Abstract 16496: Changes in Aortic-Mitral Coupling in Severe Aortic Stenosis
Background: The mitral and aortic valves (MV, AV) are coupled via fibrous tissue. Normal aortic-mitral coupling (AMC) has been described using high-resolution real-time 3D images obtained by matrix transesophageal echocardiography (mTEE). We hypothesized that MV and left ventricular (LV) function are affected by severe aortic stenosis (AS) through altered AMC. We studied changes in AMC in patients with AS undergoing aortic valve replacement (AVR) and compared them to patients without AS with normal and wiith reduced LV function.
Methods: MTEE (Philips iE33) studies were performed on 31 patients: 15 controls with normal AV and LV function; 10 with AS and normal LV function who were studied pre- and post-AVR; and 6 with systolic heart failure (SHF) and normal AV and MV. Custom software tracked the AV and MV annuli in 3D space throughout the cardiac cycle, allowing automated measurements of changes in MV and AV morphology, angle and motion.
Results: See Table. In patients post-AVR, both aortic annular (AoA) and mitral annular (MA) areas were significantly smaller throughout the cardiac cycle compared to controls and pre-AVR values. End-systolic AoA-MA angle was reduced in patients pre-AVR compared to controls. There was a trend towards wider AoA-MA angles post-AVR. MA displacement was reduced in SHF patients compared to all other groups, and reduced post-AVR compared to pre-AVR values. There was trend towards a reduction in MA motion post-AVR compared to controls.
Conclusion: Severe AS affects normal AMC by inhibiting the hinge motion between the MV and AV and is partially relieved by AVR. AVR also results in reduced AoA and MA areas throughout the cardiac cycle. Post-AVR, MA displacement is reduced but not as severe as in SHF, likely reflecting the influence of LV function. These results demonstrate for the first time that AMC is restricted in AS and continues to operate with abnormal physiology post-AVR, which may have implications for future development of prosthetic AVs.
- © 2010 by American Heart Association, Inc.