Initial studies suggested that angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), and (possibly) aldosterone antagonists might either prevent new onset and recurrent atrial fibrillation (AF) or reduce the rate of major adverse cardiovascular outcomes in these patients. However, the available data do not support the use of these drugs solely for these purposes.
In this topic ACE inhibitors and ARBs collectively will be referred to as ‘angiotensin inhibition.’
Mechanisms proposed to explain the benefit of angiotensin blockade found in the early studies included the direct effects of angiotensin blockade on the structural and electrical properties of the atria, as well as the indirect influence of improved control of heart failure and hypertension, both of which are known risk factors for atrial fibrillation (AF) . (See "The electrocardiogram in atrial fibrillation" and "Actions of angiotensin II on the heart" and "Epidemiology of and risk factors for atrial fibrillation".)
The following observations supported the proposed mechanisms:
Reduction in atrial stretch — Atrial stretch, due to increased left atrial (LA) pressure, is associated with changes in the refractory period and conduction properties of atrial myocardium. These abnormalities provide both potential triggers and the substrate for the initiation and perpetuation of AF. The hemodynamic effects of angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) result in improved ventricular function and also reductions in LA pressure and wall stress .