The abstract describes the methodology of a prospective cohort study evaluating the 1-year CMR-derived effects of mavacamten in 22 patients with obstructive hypertrophic cardiomyopathy, but reports no results.
Cohort (n=22)
Blinded outcome assessment
No
Does mavacamten improve CMR-derived functional and structural parameters in patients with obstructive hypertrophic cardiomyopathy?
This prospective cohort study evaluates the 1-year effects of mavacamten on cardiac structure and function using comprehensive CMR in patients with obstructive hypertrophic cardiomyopathy.
Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular (LV) hypertrophy and often accompanied by LV outflow tract (LVOT) obstruction (oHCM).1 By modulating myosin-actin interaction, mavacamten improves clinical symptoms and exercise capacity while leading to reduction of echocardiographic LVOT gradient and favourable cardiac remodeling.2,3 Given its non-invasive tissue characterization and assessment of function, cardiovascular magnetic resonance (CMR) is recommended for evaluation in HCM.1 CMR substudies of the EXPLORER-HCM and SEQUOIA-HCM trials using 1.5T and 3T systems from different vendors revealed beneficial shorter-term effects after 30 and 24 weeks of myosin-inhibitor therapy using mavacamten and aficamten, respectively.4,5 This prospective study evaluated 1-year CMR-derived effects of mavacamten in oHCM employing a standardized protocol at a single tertiary referral centre comprising volumetric, functional, and feature-tracking strain analysis of all chambers including LV tissue characterization. The study was approved by the institutional review board. Twenty-two oHCM patients underwent 1.5T-CMR (Ingenia, Philips Healthcare) at first referral (baseline) and 1 year later including the following sequences: (a) balanced steady-state free precession cine in short-axis and long-axis (4-chamber, 2-chamber, and 3-chamber views); (b) T1 mapping (modified Look-Locker inversion recovery) acquired in three short-axis slices before and 10 min after gadobutrol (0.2 mmol/kg); (c) late gadolinium enhancement (LGE) in the same orientations as cine sequences. After baseline, patients either remained on negative inotropic therapy (control group, n = 7) or were treated additionally with mavacamten (mavacamten group, n = 15). The treatment decision for mavacamten was based on patient’s discretion. Two blinded cardiovascular radiologists with 5 and 8 years of experience in CMR analysed the data and performed the measurements in consensus.
Seuthe et al. (Mon,) conducted a cohort in Obstructive hypertrophic cardiomyopathy (oHCM) (n=22). Mavacamten vs. Negative inotropic therapy was evaluated on CMR-derived volumetric, functional, and feature-tracking strain analysis. The abstract describes the methodology of a prospective cohort study evaluating the 1-year CMR-derived effects of mavacamten in 22 patients with obstructive hypertrophic cardiomyopathy, but reports no results.
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