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Background <p>Mavacamten is the first approved myosin inhibitor for symptomatic obstructive hypertrophic cardiomyopathy (oHCM), addressing hypercontractility and left ventricular outflow tract (LVOT) obstruction.</p> Objectives <p>This study evaluates left ventricular performance by non-invasive measurements of pressure–strain loops in patients treated with Mavacamten.</p> Methods <p>In 36 symptomatic oHCM patients, pressure–strain analysis was performed prior to 3 and 12&#xa0;months after Mavacamten therapy. Echocardiographic measurements included LVOT gradient, left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), left atrial strain (LAS), peak strain time dispersion (PSD), and myocardial work parameters (global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE)). Clinical status was evaluated using the New York Heart Association (NYHA) class and stress biomarkers (NTproBNP and high-sensitivity troponin I).</p> Results <p>Mavacamten therapy significantly reduced LVOT gradients at rest and under provocation. Gradients decreased from 69 ± 36 to 24 ± 27&#xa0;mmHg (<i>p</i> &lt; 0.001) at 3&#xa0;months and further to 11 ± 6&#xa0;mmHg (<i>p</i> = 0.003) at 12&#xa0;months. Provoked gradients decreased from 113 ± 33 to 50 ± 31&#xa0;mmHg (<i>p</i> &lt; 0.001) at 3&#xa0;months and to 31 ± 19&#xa0;mmHg (<i>p</i> = 0.01) at 12&#xa0;months. Clinical symptoms also improved. LVEF was 68 ± 6% at baseline and decreased mildly to 62 ± 5% (<i>p</i> = 0.003), while GLS and LAS remained unchanged. PSD decreased mildly from 116 ± 56 to 97 ± 36&#xa0;ms and further to 93 ± 38&#xa0;ms, but this was not statistically significant (<i>p</i> = 0.07). Under Mavacamten, GWE remained stable. In contrast, GWI, GCW, and GWW decreased significantly from baseline to 3&#xa0;months (GWI, 2098 ± 700 to 1610 ± 440&#xa0;mmHg%, <i>p</i> &lt; 0.001; GCW, 2514 ± 776 to 1951 ± 466&#xa0;mmHg%, <i>p</i> &lt; 0.001; GWW, 312 ± 163 to 249 ± 177&#xa0;mmHg%, <i>p</i> = 0.003), with only mild, non-significant further reductions at 12&#xa0;months (1538 ± 402, 1901 ± 380, and 207 ± 124&#xa0;mmHg%, respectively; <i>p</i> = 0.67, <i>p</i> = 0.74, <i>p</i> = 0.30).</p> Conclusion <p>Myocardial work indices derived from non-invasive pressure–strain analysis were feasible to obtain in patients with oHCM in this study. Mavacamten therapy decreases workload index, constructive and wasted work, and synchronizes myocardial contractility, reflecting normalization of myocardial energetics. These findings reinforce the role of Mavacamten as a targeted therapy in oHCM.</p> Graphical Abstract <p></p>

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Mavacamten optimizes myocardial work in patients with obstructive hypertrophic cardiomyopathy: a non-invasive pressure–strain analysis

  • 期刊论文

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  • 发表日期：

    2026年2月19日

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  • S. Scholtz,
  • C. Coppée,
  • K. Mohemed,
  • M. Potratz,
  • F. Langkamp,
  • V. Rudolph,
  • C. Maack,
  • W. Scholtz,
  • V. Sequeira,
  • J.-C. Reil

摘要

Background

Mavacamten is the first approved myosin inhibitor for symptomatic obstructive hypertrophic cardiomyopathy (oHCM), addressing hypercontractility and left ventricular outflow tract (LVOT) obstruction.

Objectives

This study evaluates left ventricular performance by non-invasive measurements of pressure–strain loops in patients treated with Mavacamten.

Methods

In 36 symptomatic oHCM patients, pressure–strain analysis was performed prior to 3 and 12 months after Mavacamten therapy. Echocardiographic measurements included LVOT gradient, left ventricular ejection fraction (LVEF), global longitudinal strain (GLS), left atrial strain (LAS), peak strain time dispersion (PSD), and myocardial work parameters (global work index (GWI), global constructive work (GCW), global wasted work (GWW), and global work efficiency (GWE)). Clinical status was evaluated using the New York Heart Association (NYHA) class and stress biomarkers (NTproBNP and high-sensitivity troponin I).

Results

Mavacamten therapy significantly reduced LVOT gradients at rest and under provocation. Gradients decreased from 69 ± 36 to 24 ± 27 mmHg (p < 0.001) at 3 months and further to 11 ± 6 mmHg (p = 0.003) at 12 months. Provoked gradients decreased from 113 ± 33 to 50 ± 31 mmHg (p < 0.001) at 3 months and to 31 ± 19 mmHg (p = 0.01) at 12 months. Clinical symptoms also improved. LVEF was 68 ± 6% at baseline and decreased mildly to 62 ± 5% (p = 0.003), while GLS and LAS remained unchanged. PSD decreased mildly from 116 ± 56 to 97 ± 36 ms and further to 93 ± 38 ms, but this was not statistically significant (p = 0.07). Under Mavacamten, GWE remained stable. In contrast, GWI, GCW, and GWW decreased significantly from baseline to 3 months (GWI, 2098 ± 700 to 1610 ± 440 mmHg%, p < 0.001; GCW, 2514 ± 776 to 1951 ± 466 mmHg%, p < 0.001; GWW, 312 ± 163 to 249 ± 177 mmHg%, p = 0.003), with only mild, non-significant further reductions at 12 months (1538 ± 402, 1901 ± 380, and 207 ± 124 mmHg%, respectively; p = 0.67, p = 0.74, p = 0.30).

Conclusion

Myocardial work indices derived from non-invasive pressure–strain analysis were feasible to obtain in patients with oHCM in this study. Mavacamten therapy decreases workload index, constructive and wasted work, and synchronizes myocardial contractility, reflecting normalization of myocardial energetics. These findings reinforce the role of Mavacamten as a targeted therapy in oHCM.

Graphical Abstract