Boomsma F, de Kam P J, Tjeerdsma G, van den Meiracker A H, van Veldhuisen D J
Department of Internal Medicine, Erasmus university Medical Centre Rotterdam, Rotterdam, The Netherlands.
Eur Heart J. 2000 Nov;21(22):1859-63. doi: 10.1053/euhj.2000.2176.
Experimental evidence has suggested that semicarbazide-sensitive amine oxidase is involved in vascular endothelial damage and in the process of atherosclerosis, through the formation of reactive aldehydes, hydrogen peroxide and ammonia from endogenous substrates. Recent evidence indicates that semicarbazide-sensitive amine oxidase may be identical with the vascular adhesion protein-1. In patients with diabetes mellitus and chronic heart failure the plasma activity is raised relative to the severity of the disease. The prognostic value of plasma semicarbazide-sensitive amine oxidase is not known.
Plasma semicarbazide-sensitive amine oxidase activity was measured at baseline in patients with moderate to severe chronic heart failure who participated in a large European study (PRIME-II). The 372 patients who took part in a pre-defined substudy in The Netherlands were investigated and a survival follow-up (maximum 5.4 years, mean 3.4 years) was carried out. Within the follow-up period 195 patients died. Plasma semicarbazide-sensitive amine oxidase was higher at baseline in those who died than in the survivors (653+/-258 vs 540+/-242 mU. l(-1), P<0.001). Dividing the patients into two groups according to plasma values above or below the median value of 550 mU. l(-1), semicarbazide-sensitive amine oxidase was found to be a prognostic parameter for survival, both in univariate (P<0.0001) and in multivariate (P=0.0106) analysis. Semicarbazide-sensitive amine oxidase values >550 mU. l(-1)had a 1. 50 (95% CI, 1.10-2.04) times increased risk of death.
The finding that plasma semicarbazide-sensitive amine oxidase is an independent prognostic marker for mortality in chronic heart failure supports the concept that an elevated plasma semicarbazide-sensitive amine oxidase level has deleterious effects, possibly due to vascular endothelial damage.
实验证据表明,氨基脲敏感胺氧化酶通过内源性底物形成反应性醛、过氧化氢和氨,参与血管内皮损伤和动脉粥样硬化过程。最近的证据表明,氨基脲敏感胺氧化酶可能与血管黏附蛋白-1相同。在糖尿病和慢性心力衰竭患者中,血浆活性相对于疾病严重程度升高。血浆氨基脲敏感胺氧化酶的预后价值尚不清楚。
在参与一项大型欧洲研究(PRIME-II)的中重度慢性心力衰竭患者中,于基线时测量血浆氨基脲敏感胺氧化酶活性。对荷兰参与一项预先定义的子研究的372例患者进行了调查,并进行了生存随访(最长5.4年,平均3.4年)。在随访期内,195例患者死亡。死亡患者基线时的血浆氨基脲敏感胺氧化酶高于存活者(653±258对540±242 mU·l⁻¹,P<0.001)。根据血浆值高于或低于中位数550 mU·l⁻¹将患者分为两组,发现氨基脲敏感胺氧化酶在单因素(P<0.0001)和多因素(P=0.0106)分析中均为生存的预后参数。氨基脲敏感胺氧化酶值>550 mU·l⁻¹时死亡风险增加1.50倍(95%可信区间,1.10-2.04)。
血浆氨基脲敏感胺氧化酶是慢性心力衰竭死亡率的独立预后标志物这一发现支持了血浆氨基脲敏感胺氧化酶水平升高具有有害作用的概念,可能是由于血管内皮损伤所致。