PALERMO, ITALY. There is growing evidence that the hormone aldosterone is involved in the genesis of atrial fibrillation (AF). Research has shown that an excess of aldosterone (aldosteronism, hyperaldosteronism) can cause potassium wasting, particularly in magnesium-deficient patients, and is a key player in structural remodeling (fibrosis) of the atria. Aldosterone is the "end product" of the renin-angiotensin-aldosterone system (RAAS), the body's main system for dealing with a fall in blood pressure that is too great to be dealt with by the autonomic nervous system alone. The formation of aldosterone can be inhibited by angiotensin converting enzyme II receptor blockers (ARBs) and its effect can be blocked by aldosterone antagonists such as spironolactone and triamterene.

Recent studies have shown that the ACE inhibitors enapril and trandolapril reduce the risk of AF in patients with left ventricular dysfunction, while the ARBs valsartan and candesartan have been found helpful in preventing AF in patients with chronic heart failure. The ARB irbesartan combined with amiodarone increases time to recurrence after cardioversion in patients with persistent AF. Also, 'left atrial stunning', lasting a few weeks after the cardioversion of AF and probably responsible for the increased embolic events after cardioversion, is significantly reduced by pretreatment with irbesartan.

A study involving hypertensive patients with left ventricle hypertrophy showed that the risk of both new-onset AF and stroke was markedly reduced by the treatment with the ARB, Losartan. However, there is no evidence that ACE inhibitors or ARBs have any effect in preventing AF relapses in patients with normal hearts and no hypertension (lone afibbers). A significant proportion of afibbers with no underlying heart disease suffer from hypertension. Hypertension is usually treated with diuretics, alpha- or beta-blockers, calcium channel blockers, ACE inhibitors or ARBs. The authors of the report conclude that ACE inhibitors and ARBs should be considered the drugs of choice in patients with AF and coexisting clinical conditions such as hypertension, coronary disease, heart failure and diabetes mellitus.

Novo, G, et al. The role of the renin-angiotensin system in atrial fibrillation and the therapeutic effects of ACE-Is and ARBs. British Journal of Clinical Pharmacology, Vol. 66, No. 3, 2008, pp. 345-51

Editor's comment: Although there is no evidence that ACE inhibitors and ARBs are helpful in preventing new-onset afib, or in reducing episode frequency or duration in lone afibbers without hypertension, there is some indication that they may be of benefit to afibbers with hypertension and no underlying heart disease. Thus, hypertensive afibbers who are currently on diuretics, alpha-blockers, beta-blockers, or calcium channel blockers may wish to try an ACE inhibitor or an ARB instead to see if their afib burden might be reduced.