Abstract 14061: Prostacyclin Levels in Pulmonary Hypertension: A Comparison Between Pulmonary Arterial Hypertension and Diastolic Heart Failure-Induced Pulmonary Hypertension
Background: Imbalance in endogenous prostacyclin production has long been implicated in the development of pulmonary hypertension (PH). In addition to cAMP-mediated vasodilation, prostacyclin is involved in decreasing platelet aggregation and smooth muscle cell proliferation. As such, prostacyclin therapy has become a mainstay of treatment in patients with PH. While levels of prostacyclin are known to be decreased in patients with pulmonary arterial hypertension (PAH), it has never been evaluated in patients with PH secondary to diastolic heart failure (DP)- an increasingly recognized cause of secondary PH. Therefore, we decided to compare levels of prostacyclin in patients with PAH, DP and normal controls.
Methods and Results: We measured serum levels of 6-Keto PGF1α (6KPGF) the stable metabolite of prostacyclin using the Amersham Enzymeimmunoassay Biotrak System (GE Healthcare, Buckinghamshire, United Kingdom) in patients with PAH, DP and normal controls. Thirty, 32, and 20 patients comprised the above groups, respectively. Median 6KPGF levels were significantly lower in the PAH group compared to controls (48.5 (range 24.8-785) vs. 85.4 (58.6-2516), p=0.008), while 6KPGF levels were not significantly different in the DP group as compared to controls (78.0 (25.0-966) vs. 85.4 (58.6-2516), p=0.463).
Conclusions: While prostacyclin levels are decreased in PAH as compared to controls, there is no significant difference in levels between patients with diastolic heart failure-induced PH (DP) and normal controls. This dichotomy reflects a difference in the pathogenesis of PAH as compared to DP, and may suggest a limited role for prostacyclin in the treatment of DP.
- © 2011 by American Heart Association, Inc.