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. 2023 Oct 7;44(44):4622–4633. doi: 10.1093/eurheartj/ehad637

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© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Graphical Abstract — The path to treatment of obstructive hypertrophic cardiomyopathy. (Top left) Haemodynamic observations demonstrated. Left ventricular (LV) obstruction and symptoms related to LV hypertrophy. (Bottom left) Discovery of genetic variants in ∼40% of patients. (Centre) Sarcomeres in obstructive hypertrophic cardiomyopathy (oHCM) show excess of myosin–actin cross-bridges that are normalized by mavacamten. (Top right) Pre-clinical observations in mouse and pig models of oHCM. (Bottom right) The two placebo-controlled clinical trials of mavacamten in oHCM. HCM, hypertrophic cardiomyopathy; hsTnT, high-sensitivity troponin T; LA, left atrial; LV, left ventricular; LVOT, left ventricular outflow tract; NT-proBNP, N-terminal pro-B-type natriuretic peptide; QOL, quality of life.