Just read an interesting article entitled Drug Therapy for the Management of Atrial Fibrillation: An Update Posted 10/29/2003 on Medscape at
[
www.medscape.com]
On p. 6 it states
"There has been recent interest in the role of the reninangiotensin system in atrial electrical remodelling. Inhibition of endogenous angiotensin II by captopril or candesartan prevents the shortening of atrial refractory periods during rapid atrial pacing in dogs.[46] Enalapril prevented the structural and electrical changes that promote AF initiation in an experimental heart failure model.[47] Pedersen et al. demonstrated that treatment with the angiotensin-converting enzyme (ACE) inhibitor trandolapril reduced the risk of developing AF after myocardial infarction by 55% during long-term follow-up.[48] This difference could not be explained by differences in levels of potassium or left ventricular function. Patients on ACE inhibitors have also been noted to have an improved outcome from cardioversion.[49] Madrid et al. studied 154 patients undergoing cardioversion of persistent AF.[50] Seventy-five patients were randomised to amiodarone only and 79 were randomised to amiodarone plus irbesartan. At two months, 85% of patients were still in sinus rhythm on combination therapy compared with 63% in the amiodarone only group. It is theorised that blockade of angiotensin II prevents atrial electrical remodelling by decreasing atrial stretch, modulating refractoriness, interfering with ion currents, modifying sympathetic tone and stabilising electrolyte concentrations.[46]"
Although this is more applicable to those with persistent AF, some of you LAFers with more frequent episodes often requiring cardioversion might ask your MDs about ACE inhibitors. Although not discussed in the article, ACE inhibitors also offer the additional benefit of at least partially blocking aldosterone (causes cardiac fibrosis) production secondary to the RAAS. If you have any inclination toward hypertension, ACE inhibitors should be a no brainer.
PC v54
