Author + information
- Elisa Bradley,
- John Daugherty,
- Emefah Loccoh,
- Faith Kline and
- Peter Mohler
Background: Heart failure currently affects 5.1 million adults in the U.S., leading to increased research in left ventricular (LV) failure. However, there remains scarce data on right ventricular (RV) failure despite increasing recognition of pulmonary arterial hypertension (PAH), where RV failure plays a central role in prognosis. We sought to evaluate potential pathways that may mediate RV failure.
Methods: Human mRNA was isolated from control LV (n=5), control RV (n=5), and PAH RV samples (n=2). Protein expression was then analyzed if >1.5 fold difference (positive or negative) between RV and LV control samples and confirmed with immunoblot. All samples were normalized to GAPDH and compared with the student's t-test.
Results: There was increased expression of FIGF in RV vs. LV control tissue (1.02+0.19 vs. 0.5+0.19, p<0.05). All other proteins were not differentially expressed in ventricular tissue. Descriptive analysis of protein expression in PAH-RV samples suggest increased expression of CTGF 1, CTGF 2, and TRAPP6AC (Fig 1).
Conclusion: Although fibrosis is one of the hallmark changes within the pulmonary vascular in PAH, no relationship of fibrotic changes in the RV has been reported. Our data suggests that CTGF may play a role in ventricular fibrosis and therefore, how well the RV functions in PAH. We also found increased expression of TRAPP6AC in PAH RV tissue, which may suggest that protein transport and therefore targeting/secretion play a role in PAH mediated RV dysfunction.
Poster Hall, Hall C
Saturday, March 18, 2017, 9:45 a.m.-10:30 a.m.
Session Title: Understanding Pulmonary Vascular Disease: From Bench to Bedside
Abstract Category: 35. Pulmonary Hypertension and Pulmonary Thrombo-embolic Disease
Presentation Number: 1181-006
- 2017 American College of Cardiology Foundation