Of hammers and screws: renin-angiotensin-aldosterone system inhibition to prevent atrial fibrillation in patients with hypertension

Abstract

This editorial refers to ‘Antihypertensive treatment and risk of atrial fibrillation: a nationwide study’[†][1], by S.C.W. Marott et al. , on page 1205 This editorial discusses the observation that monotherapy of uncomplicated hypertension with an ACE inhibitor or a sartan is associated with a lower risk of new-onset atrial fibrillation than treatment with a calcium channel blocker, diuretic, or beta-blocker. This association, found in a Danish nationwide database over a mean follow-up duration of 6–7 years, is put in context with the outcomes of controlled clinical trials testing similar interventions in patients without hypertension. In summary, the data suggest that different types of atrial fibrillation require different forms of preventive treatment, and that such ‘pathophysiological types of atrial fibrillation’ can be differentiated in patients using clinical characteristics supplemented by blood and ECG biomarkers, potentially opening the way towards a more personalized therapy of atrial fibrillation. Although atrial fibrillation (AF) is rarely dangerous in the acute setting, the long-term consequences are grim. Even the most modern forms of management, including adequate stroke prevention and rate control therapy,1 are not sufficient to prevent premature cardiovascular deaths in patients with AF.2,3 Furthermore, the majority of AF patients remain symptomatic,4 and many are hospitalized for AF.5,6 After its manifestation, early rhythm control treatment of AF, i.e. thorough prevention of recurrent AF after the first episode, may be useful.2 Although we do not have formal proof of this concept, preventing the first episode of AF could be an even better way to prevent these complications. The mechanisms by which AF perpetuates itself have been studied in great detail in animal models and in patients in the last … [1]: #fn-2