慢性心力衰竭患者血浆醛固酮水平升高,尽管血管紧张素转换酶被完全抑制

U. Jorde, T. Vittorio, S. Katz, P. Colombo, F. Latif, T. L. Le Jemtel
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引用次数: 116

摘要

背景:服用血管紧张素转换酶(ACE)抑制剂的慢性心力衰竭(CHF)患者血浆醛固酮水平升高。醛固酮水平升高可能反映血管转换酶在长期ACE抑制过程中的不完全抑制。我们同时测量了CHF患者血浆醛固酮水平和血管转换酶的抑制程度。方法与结果:34例CHF患者接受最大推荐剂量的ACE抑制剂治疗,持续3 ~ 105个月。测量外源性血管紧张素I (AI)的升压反应,并标准化血管紧张素II (AII)的升压反应,以评估血管转换酶(AII/AI比率)的抑制作用。固相放射免疫法测定醛固酮水平。34例受试者中有11例血浆醛固酮水平高于正常上限,即>15.0 ng/dL。11例受试者中有7例(64%)AII/AI比值≤0.05,表明血管转换酶完全抑制。在整个队列中,AII/AI比率与ACE抑制剂治疗的持续时间无关。结论:慢性心力衰竭患者在长期ACE抑制剂治疗期间血浆醛固酮水平升高,尽管血管转换酶被完全抑制。血管转换酶的完全抑制并不排除对CHF患者醛固酮受体阻断的需要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Elevated Plasma Aldosterone Levels Despite Complete Inhibition of the Vascular Angiotensin-Converting Enzyme in Chronic Heart Failure
Background—Plasma aldosterone levels are elevated in patients with chronic heart failure (CHF) taking angiotensin-converting enzyme (ACE) inhibitors. Elevated aldosterone levels may reflect incomplete inhibition of the vascular converting enzyme during long-term ACE inhibition. We simultaneously measured plasma aldosterone levels and the degree of inhibition of the vascular converting enzyme in patients with CHF. Methods and Results—Thirty-four subjects with CHF receiving the maximum recommended doses of ACE inhibitors for a duration of 3 to 105 months were studied. The pressor response to exogenous angiotensin I (AI) was measured and normalized for the pressor response to angiotensin II (AII) to assess inhibition of the vascular converting enzyme (AII/AI ratio). Aldosterone levels were determined by solid-phase radioimmunoassay. Eleven of the 34 subjects had plasma aldosterone levels above the upper limit of normal, ie, >15.0 ng/dL. Seven of these 11 subjects (64%) had an AII/AI ratio ≤0.05, indicating complete inhibition of the vascular converting enzyme. In the entire cohort, the AII/AI ratio did not correlate with the duration of ACE inhibitor therapy. Conclusions—Plasma aldosterone levels are elevated in patients with CHF during long-term ACE inhibitor therapy despite complete inhibition of the vascular converting enzyme. Complete inhibition of the vascular converting enzyme does not obviate the need for aldosterone receptor blockade in patients with CHF.
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