We evaluated 30 consecutive patients and 48 age- and sex-matched contr
ols to explore the possibility of a pathogenic contribution by plasma
endothelin-1 in the cardiac expression of systemic sclerosis. Venous p
lasma endothelin-1 was measured by radio-immunoassay and left ventricu
lar function by echocardiography. The patient group had elevated plasm
a endothelin-1 (2.6+/-0.2 vs. 1.8+/-0.1 pmol/l, P<0.001), but endothel
in-1 was not related to age, heart rate, blood pressure, total periphe
ral resistance, disease duration or systemic sclerosis score. Endothel
in-1 was related to left ventricular hypertrophy in terms of septal th
ickness (r=0.33, P<0.01) and left ventricular mass index (r=0.32, P<0.
01). Plasma endothelin-1 was further related to measures indicating re
duced left ventricular filling; left atrial emptying index (r=-0.50, P
<0.0005), the first third tilling fraction (r=-0.31, P<0.05) and the t
ime velocity integral of Doppler early/late filling velocity (r=-0.40,
P<0.001). Furthermore, circulating endothelin-1 was related to impair
ed left Ventricular contractility as estimated by pre-ejection period/
left ventricular ejection time (r=0.32, P<0.01) and end-systolic wall
stress/volume index (r=-0.30, P<0.05). We conclude that plasma endothe
lin-1 is elevated in relation to the degree of left ventricular hypert
rophy, diastolic dysfunction and impaired contractility in systemic sc
lerosis. It may be of pathogenic importance to the cardiac involvement
in systemic sclerosis which is not mediated via an increase in system
ic blood pressure. It is not yet clear whether our findings are exclus
ive to systemic sclerosis patients or represent a generalized phenomen
on in patients with impaired left ventricular function. (C) 1997 Elsev
ier Science Ireland Ltd.