CONG
CPCA
Plenary
Lily Lin
Clinical Lecturer
University of Alberta
Lily Lin
Clinical Lecturer
University of Alberta
Sanaz Hatami
Cardiac Surgeon
Darren Freed
Cardiac Surgeon
James Yashu Coe, n/a
Professor
Timothy Colen
Assistant Professor
Consolato Sergi
Professor
Richard Thompson
Associate professor
Elena Di Martino
Associate Professor
Walter Herzog
Professor
Ziad Abu Sara
Adjunct Assistant Professor
Nee Scze Khoo, MBChB, FRACP
Associate Director of Echocardiography
University of Alberta
Nee Scze Khoo, MBChB, FRACP
Associate Director of Echocardiography
University of Alberta
BACKGROUND: Tricuspid valve regurgitation (TR) develops in 25-35% of children with hypoplastic left heart syndrome (HLHS), a risk factor for morbidity and mortality. Surgical strategies for TR in HLHS are modest in success and durability, therefore warrants improved understanding and innovation. We developed a novel piglet model simulating infant HLHS RV physiology to study TV adaptation to chronic increased preload and afterload. We hypothesize that TV competency is maintained by adaptive rapid leaflet expansion despite annular dilation.
METHODS AND RESULTS: Sixteen piglets at 4-5weeks of age (maturity equivalent to infants) underwent left thoracotomy. Intervention piglets (IP, n=8) had their pulmonary valve torn to produce moderate to severe pulmonary regurgitation (volume loading) and pulmonary artery band placed to increase RV pressure. Control piglets (CP, n=8), age and gender matched, had sham surgery. Following a 4-week recovery, all piglets underwent hemodynamic assessment and 3DE of TV. We assessed TV annulus and leaflet geometry in mid-systole using a custom 3DE software (MATLAB). Ex-vivo TV total leaflet area was measured. Comparisons between IP and CP were made using Student t-test with significance at p < 0.05. Values were expressed as mean (standard deviation). IP had significant pulmonary regurgitation (mean PR reverse/forward velocity time integral ratio 0.68 (0.09)) and mean RV systolic pressure 77.9% of systemic pressure, reflected in thicker RV free wall and anterior papillary muscle, consistent with an effective model. IP and CP were similar in weight and TR grade. IP TV annulus were larger (p=0.02), more circular (p=0.03) and leaflets more tethered (p=0.02) with 43% larger total leaflet area (p=0.01) [see Table]. Greatest expansion was seen in the posterior leaflet (p=0.01). 3DE TV total leaflet area correlated with ex-vivo TV pathologic specimen area (r=0.63, p=0.02).
CONCLUSION: Following chronic exposure to increased RV preload and afterload, there is TV annular dilation and likely unchanged sub-valve apparatus, resulting in leaflet tethering. In-vivo 3DE identified rapid leaflet expansion as the main adaptive change to maintain competency from detrimental remodeling. Further research into modulation of TV leaflet growth may be important for understanding TV failure in HLHS.