Key result
Exogenous ET-1 infusion in patients with left ventricular dysfunction increased mean arterial pressure (100 to 107 mmHg, p<0.01) and systemic vascular resistance, without changing pulmonary pressure.
Why the study?
Does exogenous endothelin-1 infusion alter systemic and pulmonary haemodynamics in patients with left ventricular systolic dysfunction?
Does exogenous endothelin-1 infusion alter systemic and pulmonary haemodynamics in patients with left ventricular systolic dysfunction?
Absolute Event Rate: 107% vs 100%
p-value: p=<0.01
Exogenous ET-1 at pathophysiological concentrations causes systemic but not pulmonary vasoconstriction in patients with left ventricular dysfunction.
May support selective ET-1 targeting in LV dysfunction; leaves open whether antagonists confer clinical benefit.
OBJECTIVES: Plasma levels of immunoreactive endothelin-1 (ET-1) are raised in chronic heart failure. Whether plasma ET-1 contributes to the haemodynamic derangement found in chronic heart failure is not known. We investigated the effects of exogenous ET-1 on the pulmonary and systemic vasculature in patients with left ventricular systolic dysfunction (LVD), with or without overt heart failure. METHODS: ET-1 was infused at 1, 5 and 15 pmol/min into a distal pulmonary artery of ten patients with LVD to achieve plasma concentrations of ET-1 similar to those found in patients with heart failure and pulmonary hypertension. Haemodynamics were measured using a pulmonary thermodilution catheter and an arterial line. Intravascular Doppler and local pulmonary angiography were used to assess local pulmonary blood flow in the first four patients. RESULTS: Systemic haemodynamic changes occurred with ET-1 infusion: mean arterial pressure (100 +/- 3 [standard error of the mean]) to 107 +/- 3 mmHg; p < 0.01) and systemic vascular resistance (1699 +/- 118 to 2033 +/- 135 dynes s/cm5; p < 0.001) rose, while the cardiac index fell from 2.43 +/- 0.17 to 2.20 +/- 0.16 l/min/m2 (p < 0.002). Mean pulmonary artery pressure (21 +/- 2 mmHg) and pulmonary vascular resistance (151 +/- 14 to 147 +/- 14 dynes s/cm5) did not change however. CONCLUSIONS: Exogenous ET-1, when infused to achieve plasma concentrations similar to those in severe heart failure and pulmonary hypertension, causes systemic but not pulmonary vasoconstriction.
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P Cowburn (1998) studied left ventricular systolic dysfunction (n=10). Exogenous endothelin-1 (ET-1) vs. Baseline was evaluated on Mean arterial pressure (p=<0.01). Exogenous ET-1 infusion in patients with left ventricular dysfunction increased mean arterial pressure (100 to 107 mmHg, p<0.01) and systemic vascular resistance, without changing pulmonary pressure.
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