Mitral Valve Function in Atrial Fibrillation
Julia C. Swanson1, Gaurav Krishnamurthy1, John-Peder Escobar Kvitting1, D. Craig Miller1, Neil B. Ingels, Jr.2.
Whether mitral valve (MV) function is disturbed in the setting of atrial fibrillation (AFIB), a common clinical arrhythmia, is unknown. Recent work has shown that the MV anterior leaflet (AL) is an active structure that stiffens and relaxes during the cardiac cycle. Further, in the setting of ventricular pacing, when atrial depolarization does not precede ventricular systole, both early systolic annular septal-lateral dimension reduction and AL stiffening are abolished; thus, these phenomena depend on supra-ventricular (or “atriogenic”) depolarization. The purpose of this study was to investigate the effect of AFIB on both early systolic annular septal-lateral dimension reduction and AL stiffening.
Eight sheep had radiopaque-marker arrays implanted in the left ventricular (LV), mitral annulus, AL and papillary muscle tips. 4-D marker coordinates (x,y,z,t) were obtained from biplane videofluoroscopy at baseline (CTL) and during atrial fibrillation (AFIB) induced by application of an alternating current fibrillator to the atria. Septal-lateral annular dimensions were obtained every 16.7msec from annular markers. Circumferential and radial AL stiffness values, reflecting force generation in three leaflet regions (annular, belly, free-edge), were obtained from inverse finite element analysis of AL displacements in response to trans-leaflet pressure changes during both isovolumic contraction (IVC) and isovolumic relaxation (IVR).
AFIB abolished early systolic septal-lateral dimension reduction, but AL stiffness was unchanged (Table). Early systolic AL stiffness (IVC) was greater than late systolic AL stiffness in all three leaflet regions in both the radial and circumferential directions despite the loss of normal atrial depolarization and contraction (all p<0.002).
During acute AFIB in ovine hearts, early-systolic (IVC) septal-lateral dimension reduction was abolished, but, surprisingly, AL stiffening was unaffected. Each depolarization that traversed the atrioventricular node (AVN) also entered the AL causing early systolic AL stiffening. There appears to be two pathways: One triggering early systolic septal-lateral dimension reduction which is abolished by AFIB, and another not affected by AFIB and similar to AVN conduction.
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