Abstract 18726: Mediators in Pulmonary Hypertension: A Comparison Between Pulmonary Arterial Hypertension and Diastolic Heart Failure-Induced Pulmonary Hypertension
Background: Pulmonary arterial hypertension (PAH), defined by elevated pulmonary arterial pressure (PAP) in the setting of normal left ventricular (LV) function, results from the imbalance of vasoactive mediators causing vasoconstriction and proliferation of pulmonary-arterial vasculature. Some of these mediators have been the target of novel therapies developed to treat PAH. Diastolic heart failure (DHF) is characterized by impaired LV relaxation with preserved ejection fraction and the transmission of increased pressure to the pulmonary circulation. A common cause of secondary pulmonary hypertension, elevated PAP in DHF has been associated with increased mortality. No study has assessed the levels of vasoactive mediators in patients with PAH as compared to DHF-induced pulmonary hypertension (DHF-P).
Methods and Results: We measured vasoconstrictors, urotensin II (U-II), norepinephrine (NE) and epinephrine (EPI), and vasodilators, 6-Keto PGF2-α (6KPGF, stable metabolite of prostacyclin) and relaxin (RLX), in patients with PAH, DHF-P, DHF alone and controls. Eighteen, 13, 7 and 15 patients comprised the above groups, respectively. U-II was insignificantly elevated in patients with DHF compared to the other groups (p=0.477). NE was significantly elevated in PAH (p=0.006) and DHF (p=0.039) compared to controls. EPI was significantly elevated in DHF-P (p=0.012) though not in DHF alone or PAH as compared to controls. 6KPGF was lower in all conditions as compared to controls, though it was significantly lower in PAH and DHF alone as compared to DHF-P and controls (p<0.05). RLX was insignificantly elevated in all conditions compared to controls, with the highest levels in PAH (p=0.252).
Conclusion: Significant elevations in NE in DHF, EPI in DHF-P and significantly lower levels of 6KPGF in DHF suggest a role of such mediators in the development of these conditions. As such, these mediators should be studied as future therapeutic targets in DHF and DHF-P.
- © 2010 by American Heart Association, Inc.