Abstract
Endothelin-1 (ET-1), a potent vasoconstrictor, is elevated in heart failure states as well as in pulmonary arterial hypertension (PAH). Additionally, ET-1 receptor blockade is a mainstay of PAH treatment. Diastolic heart failure (DHF) is a common cause of secondary pulmonary hypertension, and elevated PA pressure is associated with increased mortality in DHF. As new clinical trials are designed to evaluate the role of ET-1 antagonism in DHF-induced pulmonary hypertension (D-PH), we compared serum ET-1 levels in patients with PAH, D-PH, and normal controls to more clearly understand the neurohormonal milieu of D-PH.
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