1993, 329: 1677–1683.

2. Rosengren A, Hawken S, Ounpuu S, for the INTERHEART Investigators: Association of psychosocial risk factors with risk of acute myocardial infarction in 11 119 cases and 13 648 controls from 52 countries (the INTERHEART study): case-control study. Lancet 2004, 364: 953–962.

3. Lett HS, Blumenthal JA, Babyak MA, et al.: Depression as a risk factor for coronary artery disease, mechanisms, and treatment. Psychosom Med 2004, 66: 305–315.

4. Barth J, Schumacher M, Herrmann-Lingen C: Depression as a risk factor for mortality in patients with coronary heart disease. Psychosom Med 2004, 66: 802–813.

5. Van Melle JP, de Jonge P, Spijkerman TA, et al.: Prognostic association of depression following myocardial infarction with mortality and cardiovascular events: a meta-analysis. Psychosom Med 2004, 66: 814–822.

6. Kawachi I, Colditz GA, Ascherio A, et al.: Prospective study of phobic anxiety and risk of coronary heart disease in men. Circulation 1994, 89: 1992–1997.

7. Mittleman MA, Mintzer D, Maclure M, et al.: Triggering of myocardial infarction by cocaine. Circulation 1999, 99: 2737–2741.

8. House JS, Landis KR, Umberson D: Social relationships and health. Science 1988, 241: 540–545.

9. Case RB, Moss AJ, Case N, et al.: Living alone after myocardial infarction: impact on prognosis. JAMA 1992, 267: 515–519.

10. Williams RB, Barefoot JC, Califf RM: Prognostic importance of social and economic resources among medically treated patients with angiographically documented coronary artery disease. JAMA 1992, 267: 520–524.

11. Brummett BH, Barefoot JC, Siegler IC, et al.: Characteristics of socially isolated patients with coronary artery disease who are at elevated risk for mortality. Psychosom Med 2001, 63: 267–272.

12. Barefoot JC, Dahlstrom WG, Williams RB: Hostility, CHD incidence, and total mortality: a 25-year follow-up study of 255 physicians. Psychosom Med 1984, 45: 59–63.

13. Williams JE, Paton CC, Siegler IC, et al.: Anger proneness predicts coronary heart disease risk: prospective analysis from the Atherosclerosis Risk in Communities (ARIC) Study. Circulation 2000, 101: 2034–2039.

14. Williams JE, Nieto FJ, Sanford CO, et al.: The association between trait anger and incident stroke risk: The Atherosclerosis Risk in Communities (ARIC) Study. Stroke 2002, 33: 13–20.

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15. Williams JE, Paton CC, Siegler IC, et al.: Anger proneness predicts coronary heart disease risk: prospective analysis from the Atherosclerosis Risk in Communities (ARIC) Study. Circulation 2000, 101: 2034–2039.

16. Williams JE, Nieto FJ, Sanford CO, et al.: The association between trait anger and incident stroke risk: The Atherosclerosis Risk in Communities (ARIC) Study. Stroke 2002, 33: 13–20.

17. Eng PM, Fitzmaurice G, Kubzansky LD, et al.: Anger expression and risk of stroke and coronary heart disease among male health professionals. Psychosom Med 2003, 65: 100–110.

18. Kawachi I, Colditz GA, Ascherio A, et al.: Prospective study of phobic anxiety and risk of coronary heart disease in men. Circulation 1994, 89: 1992–1997.

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19.

Porodicno opterecenje

PODATAK (CINJENICA):

Otac je umro od iznenadne srcane smrti u svojoj 54. godini

Dokaz o tacnosti podatka:

Podaci iz medicinske dokumentacije dobijeni od bolesnika

RIZICI (OPASNOSTI):

• Using data from the Framingham Offspring Study, a United States population-based epidemiologic cohort established in 1971, 2302 men and women aged 30 years or older with parents in the original Framingham Heart Study were examined for their risk of developing CVD according to the presence of premature (onset age < 55 years in father, < 65 years in mother) CVD. The definition of CVD included confirmed reports of coronary death, myocardial infarction, coronary insufficiency, angina pectoris, atherothrombotic stroke, intermittent claudication, and cardiovascular death. It appears that a premature paternal history of CVD is at least as important as a premature maternal history for men and women. When both parents have a premature history of CVD, women in particular have a considerably higher risk of developing CVD, with 2.8 times the risk compared with women lacking any premature parental history. When the presence of nonpremature (onset age 55 years or older in father, 65 years or older in mother) CVD was considered, the relative risks were greatly reduced and not significant. These data suggest that only an early or premature parental history of CVD may be clinically relevant in patients when considering the long-term risk of developing cardiovascular disease.

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DOKAZI:

Possible combinations of family members that may comprise a family history of cardiovascular disease and risk of CHD

Possible combinations of family members that may comprise a family history of cardiovascular disease and risk of coronary heart disease. In an Australian study of 403 cases of coronary heart disease and 236 controls, various definitions of family history of coronary heart disease were considered attempted to estimate the additional information provided by more complex or comprehensive family history definitions . This figure compares the odds ratios of coronary heart disease for different family history definitions, as well as considering premature history (< 55 men or < 60 women) or any history at all. All definitions were predictive of coronary heart disease, and with premature family history having a slightly stronger magnitude of risk. Models were then fit to quantitate the improvement in the prediction of coronary heart disease with more this more detailed information compared with a "simple" definition of one or more first-degree family member with coronary heart disease at any age.

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ZAKLJUCAK: � Istrazivanjima je dokazan izvestan nivo genetske veze izmedju iznenadne srcane

smrti kod bliskog clana porodice i grupe bolesnika koje su pracene u tim istrazivanjima.

� Iznenadna srcana srcana smrt oca predstavlja snazan factor rizika za nastanak iznenadne srcane smrti cak i bez obzira na postojanje ili ne postojanje strukturnih ostecenja miokarda.

� Dakle treba biti oprezan u sveukupnom kardiovaskularnom pracenju ovog bolesnika /bez obzira na relativno dobre dosadasnje nalaze/ jer se iznenadni fatalni dogadjaj prvenstveno zbog fatalnog poremecaja srcanog ritma kod ovog bolesnika ne moze iskljuciti.

Literatura:

1. Lloyd-Jones DM, Nam BH, D'Agostino RB Sr, et al.: Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring. JAMA 2004, 291: 2204–2211.

2. Sesso HD, Lee IM, Gaziano JM, et al.: Maternal and paternal history of myocardial infarction and risk of cardiovascular disease in men and women. Circulation 2001, 104: 393–398.

3. Silberberg JS, Wlodarczyk J, Fryer J, et al.: Risk associated with various definitions of family history of coronary heart disease. The Newcastle Family History Study II. Am J Epidemiol 1998, 147: 1133–1139.

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EKG promene:

PODATAK (CINJENICA): Povremene komorske ekstrasistole u mirovanju

Dokaz o tacnosti podatka:

EKG uradjen tokom pregleda u pritvorskoj jedinici H askog tribunala.

RIZICI (OPASNOSTI):

• Najnovija istrazivanja revijalno publikovana u J. Am. Coll. Cardiol. 2009., pokazuju da je verovatnoca iznenadne srcane smrti kod ove grupe bolesnika na godisnjem nivou oko 2%- 3%.

• One of the main clinical problems of patients with arterial hypertension is the presence of arrhythmias, especially if left ventricular hypertrophy exists. Recent results from our group and all data available via Med-Line-search have been analysed. The analysis was focused on atrial and ventricular arrhythmias and arrhythmic risk prediction, using non-invasive markers.

• Arterial hypertension is a major cause of non-rheumatic atrial fibrillation and other supraventricular arrhythmias. The prevalence of ventricular arrhythmias is increased in hypertensive patients without left ventricular hypertrophy, compared to normotensives.

DOKAZI:

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J. Am. Coll. Cardiol. 2009;54;747-763. doi:10.1016/j.jacc.2009.03.078

Am J Med 1988; 84 (suppl. 1B):65±68.

Systolic blood pressure and risk of sudden cardiac death

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Correlation of rate of ventricular premature beats and left ventricular ejection fraction. Group 1, patients with a duration of arterial hypertension of 4.6 _ 8 years; group 2, patients with a duration of arterial hypertension of 8.7 _ 12 years and heart failure. EDV, end diastolic volume; ESV, endsystolic volume; EF, ejection fraction.

In this series of 29,244 subjects, frequent ventricular ectopy occurred in 3 percent of subjects only during exercise, in 2 percent of subjects only during recovery from exercise, and in 2 percent of subjects during both exercise and recovery. The prognosis of patients who had postexercise-induced frequent ventricular ectopy was worse than the prognosis of subjects who had frequent ventricular ectopy only during exercise. The mean follow-up time was 5.3 years.

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Kaplan-Meier cumulative survival plot for cardiac death: QT interval dispersion (QTd). QTd > 80 ms was significantly related to cardiac death (P=0-0002). ^cumulative survival QTd >80 ms, O = event times; —=cumulative survival QTd <80 ms, O=event times.

Kaplan-Meier cumulative survival plot for global death: Lown classes. Lown class IV b was significantly related to global death (P=0-0025). =cumulative survival Lown class IV b, O=event times; =cumulative survival Lown classes 0 to IV a, D= event times.

ZAKLJUCAK: � Znajuci da bolesnik ima povremeno sistolni pritisak veci od 155 mmHg, relativni

rizik od razvoja iznenadne smrti se krece oko 1.4 na 1000 tokom jedne godine.

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� Registrovane ventrikularne ekstrasistolne aritmije u mirovanju /PVC/ u odredjenom procentu smanjuju verovatnocu prezivljavanja ovih bolesnika u periodu od 80 meseci.

� Uocene ventrikularne ekstrasistole u mirovanju ukazuju da ovaj bolesnik moze imati sklonost poremecajima srcanog ritma, a sto je i detektovano epizodom atrijalne fibrilacije /prema podacima iz Vaseg E-maila iz avgusta 2009 g./

� Neophodno je pratiti bolesnika i povremeno monitorirati /24 casovni holter EKG itd./ mogucu pojavu kompleksnih poremecaja srcanog ritma i po potrebi sprovoditi sve neophodne dijagnosticke i terapijske procedure.

Literatura:

1. Robert J. Myerburg, Vivek Reddy, and Agustin Castellanos. Indications for Implantable Cardioverter-Defibrillators Based on Evidence and Judgment. J. Am. Coll. Cardiol. 2009;54;747-763.

2. Le Heuzey JY, Guize L. Cardiac prognosis in hypertensive patients.Incidence of sudden death and ventricular arrhythmias. Am J Med 1988; 84 (suppl. 1B):65±68.

3. Hennersdorf, Marcus G.Strauer, Bodo E. Arterial hypertension and cardiac arrhythmias

Journal of Hypertension:February 2001 - Volume 19 - Issue 2 - pp 167-177.

4. Bethge C, Motz W, von Hehn A, Strauer BE. Ventricular arrhythmias in hypertensive heart disease with and without heart failure. J Cardiovasc Pharmacol 1987; 10(suppl. 6):S119±S128.

5. Frolkis JP, Pothier CE, Blackstone EH, et al: Frequent ventricular ectopy after exercise as

a predictor of death. N Engl J Med 348:781, 2003.

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EHOKARDIOGRAFSKE promene:

PODATAK (CINJENICA):

Leva pretkomora je 4,7cm ( lako uvecana )

Aorta u korenu 4,2cm

Trag aortne regurgitacije

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Dokaz o tacnosti podatka:

Originalne slike transtorakalne ehokardiografije iz medicinske dokumentacije.

RIZICI (OPASNOSTI):

� Blago povecana leva pretkomora ukazuje na pocetno strukturno ostecenje miokarda. Slicno patofiziolosko znacenje ima i blaga aortna regurgitacija.

� U daljem toku je moguca progresija ovih poremecaja, pojava dodatnih strukturnih ostecenja srca i pojava novih kardiovaskularnih dogadjaja kao sto su poremecaji srcanog ritma tipa atrijalne fibrilacije itd.

DOKAZI:

Percentage of patients free of atrial fibrillation (AF) during a 5-year period after baseline echocardiography, stratified by left atrial volume quartiles.

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Incremental prognostic value of left atrial (LA) size variables in models for prediction of atrial fibrillation.

ZAKLJUCAK: � Zbog blago povecanog dijametra leve pretkomore ovaj bolesnik ima verovatnocu

pojave ponovljenih epizoda atrijalne fibrilacije kao i drugih poremecaja srcanog ritma ili nepovoljnih kardiovaskularnih dogadjaja.

� Neophodno je ehokardiografsko pracenje ovog bolesnika, povremena kontrola srcanog ritma, stroga kontrola krvnog pritiska /jer je poznato da je arterijska hipertenzija jedan od najvaznijih faktora koji dovode do nastanka atrijalne fibrilacije u bolesnika koji nemaju znacajna ostecenja srcanih zalistaka/.

Literatura:

1. Hennersdorf, Marcus G.; Strauer, Bodo E. Arterial hypertension and cardiac arrhythmias.Journal of Hypertension. February 2001 - Volume 19 - Issue 2 - pp 167-177.

2. Teresa S. M. Tsang, Marion E. Barnes, Kent R. Bailey et al. Left Atrial Volume: Important Risk Marker of Incident Atrial Fibrillation in 1655 Older Men and Women. Mayo Clin Proc. 2001;76:467-475.

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1.

PAROKSIZAM ATRIJALNE FIBRILACIJE:

PODATAK (CINJENICA): Paroxisam atrijalne fibrilacije

Dokaz o tacnosti podatka:

E-mail od 04. Avgusta 2009. godine

RIZICI (OPASNOSTI):

• Arterijska hipertenzija je najcesci uzrok atrijalne fibrilacije ili drugih oblika supraventrikularnih poremecaja srcanog ritma u bolesnika koji nemaju reumatsku manu.

• U bolesnika zivotne dobi 50-59 godina atrijalna fibrilacija ima verovatnocu razvoja mozdanog udara od oko 3% na godisnjem nivou.

• Takodje atrijalna fibrilacija dodatno dovodi do str ukturnih ostecenja miokarda i razvoja novih nepovoljnih kardiovaskularnih dogadjaja.

DOKAZI:

Relative risk of stroke and mortality in patients with AF compared with patients without AF. Source data from the Framingham Heart Study, Regional Heart Study, Whitehall study, and Manitoba study.

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Framingham Study

Age & Risk of Stroke in Atrial Fibrillation

Thromboembolic Events

Control Patients in AF Trials

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Antithrombotic therapy for prevention of stroke (ischemic and hemorrhagic) in patients with nonvalvular AF: warfarin compared with aspirin and aspirin compared with placebo. Adapted with permission from Hart et al. Ann Intern Med 1999;131:492–501. (The American College of Physicians–American Society of Internal Medicine is not responsible for the accuracy of the translation.)

ZAKLJUCAK: � Sva strukturna ostecenja miokarda, kao i registrovane ventrikularne

ekstrasistole /PVC/ kao i epizoda atrijalne fibrilacije, mogu dovesti do embolijskih dogadjaja u centralnom nervnom sistemu /mozdani udar/ kao i do svih drugih fatalnih komplikacija.

� U procesu pracenja i lecenja, neophodno je preduzeti sve mere sprecavanja nastanka ventrikularnih ekstrasistola /PVC/ , mogucih epizoda atrijalne fibrilacije, drugih fatalnih poremecaja srcanog ritma, kao i sprecavanja nastanka emoblijskih dogadjaja, a posebno infarkta mozga.

Literatura:

1. Flegel KM, Shipley MJ, Rose G. Risk of stroke in non-rheumatic atrial fibrillation [published erratum appears in Lancet 1987;1:878]. Lancet 1987;1:526 –9.

2. Kannel WB, Abbott RD, Savage DD, McNamara PM. Coronary heart disease and atrial fibrillation: the Framingham Study. Am Heart J 1983;106:389 –96.

3. Krahn AD, Manfreda J, Tate RB, Mathewson FA, Cuddy TE. The natural history of atrial

fibrillation: incidence, risk factors, and prognosis in the Manitoba Follow-Up Study. Am J Med 1995;98:476–84.

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4. Hart RG, Pearce LA, McBride R, Rothbart RM, Asinger RW, for the Stroke Prevention in

Atrial Fibrillation (SPAF) Investigators. Factors associated with ischemic stroke during aspirin therapy in atrial fibrillation: analysis of 2012 participants in the SPAF I-III clinical trials. Stroke 1999;30:1223–9.

5. Hart RG, Benavente O, McBride R, Pearce LA. Antithrombotic therapy to prevent stroke in patients with atrial fibrillation: a meta-analysis. Ann Intern Med 1999;131:492–501.

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1.

ZAKLJUCAK

Na osnovu svega navedenog, radi se bolesniku sa sledecim faktorima rizika za kardiovaskularna obolenja:

• Zivotna dob 55 godina • Gojaznost, TT = 120 kg, TV = 1,97m, BMI = 30,9 kg/m2 • Hypercholesterolemia ( holesterol 5,4 mmol/l, LDL holesterol 3,4 mmol/l ) • Arterijska hipertenzija ( max 190/120 mmHg, najcesce za sistolni 120-140

mmHg, a za dijastolni 80-100 mmHg ) • Stresovi • Porodicno opterecenje (otac je umro od iznenadne srcane smrti u svojoj 54.

godini)

Dosadasnjim ispitivanjima je dokazano postojanje sledecih obolenja:

Hypertensio arterialis Fibrilatio atriorum parosismalis ( na osnovu E-maila od 04. avgusta 2009. godine) Hypercholesterolemia Obesitas Hemangioma hepatis Asthma bronchiale Discopathia C5/C6 Status post operationem hearnie ingvinalis lat. sin.

Moguci kardiovaskularni rizici u buducnosti kod ovog bolesnika su sledeci:

� Zbog znacaja zivotne dobi od 55 godina kao faktora rizika, moguc je nastanak koronarne arterijske bolesti u skorijem vremenskom intervalu, bez obzira sto su ostali testovi na ishemiju za sada uglavnom normalni.

� Samo na osnovu pola, muskarci , koji uz to jos imaju i arterijsku hipertenziju, imaju relativni rizik oko 2 za razvoj srcanih bolesti, cak i kada su im svi drugi zdravstveni parametri normalni.

� Najveci broj muskaraca zivotne dobi od 50 do 59 godina, u desetogodisnjem period, ima rizik od nastanka kardiovaskularnih bolesti od 6% do preko 20%.

� Osobe muskog pola, sa povecanom telesnom masom ( gojaznost BMI ≥ 30,9 kg/m2

), imaju i do 30 procenata veci rizik za razvoj kardiovaskularnih obolenja u odnosu na normalno uhranjene osobe.

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� Ukoliko ove osobe imaju i hipertenziju, tada je relativni rizik za razvoj kardiovaskularnih bolesti veci od 3.

� Obesity is associated with an increased risk of morbidity and mortality as well as reduced life expectancy. On the whole, overweight and obesity predispose to or are associated with numerous cardiac complications such as coronary heart disease, heart failure, and sudden death because of their impact on the cardiovascular system.

� Ovaj bolesnik ima povisene vrednosti LDL holesterola i blago povisene vrednosti ukupnog holesterola te prema tome ima znacajan rizik za razvoj ateroskleroze i svih drugih kardiovaskularnih komplikacija.

� Prediktivna verovatnoca razvoja nepovoljnih kardiovaskularnih dogadjaja kada se uzme u obzir ovaj faktor rizika je oko 30 %.

� Uzimajuci u obzir vrednosti pritiska koje su se kretale i preko 175/105 mmHg., ovaj bolesnik ima i do osam puta /8x/ veci rizik za kardiovaskularnu smrt u odnosu na kontrolnu grupu /videti grafikone/.

� Kako pacijent ima i druge faktore rizika koji su udruzeni sa arterijskom hipertenzijom to znaci da je verovatnoca nastanka nepovoljnih kardiovaskularnih dogadjaja opisana eksponencijalnom krivuljom u funkciji vremena.

� U slucajevima izenadnog besa ili ljutnje relativni rizik od nastanka infarkta srca je izmedju 2 i 4.

� Ukoliko bi doslo do razvoja infarkta srca dalje depresivne reakcije bi za 24% pogorsale tok te bolesti u odnosu na 17.6% koliko bi se desavalo u kontrolnoj grupi ovih bolesnika.

� Zbog socijalne izolacije stopa mortaliteta kod ovih bolesnika je znacajno povecana u odnosu na grupe koje nisu u uslovima socijalne izolacije / pritvora/.

� Iznenadna srcana srcana smrt oca predstavlja snazan factor rizika za nastanak iznenadne srcane smrti cak i bez obzira na postojanje ili ne postojanje strukturnih ostecenja miokarda.

� Znajuci da bolesnik ima povremeno sistolni pritisak veci od 155 mmHg, relativni rizik od razvoja iznenadne smrti se krece oko 1.4 na 1000 tokom jedne godine.

� Registrovane ventrikularne ekstrasistolne aritmije u mirovanju /PVC/ u odredjenom procentu smanjuju verovatnocu prezivljavanja ovih bolesnika u periodu od 80 meseci.

� Uocene ventrikularne ekstrasistole u mirovanju ukazuju da ovaj bolesnik moze imati sklonost poremecajima srcanog ritma, a sto je i detektovano epizodom atrijalne fibrilacije /prema podacima iz Vaseg E-maila iz avgusta 2009 g./

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� Blago povecana leva pretkomora ukazuje na pocetno strukturno ostecenje miokarda. Slicno patofiziolosko znacenje ima i blaga aortna regurgitacija.

� U daljem toku je moguca progresija ovih poremecaja, pojava dodatnih strukturnih ostecenja srca i pojava novih kardiovaskularnih dogadjaja kao sto su poremecaji srcanog ritma tipa atrijalne fibrilacije itd.

� Arterijska hipertenzija je najcesci uzrok atrijalne fibrilacije ili drugih oblika supraventrikularnih poremecaja srcanog ritma u bolesnika koji nemaju reumatsku manu.

� U bolesnika zivotne dobi 50-59 godina atrijalna fibrilacija ima verovatnocu razvoja mozdanog udara od oko 3% na godisnjem nivou.

� Takodje atrijalna fibrilacija dodatno dovodi do str ukturnih ostecenja miokarda i razvoja novih nepovoljnih kardiovaskularnih dogadjaja.

� Zbog uzimanja bronhodilatatora /lekovi za astmu/ povecana je verovatnoca nastanka srcanih aritmija koje u odredjenim stanjima mogu biti potencijalno veoma opasne.

� Iz istih razloga otezana je medikamentozna kontrola krvnog pritiska i srcanog ritma /Beta adrenergicka stimulacija/.

U cilju smanjenja rizika za nastanak nepovoljnih ili fatalnih dogadjaja u buducnosti, potrebno je sledece:

1. Redovno uzimanje odgovarajuce terapije

2. Neophodna je redukcija telesne mase ( gojaznosti ) koja moze pomoci znacajnom smanjenju krvnog pritiska, a time i smanjenju sveukupnih kardiovaskularnih rizika ovog bolesnika.

3. Neophodno sprovesti sve mere prevencije / lecenja/ poremecaja lipida u krvi /

holesterola i LDL/ kako primenom higijensko –dijetetskog rezima, tako i kontrolisanim i razumnim koriscenjem hipolipemika /statina/.

4. Izuzetno je vazno, kako ne medikamentoznim tako i medikamentoznim

nacinima lecenja krvni pritisak drzati u granicama normale / manje slana ishrana itd/.

5. Preduzeti sve razumne, a realno moguce mere, radi sprecavanja iznenadnih

mentalnih stresnih situacija kod ovog bolesnika /ukoliko je potrebno i medikamentoznim tretmanom/.

6. Neophodno je pratiti bolesnika i povremeno monitorirati /24 casovni holter EKG

itd./ mogucu pojavu kompleksnih poremecaja srcanog ritma i po potrebi sprovoditi sve neophodne dijagnosticke i terapijske procedure.

7. Neophodno je povremeno ehokardiografsko pracenje ovog bolesnika, povremena kontrola srcanog ritma, stroga kontrola krvnog prit iska /jer je poznato da je

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arterijska hipertenzija jedan od najvaznijih faktor a koji dovode do nastanka atrijalne fibrilacije u bolesnika koji nemaju znacajna ostecenja srcanih zalistaka, a imaju verifikovane povecane dimenzije leve srcane pretkomore/.

8. Neophodno je preduzeti sve mere sprecavanja nastanka ventrikularnih ekstrasistola /PVC/ , mogucih epizoda atrijalne fibrilacije, drugih fatalnih poremecaja srcanog ritma, kao i sprecavanja nastanka emoblijskih dogadjaja, a posebno infarkta mozga.

9. Potrebne su redovne kontrole kod kardiologa, pulmologa, alergologa, gastroenterologa, neurologa, hirurga, hepatologa, a po potrebi i drugih specijalnosti.

10. Savetuje se i izvrsiti ultrazvucni pregled stomaka / kako je preporuceno od strane hirurga, ali prema meni dostupnoj dokumentaciji to do sada nije ucinjeno/.

16. Oktobar 2009. U Beogradu, Serbia

Zdravko M. Mijailovic, MD, PhD, Cardiologyst Head of the Clinic for Cardiology Military Medical Academy – Belgrade, Serbia American Registred for Diagnostic Cardiac Sonography Associate Professor of Internal medicine / Cardiology/ Fellow of European Society of Cardiology Fellow of American Colledge of Cardiology Member of American Heart Association Member of American Society of Echocardiography

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