Plasma semicarbazide-sensitive amine oxidase is elevated in patients with congestive heart failure
Plasma semicarbazide-sensitive amine oxidase is elevated in patients with congestive heart failure
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DOI：
10.1016/s0008-6363(96)00209-x
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发表时间：
1997-02-01
影响因子：
10.8
通讯作者：
Schalekamp, MADH
中科院分区：
文献类型：
--
作者：
Boomsma, F;vanVeldhuisen, DJ;Schalekamp, MADH
目的：缩氨基脲敏感胺氧化酶（SSAO）存在于多种哺乳动物组织中，尤其是血管平滑肌细胞，但也存在于血浆中。该酶已被认为在血管内皮损伤中发挥作用，通过将胺转化为细胞毒性醛、氨和过氧化氢。内皮功能障碍存在于糖尿病（DM）和充血性心力衰竭（CHF）。糖尿病患者血浆SSAO活性升高已有报道，但CHF患者尚无相关数据。方法和结果：对271例CHF患者的血浆SSAO进行了测量，并与77例对照组进行了比较。与对照组相比，CHF患者的SSAO升高（589 +/- 252 vs 355 +/- 114 mU/l; P < 0.0001）。NYHA III/IV级患者血浆SSAO高于III级患者（662 +/- 288 vs. 555 +/- 226 mU/l, P = 0.004），合并DM患者血浆SSAO高于无DM患者（706 +/- 248 vs. 557 +/- 245 mU/l, P < 0.0001）。血浆SSAO与血浆房利钠肽（r = 0.421 P < 0.0001）、血浆去甲肾上腺素（r = 0.27 P < 0.0001）、左心室射血分数（r = -0.13 P = 0.0162）相关。多元回归分析显示，心房利钠肽、去甲肾上腺素、糖尿病和心胸比值是影响血浆SSAO的主要因素。结论：CHF患者血浆SSAO水平升高，且随着病情的严重程度和糖尿病的出现而升高，这支持了SSAO可能参与血管内皮损伤的发病机制的观点。血浆SSAO可能是评估CHF严重程度和预后评估的有用参数。药理学操作SSAO活性可能是预防各种血管疾病中血管内皮损伤的一个有趣的新概念。
Objective: Semicarbazide-sensitive amine oxidase (SSAO) is present in various mammalian tissues, especially in vascular smooth muscle cells, but also in plasma. The enzyme has been suggested to play a role in vascular endothelial damage through conversion of amines into cytotoxic aldehydes, ammonia and hydrogen peroxide. Endothelial dysfunction is present in diabetes mellitus (DM) and congestive heart failure (CHF). Elevated plasma SSAO activities have been reported in patients with DM, bur no data on patients with CHF are as yet available. Methods and Results: Plasma SSAO was measured in 271 patients with CHF and compared to values in 77 controls. SSAO was found to be elevated in patients with CHF compared to controls (589 +/- 252 vs. 355 +/- 114 mU/l; P < 0.0001). Plasma SSAO was higher in NYHA class III/IV than in class III (662 +/- 288 vs. 555 +/- 226 mU/l; P = 0.004) and also higher in patients with concomitant DM than in those without (706 +/- 248 vs. 557 +/- 245 mU/l; P < 0.0001). Plasma SSAO correlated with plasma atrial natriuretic peptide (r = 0.421 P < 0.0001), with plasma norepinephrine (r = 0.27: P < 0.0001) and with left ventricular ejection fraction (r = -0.13; P = 0.0162). Multiple regression analysis showed atrial natriuretic peptide, norepinephrine, DM and cardiothoracic ratio to be the main determinants of plasma SSAO. Conclusion: The finding of elevated plasma SSAO in CHF, increasing with severity of the disease and with the concomitant presence of DM, supports the suggestion that SSAO may be involved in the pathogenesis of vascular endothelial damage. Plasma SSAO may be a useful parameter in assessing severity of CHF and in prognostic evaluation. Pharmacologic manipulation of SSAO activity might be an interesting new concept for prevention of vascular endothelial damage in various vascular disease entities.