Abstract 11577: Systemic Inflammatory Burden in Heart Failure with Preserved Ejection Fraction induced Pulmonary Hypertension Compared to Pulmonary Arterial Hypertension
Background: High sensitivity C-reactive protein (hs-CRP) is a robust and reproducible marker of inflammation. Heart failure with preserved ejection fraction (HFpEF) is a common cause of secondary pulmonary hypertension (HFpEF-PH). Recently, studies have shown that similar to Pulmonary Arterial Hypertension (PAH), HFpEF-PH has additional pre-capillary active pro-inflammatory changes. We compared levels of pulmonary arterial (PA) hs-CRP in patients with both PAH and HFpEF-PH to assess the inflammatory burden in the pathophysiology of these two diseases.
Methods: Prior to the initiation of treatment, PA levels during right heart catheterization (RHC) of hs-CRP were measured in consecutive patients with PAH (mean PA pressure>25mmHg, PCWP<15mmHg, gradient PA-diastolic PCWP >5mmHg and transpulmonary gradient [TPG] >12mmHg) and HFpEF-PH (clinical symptoms of CHF, transthoracic echocardiographic (TTE) parameters consistent with diastolic dysfunction, left ventricular ejection fraction ≥50% and PASP>35mmHg on TTE, RHC mean PA pressure>25mmHg, gradient PA-diastolic PCWP <5mmHg and TPG ≤12mmHg). Patients with significant valvular disease were excluded.
Results: After controlling for co-morbid diseases, Patients with HFpEF-PH (n=18) had significantly elevated hs-CRP (15±3mg/L) compared to both PAH (n=13, 6±1mg/L, p=0.01) and controls (n=6, 5±2mg/L, p=0.04; overall p=0.007). However, no significant difference in hs-CRP levels were found between the PAH and controls (p=0.5).
Conclusion: This study is the first to measure and compare PA hs-CRP levels in HFpEF-PH and PAH and highlights the increased systemic inflammatory burden in the pathogenesis of HFpEF-PH compared to PAH. As both PAH and HFpEF-PH share many echocardiographic features making them difficult to distinguish, hs-CRP may assist in differentiating these two diseases. Further multicenter studies are warranted to investigate these findings.
- © 2012 by American Heart Association, Inc.