Abstract 15675: Local Inflammatory Mediators in Diastolic Heart Failure Induced Reactive Pulmonary Hypertension Are Similar to Pulmonary Arterial Hypertension
Background: Tumor Necrosis Factor-α (TNF) and Interleukin-6 (IL6) act as local cytokine mediators of remodeling, endothelial activation, and inflammation. Diastolic heart failure is the most common cause of secondary pulmonary hypertension (DHF-PH). In vitro, similar to PAH, DHF-PH has additional pre-capillary active pro-inflammatory changes. We studied the pathophysiological contribution of localized endothelial remodeling and dysfunction in DHF-PH through measuring in-vivo pulmonary arterial (PA) TNF and IL6 levels in patients with PAH and DHF-PH.
Methods: Prior to the initiation of treatment, PA levels of TNF and IL6 were measured during right heart catheterization (RHC) in consecutive patients with PAH (mPAP>25mmHg, PCWP<15mmHg, gradient dPAP-PCWP >5mmHg and transpulmonary gradient [TPG] >12mmHg) and DHF-PH (clinical symptoms of CHF, TTE parameters consistent with diastolic dysfunction, LVEF≥50% and PASP>35mmHg on TTE, RHC mPAP>25mmHg, gradient dPAP-PCWP <5mmHg and TPG ≤12mmHg). Patients with significant valvular disease were excluded.
Results: Patients with both DHF-PH (I, n=17) and PAH (II, n=11) had significantly elevated levels of TNF (figure A) and IL6 (figure B) compared to no-PH (III, n=8). However, no significant difference in TNF and IL6 were found in I vs. II.
Conclusions: This study is the first to measure and compare levels of PA TNF and IL6 levels in DHF-PH and PAH and highlights the similar role of activated endothelial remodeling in the pathophysiology of both DHF-PH and PAH.
- © 2013 by American Heart Association, Inc.