Σάββατο 31 Ιανουαρίου 2009

CCBs ACEIs AND EDEMA

J Hum Hypertens. 2009 Jan 15. [Epub ahead of print]Related Articles, LinkOut
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Mitigation of calcium channel blocker-related oedema in hypertension by antagonists of the renin-angiotensin system.

de la Sierra A.

1University of Barcelona, Barcelona, Spain.

This review is aimed at examining calcium channel blocker (CCB)-related oedema and how this can be attenuated through the use of agents that inhibit the renin-angiotensin system. CCBs are effective antihypertensive agents, but their propensity for causing oedema may reduce compliance. A review of the literature has indicated that the absolute incidence of this side effect is difficult to determine because reported rates vary widely, a factor that may stem from differences in the surveillance technique (active vs passive). In a recent trial incorporating active surveillance, 25% of patients who received amlodipine 10 mg per day experienced oedema. CCB-induced oedema is caused by increased capillary hydrostatic pressure that results from preferential dilation of pre-capillary vessels. Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) cause post-capillary dilation and normalize hydrostatic pressure, and are thus ideally suited for prevention/reversal of CCB-induced oedema. The efficacy of this strategy was proven using both subjective and objective techniques. ARB/CCB and ACEI/CCB combination therapy is also more effective than CCB monotherapy in controlling blood pressure. These combinations represent an important advance in the management of hypertension.Journal of Human Hypertension advance online publication, 15 January 2009; doi:10.1038/jhh.2008.157.

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