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Endothelin may be pathogenic in systemic sclerosis of the heart
E Kazzam1, A Waldenström, T Hedner
1Department of Internal Medicine, Umeå University Hospital, Sweden.
Insights
Elevated plasma endothelin-1 in systemic sclerosis patients correlates with cardiac dysfunction, including hypertrophy and impaired contractility. This suggests endothelin-1 may play a role in heart problems associated with systemic sclerosis.
Area of Science:
- Cardiology
- Endocrinology
- Rheumatology
Background:
- Systemic sclerosis (SSc) can involve cardiac complications.
- The role of endothelin-1 in SSc cardiac expression is not fully understood.
Purpose of the Study:
- To investigate the association between plasma endothelin-1 levels and cardiac function in patients with systemic sclerosis.
Main Methods:
- Radio-immunoassay measured plasma endothelin-1 in 30 SSc patients and 48 controls.
- Echocardiography assessed left ventricular function, including hypertrophy and filling parameters.
Main Results:
- SSc patients exhibited significantly higher plasma endothelin-1 levels compared to controls.
- Elevated endothelin-1 correlated with left ventricular hypertrophy (septal thickness, mass index).
- Plasma endothelin-1 was linked to reduced left ventricular filling and impaired contractility.
Conclusions:
- Plasma endothelin-1 is elevated in systemic sclerosis and associated with cardiac structural and functional abnormalities.
- Endothelin-1 may be pathologically important in SSc cardiac involvement, independent of systemic blood pressure.
- Further research is needed to determine if these findings are specific to SSc or indicative of a broader phenomenon in cardiac dysfunction.
Abstract:
We evaluated 30 consecutive patients and 48 age- and sex-matched controls to explore the possibility of a pathogenic contribution by plasma endothelin-1 in the cardiac expression of systemic sclerosis. Venous plasma endothelin-1 was measured by radio-immunoassay and left ventricular function by echocardiography. The patient group had elevated plasma endothelin-1 (2.6 +/- 0.2 vs. 1.8 +/- 0.1 pmol/1, P < 0.001), but endothelin-1 was not related to age, heart rate, blood pressure, total peripheral resistance, disease duration or systemic sclerosis score. Endothelin-1 was related to left ventricular hypertrophy in terms of septal thickness (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 reduced left ventricular filling; left atrial emptying index (r = -0.50, P < 0.0005), the first third filling fraction (r = -0.31, P < 0.05) and the time velocity integral of Doppler early/late filling velocity (r = -0.40, P < 0.001). Furthermore, circulating endothelin-1 was related to impaired 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 endothelin-1 is elevated in relation to the degree of left ventricular hypertrophy, diastolic dysfunction and impaired contractility in systemic sclerosis. It may be of pathogenic importance to the cardiac involvement in systemic sclerosis which is not mediated via an increase in systemic blood pressure. It is not yet clear whether our findings are exclusive to systemic sclerosis patients or represent a generalized phenomenon in patients with impaired left ventricular function.