The incidence and prevalence of atrial fibrillation (AF) are projected to increase significantly worldwide, imposing a significant burden on healthcare resources. The disease itself is extremely heterogeneous in its epidemiology, pathophysiology, and treatment options based on individual patient characteristics. Whilst ageing is well recognised to be an independent risk factor for the development of AF, this condition also affects the young in whom the condition is frequently symptomatic and troublesome. Traditional thinking suggests that the causal factors and pathogenesis of the condition in the young with structurally normal atria but electrophysiological “triggers” in the form of pulmonary vein ectopics leading to lone AF are in stark contrast to that in the elderly who have AF primarily due to an abnormal substrate consisting of fibrosed and dilated atria acting in concert with the pulmonary vein triggers. However, there can be exceptions to this rule as there is increasing evidence of structural and electrophysiological abnormalities in the atrial substrate in young patients with “lone AF,” as well as elderly patients who present with idiopathic AF. These reports seem to be blurring the distinction in the pathophysiology of so-called idiopathic lone AF in the young versus that in the elderly. Moreover with availability of improved and modern investigational and diagnostic techniques, novel causes of AF are being reported thereby seemingly consigning the diagnosis of “lone AF” to a rather mythical existence. We shall also elucidate in this paper the differences seen in the epidemiology, causes, pathogenesis, and clinical features of AF in the young versus that seen in the elderly, thereby requiring clearly defined management strategies to tackle this arrhythmia and its associated consequences. 1. Epidemiology There has been a worldwide increase in the ageing population, and as age is the most significant risk factor for AF, AF cases are predicted to reach nearly 16 million in the USA and 25 to 30 million in Europe by 2050 [1, 2]. The prevalence of AF shows a strong age dependence varying from 0.5% in patients aged <40 years to 5% in patients aged >65 years and nearly 10% amongst octogenarians [3–6]. Both the Framingham Heart Study and the Rotterdam Study estimated that the lifetime risk for development of AF in adults >40 years and at the age of 55 years respectively to be approximately 1 in 4 [7, 8]. The Cardiovascular Health Study which was a large population study of 5201 elderly adults ( years) showed an incidence of 17.6 and 42.7 events per
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