WARSAW, POLAND. In my March 2003 research report Aldosterone: Villain of the Peace?, I speculated that excess aldosterone or
cortisol was implicated in the initiation of paroxysmal atrial fibrillation (AF)
episodes and also was responsible for fibrosis of the heart tissue eventually leading
to persistent or permanent AF. I also suggested that blocking mineralocorticoid (MC)
receptors with aldosterone antagonists (spironolactone or eplerenone) may be effective
in preventing AF episodes.
Now Polish cardiologists suggest that blocking excess aldosterone with spironolactone
or eplerenone may be effective in preventing paroxysmal and persistent AF and in inhibiting
the formation of fibrosis in the heart muscle. They point out that aldosterone promotes
inflammation, oxidative stress, dysfunction of the autonomic nervous system, attenuation
of baroreceptor activity, fibrosis and necrosis (cell death) of cardiomyocytes
(heart muscle cells). They also point out that patients with AF have more MC receptors
in the atria than do subjects without AF, and that patients with primary aldosteronism
(excessive blood levels of aldosterone) have a 12-fold higher risk of AF. They suggest
that therapy with spironolactone or eplerenone may reduce the deleterious effects of aldosterone.
A recent trial (EMPHASIS) involving over 2700 patients with mild heart failure found that
therapy with 25 � 50 mg/day of eplerenone reduced the incidence of new-onset AF by almost
50%. Another trial (SPIR-AF) found that a combination of spironolactone and the beta-blocker
atenolol significantly reduced the incidence of paroxysmal AF episodes over a 12-month period.
Spironolactone on its own has also been found to reduce left atrial dimension and extent of
fibrosis when taken on a long-term basis (25 mg/day). The researchers conclude that
aldosterone antagonist therapy may be a simple and valuable option to the treatment of
paroxysmal and persistent AF.
Editor�s comment: It is encouraging to see the idea of aldosterone blockage as a means of
preventing atrial fibrillation taken up by other researchers. It would be even more encouraging
to see large-scale clinical trials evaluating the merits of aldosterone blockage in the
prevention of AF.
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