Anti-Inflammatory Action of Angiotensin-Converting Enzyme Inhibitors and Angiotensin Receptor Blockers
Letter to the Editor
Introduction
The meta-analysis by Healey et al. (1) indicated that both angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) appear to be effective in the prevention of atrial fibrillation. However, among the plausible underlying mechanisms, they did not mention the potential role of low-grade systemic inflammation.
Increasing levels of C-reactive protein (CRP), the classic marker of systemic inflammation, have been shown to be associated with atrial fibrillation (2,3). Furthermore, CRP appears also to predict patients at increased risk for developing future atrial fibrillation (4).
Because angiotensin receptor blockade has been shown to be related to a decrease in markers of systemic inflammation (5,6), this anti-inflammatory action may help explain the beneficial effect of ACEIs and ARBs in the prevention of atrial fibrillation.
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2. : "C-reactive protein elevation in patients with atrial arrhythmias: inflammatory mechanisms and persistence of atrial fibrillation". Circulation 2001; 104: 2886.
3. : "Frequency of elevation of C-reactive protein in atrial fibrillation". Am J Cardiol 2004; 94: 1255.
4. : "Inflammation as a risk factor for atrial fibrillation". Circulation 2003; 108: 3006.
5. : "Antiinflammatory effects of angiotensin II subtype 1 receptor blockade in hypertensive patients with microinflammation". Circulation 2004; 110: 1103.
6. : "Angiotensin receptor blockade decreases markers of vascular inflammation". J Cardiovasc Pharmacol 2004; 44: 335.