Syndrome X may be caused by a coronary microvascular dysfunction, possibly
due to abnormalities in coronary endothelial function. Previous studies sug
gested that endothelin-l (ET-1) might be involved in the pathogenesis of sy
ndrome X. Baseline arterial and coronary sinus ET-I levels were measured in
13 patients with syndrome X (10 women, 52 +/- 7 years) and in 8 control pa
tients (5 women, 46 +/- 11 years). ET-I was also measured after atrial paci
ng in 12 patients with syndrome X and all controls. To simultaneously asses
s the activity of nitric oxide, guanosine 3'-5'-cyclic monophosphate (cGMP)
was also measured in 11 patients with syndrome X and 7 controls. Baseline
arterial (2.27 +/- 0.46 vs 1.90 +/- 0.22 pg/ml, p < 0.05) and coronary sinu
s (2.03 +/- 0.43 vs 1.68 +/- 0.28 pg/ml, p = 0.06) ET-I plasma levels were
higher in patients than in controls. After pacing, arterial ET-I levels did
not change in either group and coronary sinus ET-1 levels were also unchan
ged in controls. In contrast, coronary sinus ET-I increased significantly i
n response to atrial pacing in patients with syndrome X (p = 0.023), and di
fferences between coronary sinus ET-I levels of patients with syndrome X an
d controls after pacing became highly significant (2.22 +/- 0.45 vs 1.69 +/
- 0.20 pg/ml, respectively, p = 0.006). No significant differences in arter
ial and coronary sinus cGMP concentrations were found between the 2 groups,
both at baseline and after pacing. Our findings suggest that an increased
vasoconstrictor activity of microvascular endothelium is present in at leas
t some patients with syndrome X and may be involved in the pathogenesis of
the syndrome. (C) 1999 by Excerpta Medico, Inc.