Defining the major health modifiers causing atrial fibrillation: a roadmap to underpin personalized prevention and treatment

Abstract

Despite the important advances that have enabled better stroke prevention in atrial fibrillation (AF) and more effective maintenance of sinus rhythm over the past decades, a large unmet need to improve the prevention and treatment of AF remains. Mortality for AF remains at 3.5% per year, and death is often experienced as sudden death or as a result of heart failure 1,2 . Each year, approximately 20% of patients with AF need to be hospitalized 3,4 , and stroke occurs in 1.5% of patients with AF who are receiving anticoagulant drugs 5 . Furthermore, more than half of the patients with AF are symptomatic despite adequate anticoagulation and rate control 4,6 . In view of the projected increase in the incidence and prevalence of AF 7-9 , as well as the substantial burden of death and dis ability that is still associated with this condition 10 , the status quo is unacceptable.Current management of patients with AF comprises treatment of the accompanying cardiovascular conditions, oral anticoagulation, rate control -with medications that slow atrioventricular nodal recovery or, rarely, with atrioventricular nodal ablation -and rhythm-control therapy with antiarrhythmic drugs, electrical cardioversion, catheter ablation or, at times, AF surgery 11,12 . Unfortunately, most of these current approaches are disconnected from our understanding of the major mechanisms that cause AF 1,13,14 1,2,7,19,20 Abstract | Despite remarkable advances in antiarrhythmic drugs, ablation procedures, and stroke-prevention strategies, atrial fibrillation (AF) remains an important cause of death and disability in middle-aged and elderly individuals. Unstructured management of patients with AF sharply contrasts with our detailed, although incomplete, knowledge of the mechanisms that cause AF and its complications. Altered calcium homeostasis, atrial fibrosis and ageing, ion-channel dysfunction, autonomic imbalance, fat-cell infiltration, and oxidative stress, in addition to a susceptible genetic background, contribute to the promotion, maintenance, and progression of AF. However, clinical management of patients with AF is currently guided by stroke risk parameters, AF pattern, and symptoms. In response to this apparent disconnect between the known pathophysiology of AF and clinical management, we propose a roadmap to develop a set of clinical markers that reflect the major causes of AF in patients. Thereby, the insights into the mechanisms causing AF will be transformed into a format that can underpin future personalized strategies to prevent and treat AF, ultimately informing better patient care.230 | APRIL 2016 | VOLUME 13 www.nature.com/nrcardio CONSENSUS STATEMENT © 2 0 1 6 M a c m i l l a n P u b l i s h e r s L i m i t e d . A l l r i g h t s r e s e r v e d .

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

“…W celu lepszego zdefiniowania różnych typów AF niewątpliwie potrzebne są systematyczne badania dotyczące głównych czynników prowadzących do AF [176].…”

“…Potrzeba większej liczby badań dotyczących głównych przyczyn (i mechanizmów elektrofizjologicznych) AF w różnych grupach pacjentów [176,1024]. W takich badaniach należy wziąć pod uwagę główne choroby współistniejące związane z AF i scharakteryzować odpowiedź na leczenie AF u pacjentów z różnymi, patofizjologicznie odrębnymi typami AF.…”

2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS

“…Table 6 provides such a taxonomy, informed by expert consensus, 76,120,175 but without much evidence to underpin its clinical use. 176 Systematic research defining the major drivers of AF is clearly needed to better define different types of AF. 176 …”

“…176 Systematic research defining the major drivers of AF is clearly needed to better define different types of AF. 176 …”

The Unresolved Issues and Modern View on Atrial Fibrillation Patients Management

“…Необ-ходимо проведение большего количества исследова-ний, направленных на изучение основных причин электрофизиологических механизмов развития ФП в разных группах пациентов [2,3]. Современный кли-нический подход к лечению пациентов с ФП вклю-чает огромный пласт знаний о разнообразных причи-нах развития и поддержания данной аритмии, таких как фиброз предсердий, нарушения обмена электро-литов, ионно-канальная дисфункция и генетические изменения, вегетативный дисбаланс, окислительный стресс, инфильтрация жировыми клетками, а также наличие сопутствующих хронических заболеваний (например, почек, легких, ЖКТ).…”