Diastolic mechanics of EHT and effect of acute mavacamten treatment. (A) Representative diastolic force–length traces of WT2 and HCM EHTs. (B) HCM EHTs had a significantly elevated diastolic force compared with WT2 (WT versus HCM, 0.13 ± 0.04 versus 0.44 ± 0.07 mN, P = 0.002, Mann–Whitney U test). (C) Representative paired acute measurement of HCM EHT isometric twitch before and after mavacamten. (D) Representative paired acute measurement of HCM EHT diastolic force–length relation before and after mavacamten. (E) Mavacamten drastically decreased active contractile for production in HCM EHTs, specifically reducing PF by ∼73% compared with untreated paired HCM EHTs (P = 0.02, paired ratio t test). (F) Mavacamten reduced diastolic force by ∼15% compared with paired untreated HCM EHTs (P = 0.002, paired ratio t test). (G) Mavacamten reduced RT50 by 26% (P = 0.006, paired ratio t test). (H) Mavacamten reduced nTTI by 18% (P = 0.01, paired ratio t test). (I) Mavacamten had no effect on TTP in HCM EHTs. Data are mean ± standard error. *, P < 0.05; **, P < 0.01. mava, mavacamten.