F. Boomsma et al., Plasma semicarbazide-sensitive amine oxidase (SSAO) is an independent prognostic marker for mortality in chronic heart failure, EUR HEART J, 21(22), 2000, pp. 1859-1863
Aims Experimental evidence has suggested that semicarbazide-sensitive amine
oxidase is involved in vascular endothelial damage and in the process of a
therosclerosis, through the formation of reactive aldehydes, hydrogen perox
ide and ammonia from endogenous substrates. Recent evidence indicates that
semicarbazide-sensitive amine oxidase may be identical with the vascular ad
hesion protein-1. In patients with diabetes mellitus and chronic heart fail
ure the plasma activity is raised relative to the severity of the disease.
The prognostic value of plasma semicarbazide-sensitive amine oxidase is not
known.
Methods and Results Plasma semicarbazide-sensitive amine oxidase activity w
as measured at baseline in patients with moderate to severe chronic heart f
ailure who participated in a large European study (PRIME-II). The 372 patie
nts who took part in a pre-defined substudy in The Netherlands were investi
gated and a survival follow-up (maximum 5.4 years, mean 3.4 years) was carr
ied out. Within the follow-up period 195 patients died. Plasma semicarbazid
e-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 medi
an value of 550 mU.l(-1), semicarbazide-sensitive amine oxidase was found t
o be a prognostic parameter for survival, both in univariate (P<0.0001) and
in multivariate (P = 0.0106) analysis. Semicarbazide-sensitive amine oxida
se values >550 mU.l(-1) had a 1.50 (95% CI, 1.10-2.04) times increased risk
of death.
Conclusion The finding that plasma semicarbazide-sensitive amine oxidase is
an independent prognostic marker for mortality in chronic heart failure su
pports the concept that an elevated plasma semicarbazide-sensitive amine ox
idase level has deleterious effects, possibly due to vascular endothelial d
amage. (Eur Heart J 2000; 21: 1859-1863, doi:10,1053/euhj.2000. 2176) (C) 2
000 The European Society of Cardiology.