Title Fibrilacija atrija i zatajivanje srca
Title (english) Atrial fibrillation and heart failure
Author Ana-Maria Kašnar
Mentor Vedran Velagić (mentor)
Committee member Maja Čikeš (predsjednik povjerenstva)
Committee member Martina Lovrić Benčić (član povjerenstva)
Committee member Vedran Velagić (član povjerenstva)
Granter University of Zagreb School of Medicine (Department of Internal Medicine) Zagreb
Defense date and country 2021-07-16, Croatia
Scientific / art field, discipline and subdiscipline BIOMEDICINE AND HEALTHCARE Clinical Medical Sciences Internal Medicine
Abstract Zatajivanje srca (ZS) i fibrilacija atrija (FA) česti su kardiovaskularni poremećaji koji međusobno kompliciraju klinički tijek. FA može dovesti do disfunkcije lijevog ventrikula (LV) uzrokujući gubitak atrijske kontrakcije, brze frekvencije ventrikula i nepravilni ventrikularni ritam. Disfunkcija LV uključuje hemodinamski stres, aktivaciju neurohormonalnog sustava, remodeliranje miokarda i indukciju apoptoze te staničnu smrt i stvaranje fibroze. Ulogu u disfunkciji LV imaju i genetičke mutacije poput veće učestalosti polimorfizama gena za angiotenzin-konvertirajući enzim (ACE). S druge strane, ZS može stvoriti uvjete koji pogoduju nastanku FA utjecajem na atrijsko remodeliranje povišenim tlakovima punjenja, promjenama u prometu kalcija i promjenama atrijskih električnih svojstava. Srčano zatajivanje povezano je s usporenim provođenjem impulsa i fibrozom atrijskog miokarda. Povišeni završni dijastolički tlak u LV dovodi do povišenog tlaka u lijevom atriju što potiče stvaranje promjena u njegovoj stijenci i rezultira promjenama u renin-angiotenzin sustavu, profibrotičkim i upalnim djelovanjem. Nekoliko neurohormonalnih puteva povezano je s disfunkcijom LV, od kojih je najvažniji renin-angiotenzin sustav i njegova patološka aktivacija. Ovaj maladaptivni sustav potiče hipertrofiju miocita, apoptozu, odlaganje kolagena i intersticijsko remodeliranje, što sve potiče strukturne promjene atrija i razvoj FA. FA i ZS dijele mnoge patofiziološke mehanizme te stoga često postoje istodobno. Najbitniji ciljevi u terapiji FA jesu prevencija moždanog udara, kontrola frekvencije ventrikula i olakšavanje simptoma, a to su ujedno i prioriteti kod pacijenata čije se stanje komplicira ZS. Postoje novi dokazi koji govore kako je kontrola ritma superiornija u odnosu na kontrolu frekvencije, osobito kontrola ritma kateterskom ablacijom u srčanom zatajivanju. Iako se pokazalo kako kateterska ablacija potencijalno ima bolje terapijske ishode, potrebna su daljnja istraživanja koja će dokazati njezinu učinkovitost u pacijenata s FA i ZS.
Abstract (english) Heart failure (HF) and atrial fibrillation (AF) are common cardiovascular disorders that frequently complicate one another. Atrial fibrillation can provoke left ventricular (LV) dysfunction causing the loss of atrial contraction, rapid ventricular rates, and irregular ventricular rhythm. Dysfunction of left ventricle includes haemodynamic stress, activation of neurohormonal systems, myocardial remodelling and induction of apoptosis, cell death and replacement fibrosis. There is a great role of other contributing factors in those patients susceptible to LV dysfunction such as genetic mutations- for instance, a higher frequency of the angiotensin converting enzyme (ACE) gene polymorphism. On the other hand, heart failure has the capacity to create a physiological environment favourable to AF by contributing to atrial remodelling due to increased filling pressures, alterations in calcium handling and alterations to the electrical properties of the atrial tissue. Heart failure is associated with slower regional conduction and atrial fibrosis. In LV dysfunction, an elevated LV end-diastolic pressure leads to the increased left atrial pressure, which increases atrial wall stress resulting in changes in the renin angiotensin system, profibrotic and proinflammatory pathways. Left ventricular dysfunction is associated with the activation of several neurohormonal pathways, the most important of which is the pathological activation of the renin angiotensin system. This maladaptive system promotes myocyte hypertrophy, apoptosis, collagen deposition and interstitial remodelling, which all contribute to structural remodelling of the atria and the development of AF. Atrial fibrillation and heart failure share pathophysiological mechanisms and therefore frequently coexist. The major goals of the therapy in patients with AF are to prevent stroke, control the ventricular rate and reduce symptoms. These priorities are the same in patients with AF complicated by HF. Current data suggest that therapy strategy of the rhythm control is superior to the rate control, especially the rhythm control in HF with a catheter ablation. Although several clinical trials have shown that catheter ablation may lead to better outcomes, further studies in the future are needed.
Keywords
fibrilacija atrija
zatajivanje srca
antikoagulacija
kateterska ablacija
moždani udar
Keywords (english)
atrial fibrillation
heart failure
anticoagulation
catheter ablation
stroke
Language croatian
URN:NBN urn:nbn:hr:105:369948
Study programme Title: Medicine Study programme type: university Study level: integrated undergraduate and graduate Academic / professional title: doktor/doktorica medicine (doktor/doktorica medicine)
Type of resource Text
File origin Born digital
Access conditions Open access
Terms of use
Created on 2022-02-24 10:20:43