9 Myocardial Remodelling Patterns in Severe Aortic Stenosis with Bicuspid and Tricuspid Valve Disease, and Reverse Remodelling after Aortic Valve Replacement

Background Bicuspid aortic valve (BAV) is a common congenital heart disease and a major risk factor for aortic stenosis (AS). Myocardial remodelling response to AS plays an important prognostic role1. Cardiovascular magnetic resonance (CMR) allows evaluation of myocardial structure, function and perfusion in AS. Phosphorus magnetic resonance spectroscopy (31P-MRS) allows assessment of myocardial energetic consequences of AS2. Purpose To assess differences in myocardial remodelling between tricuspid aortic valve (TAV) and BAV-associated severe-AS, and their recovery 6 months post aortic valve replacement (AVR). Methods Eighty severe-AS patients (70[69–72]years) undergoing AVR (40 TAV, 40 BAV) and 21 demographically-matched controls were recruited. The AS groups were matched for demographics, AS severity, surgical risk scores and comorbidities. One month before and 6 months post-AVR, patients underwent CMR and 31P-MRS for measuring left ventricular (LV) mass, concentricity-index (LV mass to LV end-diastolic volume ratio), global longitudinal shortening (GLS), rest and adenosine-stress myocardial blood flow (MBF), myocardial perfusion reserve (MPR) and energetics-index phosphocreatine to ATP ratio (PCr/ATP). Results Pre-AVR, there was no significant differences between the three cohorts when assessing LV ejection fraction, indexed LV end-diastolic volume and indexed end-systolic volume. Pre-AVR, both AS groups showed higher LV-concentricity (controls:0.53[0.51,0.60], TAV:0.95[0.82,1.07], BAV:0.92[0.82,1.08]g/ml;P<0.0001), higher mass-index (controls:45[39,50], TAV:73[67,78], BAV:74[68,80]g/m2;P<0.0001), impaired GLS (controls:18.8[16.5,19.5], TAV:12.6[11.3,13.9], BAV:13.6[10.9,16.6]%;P<0.0001). Reductions in both AS groups were also seen in PCr/ATP (controls:2.19[1.85,2.63], TAV:1.64[1.39,1.85], BAV:1.85[1.60,2.10];P=0.0004), stress-MBF (controls:2.16[1.88,2.27], TAV:1.35 [1.16,1.56], BAV:1.36[1.00,1.66]ml/min/g;P<0.0001), and MPR (controls:3.38[2.65,3.92], TAV:2.04 [1.78,2.46], BAV:1.83[1.58,2.78]ml/min/g;P<0.0001) against controls, with no significant differences between TAV and BAV. No significant difference was seen in the proportion of patients with TAV and BAV undergoing transcatheter or surgical AVR (table 1). Post-AVR, the TAV and BAV groups experienced similar magnitudes of reverse LV-remodelling, with no significant differences in LV-concentricity (TAV:0.86[0.71,0.98], BAV:0.81[0.65,0.96];P=0.41), LV-mass-index (TAV:60[54,65], BAV:61[55,66];P=0.81), GLS (TAV 15.4[13.6,17.9], BAV 16.3[12.8,18.1];P=0.82. Perfusion and cardiac energetic improvements were also similar between the AS cohorts: PCr/ATP (TAV:1.96[1.68,2.26], BAV:1.96[1.79,2.13];P=0.91), stress-MBF (TAV:1.63[1.37,1.97], BAV:1.56[1.25,1.97];P=0.86), and MPR (TAV:2.64[1.91,3.26], BAV:2.55[2.07,3.28];P=0.70). Conclusions Patients with severe AS, irrespective of BAV or TAV morphology, show a similar myocardial phenotype pre-AVR, with similar magnitudes of reverse remodelling post-AVR. Conflict of Interest None