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 (Ec) and radial (Er) stiffness was determined during IVC (Δt1), end IVC to midsystole (Δt2), midsystole to IVR onset (Δt3), and IVR (Δt4). Group mean stiffness (Ec ± SD; Er ± 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
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