TY - JOUR
T1 - The renin-angiotensin-aldosterone system (RAAS) and cardiac arrhythmias
AU - Iravanian, Shahriar
AU - Dudley, Samuel C.
PY - 2008/6
Y1 - 2008/6
N2 - The role of the renin-angiotensin-aldosterone system (RAAS) in many cardiovascular disorders, including hypertension, cardiac hypertrophy, and atherosclerosis, is well established, whereas its relationship with cardiac arrhythmias is a new area of investigation. Atrial fibrillation and malignant ventricular tachyarrhythmias, especially in the setting of cardiac hypertrophy or failure, seem to be examples of RAAS-related arrhythmias because treatment with RAAS modulators, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor blockers, reduces the incidence of these arrhythmias. RAAS has a multitude of electrophysiological effects and can potentially cause arrhythmia through a variety of mechanisms. We review new experimental results that suggest that RAAS has proarrhythmic effects on membrane and sarcoplasmic reticulum ion channels and that increased oxidative stress is likely contributing to the increased arrhythmic incidence. A summary of ongoing clinical trials that will address the clinical usefulness of RAAS modulators for prevention or treatment of arrhythmias is presented.
AB - The role of the renin-angiotensin-aldosterone system (RAAS) in many cardiovascular disorders, including hypertension, cardiac hypertrophy, and atherosclerosis, is well established, whereas its relationship with cardiac arrhythmias is a new area of investigation. Atrial fibrillation and malignant ventricular tachyarrhythmias, especially in the setting of cardiac hypertrophy or failure, seem to be examples of RAAS-related arrhythmias because treatment with RAAS modulators, including angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor blockers, reduces the incidence of these arrhythmias. RAAS has a multitude of electrophysiological effects and can potentially cause arrhythmia through a variety of mechanisms. We review new experimental results that suggest that RAAS has proarrhythmic effects on membrane and sarcoplasmic reticulum ion channels and that increased oxidative stress is likely contributing to the increased arrhythmic incidence. A summary of ongoing clinical trials that will address the clinical usefulness of RAAS modulators for prevention or treatment of arrhythmias is presented.
KW - Angiotensin receptor blocker
KW - Angiotensin-converting enzyme inhibitor
KW - Arrhythmias
KW - Atrial fibrillation
KW - Gap junction
KW - Mineralocorticoid receptor blocker
KW - Oxidative stress
KW - Renin-angiotensin-aldosterone system
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U2 - 10.1016/j.hrthm.2008.02.025
DO - 10.1016/j.hrthm.2008.02.025
M3 - Article
C2 - 18456194
AN - SCOPUS:43049107973
SN - 1547-5271
VL - 5
SP - S12-S17
JO - Heart Rhythm
JF - Heart Rhythm
IS - 6 SUPPL.
ER -