Atrial fibrillation (AF) is not a benign disease. It is associated with an increased risk of death, stroke, heart failure and hospitalisation, an impaired quality of life, and reduced exercise capacity and left ventricular dysfunction. Development of AF is a result of continuous remodelling of the atria, altered metabolism and autonomic changes secondary to ageing, progression of the underlying heart disease, and genetic and environmental factors. Hypertension, congestive heart failure, ischaemic heart disease, and diabetes are all wellknown risk factors for the development of AF.
1 The first manifestation of AF usually occurs after years of atrial and ventricular remodelling, caused by hypertension or heart failure (figure 1).
2 Important substrates for AF are fibrosis and inflammation, which form the basis of atrial and ventricular remodelling. One mechanism involved in these processes is activation of the renin-angiotensin-aldosterone system (RAAS), causing increased levels of angiotensin-II and aldosterone, which stimulate fibrosis, hypertrophy and inflammation.
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