Boomsma F, van Veldhuisen D J, de Kam P J, Man in't Veld A J, Mosterd A, Lie K I, Schalekamp M A
Cardiovascular Research Institute COEUR, Division of Internal Medicine 1, Erasmus University, Rotterdam, Netherlands.
Cardiovasc Res. 1997 Feb;33(2):387-91. doi: 10.1016/s0008-6363(96)00209-x.
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, but no data on patients with CHF are as yet available.
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. 455 +/- 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 = 0.42; 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.
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.
氨基脲敏感胺氧化酶(SSAO)存在于多种哺乳动物组织中,尤其在血管平滑肌细胞中,血浆中也有。该酶被认为通过将胺类转化为细胞毒性醛、氨和过氧化氢,在血管内皮损伤中发挥作用。糖尿病(DM)和充血性心力衰竭(CHF)患者存在内皮功能障碍。已有报道DM患者血浆SSAO活性升高,但尚无CHF患者的数据。
测定了271例CHF患者的血浆SSAO,并与77例对照者的值进行比较。发现CHF患者的SSAO高于对照组(589±252对455±114 mU/l;P<0.0001)。纽约心脏协会(NYHA)心功能Ⅲ/Ⅳ级患者的血浆SSAO高于Ⅲ级患者(662±288对555±226 mU/l;P=0.004),合并DM的患者也高于未合并DM的患者(706±248对557±245 mU/l;P<0.0001)。血浆SSAO与血浆心房利钠肽相关(r=0.42;P<0.0001),与血浆去甲肾上腺素相关(r=0.27;P<0.0001),与左心室射血分数相关(r=-0.13;P=0.0162)。多元回归分析显示心房利钠肽、去甲肾上腺素、DM和心胸比是血浆SSAO的主要决定因素。
CHF患者血浆SSAO升高,且随疾病严重程度及合并DM而增加,这一发现支持了SSAO可能参与血管内皮损伤发病机制的观点。血浆SSAO可能是评估CHF严重程度和预后的有用参数。对SSAO活性进行药物调控可能是预防各种血管疾病实体中血管内皮损伤的一个有趣的新概念。