Abstract

With an estimated prevalence of 1–2% in the general population and up to 15% of people over 80 years, atrial fibrillation (AF) is the most common sustained cardiac arrhythmia. In Europe 4.5- 6.0 million people are estimated to have AF. As two thirds of the AF cases involve patients older than 65 years of age, owing to aging of the population a pandemic of AF is expected to occur over the next decades. This will impose a major burden on all health care systems; moreover, AF increases the risk of heart failure, doubles the risk of death independently of other known predictors of mortality, is the major cause of cardio-embolic stroke and thereby long-term disability. Hence, AF worsens the quality of life and, by causing silent and recurring stroke, leads to cognitive dysfunction and dementia. Arterial hypertension is the most common cause of nonvalvular AF and is known to anticipate the incidence of AF in susceptible individuals. A relative or absolute aldosterone excess drives the development of arterial hypertension in many individuals; moreover, in primary aldosteronism, the most common curable cause of arterial hypertension, a 12-fold increase of relative risk of AF, as compared with blood pressure-matched patience with essential hypertension, was documented. In PAPPHY, a 3-center prospective study, we showed that among 73 the patients who presented with lone AF and arterial hypertension, 42% had primary aldosteronism that was surgically cured in half of them. Moreover, in the PAPY Longitudinal study we showed that AF occurred more commonly at long-term in medically treated than in surgically cured PA patients. These findings are consistent with elegant experimental studies in rodents that documented an increase susceptibility to develop AF with induced hyperaldosteronism. The mechanisms underlying AF in arterial hypertension and hyperaldosteronism will be discussed.

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