TY - JOUR
T1 - Impact of pulmonary hypertension on tricuspid valve function
AU - Casa, Lauren D.C.
AU - Dolensky, Joseph R.
AU - Spinner, Erin M.
AU - Veledar, Emir
AU - Lerakis, Stamatios
AU - Yoganathan, Ajit P.
N1 - Funding Information:
The authors thank Holifield Farms for the donation of porcine hearts. LDCC was funded with Government support under and awarded by DoD, Air Force Office of Scientific Research, National Defense Science and Engineering Graduate (NDSEG) Fellowship, 32 CFR 168a. JRD was funded by the Georgia Institute of Technology Petit Undergraduate Research Scholarship, and EMS was funded by the American Heart Association Predoctoral Fellowship (09PRE2380090). Funds were also provided by the Wallace H. Coulter Distinguished Faculty Chair Endowment.
PY - 2013/4
Y1 - 2013/4
N2 - Pulmonary arterial hypertension (PAH) results in increased right ventricle (RV) afterload leading to RV remodeling, tricuspid regurgitation (TR), and RV failure. Though characterizing the mechanisms of TR in PAH may suggest new treatment strategies, the mechanisms leading to TR in PAH have not been characterized. In the present study, eleven porcine tricuspid valves were studied in an in vitro right heart simulator. Annular dilatations of 1.2 and 1.4 times normal area, papillary muscle (PM) displacement simulating concentric RV dilatation and eccentric RV dilatation due to concomitant left ventricle dysfunction, and two levels of PAH hemodynamics were simulated independently and in combination. Relative TR, tenting area (TA) along each coaptation line, and coaptation area (CA) of each leaflet were quantified. Results showed a significant increase (p ≤ 0.05) in TR with both increased mean pulmonary artery pressure (mPAP) and annular dilatation of 1.4 times normal. Increased mPAP significantly decreased TA but tended to increase CA, while PM displacement significantly increased TA but did not affect CA, suggesting competing effects of transvalvular pressure and leaflet tethering. Annular dilatation significantly decreased anterior and posterior CA but did not affect TA. These results may inform future TV repairs in PAH to reduce TR and improve RV hemodynamics.
AB - Pulmonary arterial hypertension (PAH) results in increased right ventricle (RV) afterload leading to RV remodeling, tricuspid regurgitation (TR), and RV failure. Though characterizing the mechanisms of TR in PAH may suggest new treatment strategies, the mechanisms leading to TR in PAH have not been characterized. In the present study, eleven porcine tricuspid valves were studied in an in vitro right heart simulator. Annular dilatations of 1.2 and 1.4 times normal area, papillary muscle (PM) displacement simulating concentric RV dilatation and eccentric RV dilatation due to concomitant left ventricle dysfunction, and two levels of PAH hemodynamics were simulated independently and in combination. Relative TR, tenting area (TA) along each coaptation line, and coaptation area (CA) of each leaflet were quantified. Results showed a significant increase (p ≤ 0.05) in TR with both increased mean pulmonary artery pressure (mPAP) and annular dilatation of 1.4 times normal. Increased mPAP significantly decreased TA but tended to increase CA, while PM displacement significantly increased TA but did not affect CA, suggesting competing effects of transvalvular pressure and leaflet tethering. Annular dilatation significantly decreased anterior and posterior CA but did not affect TA. These results may inform future TV repairs in PAH to reduce TR and improve RV hemodynamics.
KW - In vitro simulation
KW - Right ventricular remodeling
KW - Tricuspid regurgitation
UR - https://www.scopus.com/pages/publications/84876478752
U2 - 10.1007/s10439-012-0713-2
DO - 10.1007/s10439-012-0713-2
M3 - Article
C2 - 23519531
AN - SCOPUS:84876478752
SN - 0090-6964
VL - 41
SP - 709
EP - 724
JO - Annals of Biomedical Engineering
JF - Annals of Biomedical Engineering
IS - 4
ER -