Transient stiffening of mitral valve leaflets in the beating heart

Anterior mitral leaflet stiffness during isovolumic contraction (IVC) is much greater than that during isovolumic relaxation (IVR). We have hypothesized that this stiffening is due to transient early systolic force development in the slip of cardiac myocytes in the annular third of the anterior leaflet. Because the atrium is excited before IVC and leaflet myocytes contract for ≤250 ms, this hypothesis predicts that IVC leaflet stiffness will drop to near-IVR values in the latter half of ventricular systole. We tested this prediction using radiopaque markers and inverse finite element analysis of 30 beats in 10 ovine hearts. For each beat, circumferential (E_c) and radial (E _r) stiffness was determined during IVC (Δt₁), end IVC to midsystole (Δt₂), midsystole to IVR onset (Δt ₃), and IVR (Δt₄). Group mean stiffness (E _c ± SD; E_r ± SD; in N/mm²) during Δt₁ (44 ± 16; 15 ± 4) was 1.6 -1.7 times that during Δt₄ (28 ± 11; 9 ± 3); Δt₂ stiffness (39 ± 15; 14 ± 4) was 1.3-1.5 times that of Δt₄, but Δt₃ stiffness (32 ± 12; 11 ± 3) was only 1.1-1.2 times that of Δt₄. The stiffness drop during Δt₃ supports the hypothesis that anterior leaflet stiffening during IVC arises primarily from transient force development in leaflet cardiac myocytes, with stiffness reduced as this leaflet muscle relaxes in the latter half of ventricular systole.