20 CHAPTER 2 INTRODUCTION Atrial fibrillation (AF) is one of the most common cardiac conditions with a prevalence of around 1-2% in the general population, and with higher rates among those with advancing age. The prevalence of AF is expected to double in the next few decades, mainly due to the ageing of the population.1 The latest ESC guidelines on AF recommend integrated care across all healthcare levels and among different specialties for all AF patients according to the ‘Atrial Fibrillation Better Care (ABC) holistic pathway’. In this acronym, the A represents ‘anticoagulation/ avoid stroke’, the B ‘better symptom management’, and the C ‘cardiovascular and comorbidity optimisation’.2 Currently, with the publications of the landmark EASTAFNET randomised controlled trials reporting positive effects of (systematic) early ablation on improving patient outcomes, scientific focus is on ‘better symptom management’.3,4 Avoiding stroke and optimising the cardiovascular risk-factor burden and comorbidities are, however, at least equally important. By reaching back to the pathophysiology of increased stroke risk in patients with AF, we want to further explain the rationale behind the ABC strategy and provide suggestions on how to achieve optimal AF care. THE CLASSIC PARADIGM IN PATHOPHYSIOLOGY In the famous Framingham Heart cohort in which patients are followed for many years to study risk factors for cardiovascular disease, stroke risk in AF patients was found to be up to five times higher compared to patients without AF.5 It is important to note, however, that this evidence originates from 1991. Therefore, it is very well possible that this risk is slightly different in today’s AF population, which experiences more comorbidities but also benefits from advancements in healthcare. More importantly, why is it that stroke risk is so much higher in AF patients? Post mortem studies reported on cerebral emboli in a significant amount of AF patients,6,7 which led to the theoretical concept that in fibrillating atria cardiac thrombi may develop because of blood stasis, most commonly in the left atrial appendage. When these thrombi migrate, they can cause ischaemic stroke further upstream. However, it is not likely that this is the only causal mechanism for ischaemic stroke in patients with AF for a variety of reasons. First, there is often a temporal dissociation between ischaemic stroke and AF, in which ischaemic stroke precedes a period of AF or in which ischaemic stroke occurs after having had AF for a long period of time.8,9 Second, many studies have shown that there is a persistently increased stroke risk in AF patients, even after sinus rhythm is restored, thus after the period of fibrillating atria and blood stasis in the left atrial appendage.10 Third, there is clear bidirectionality between AF and venous thromboembolism, where AF is associated with an increased risk not only of pulmonary embolism but also of
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