Key result
Mavacamten is linked to an ~81% reduction in resting LVOT gradient in oHCM.
Why the study?
Does mavacamten therapy improve left atrial strain adaptation in patients with obstructive hypertrophic cardiomyopathy?
Observational (n=38)
No
Does mavacamten therapy improve left atrial strain adaptation in patients with obstructive hypertrophic cardiomyopathy?
In oHCM patients treated with mavacamten, left atrial strain trajectories are heterogeneous and depend on baseline atrial function, improving in patients with lower baseline strain while decreasing in those with higher baseline strain despite overall improvements in LVOT gradients and diastolic function.
Mavacamten-associated LA strain gains in oHCM appear limited to low-baseline patients; hypothesis-generating and requires prospective validation before clinical use.
Background/Introduction Mavacamten improves symptoms and left ventricular outflow tract (LVOT) obstruction in obstructive hypertrophic cardiomyopathy (oHCM). While favorable changes in left ventricular (LV) diastolic function are also well established, the mechanistic response of left atrial (LA) function remains insufficiently characterized. LA strain may capture distinct stages of atrial adaptation to chronic LV pressure overload and its resolution. Purpose This study aimed to evaluate LA strain adaptation during mavacamten therapy in oHCM patients. Methods We analyzed clinical, biochemical, and echocardiographic data from 38 oHCM patients treated with mavacamten at the University Hospital Zurich. LA strain was assessed at baseline, 6 months and last available follow-up. Results Over a median follow-up of 56 ± 21.7 weeks, mavacamten led to reductions in resting LVOT gradient by 81.3% (from 50.0 ± 33.3 to 9.3 ± 6.2 mmHg) and Valsalva LVOT gradient by 76.7% (from 89.0 ± 38.0 to 20.7 ± 16.2 mmHg), respectively (both p<0.001). LA volume index decreased by 21.2% (from 47.6 ± 12.9 to 37.5 ± 11.7 ml/m2, p<0.001). Diastolic function and atrioventricular coupling improved, including decreases in average E/e′ (-31%, p<0.001), left atrioventricular coupling index (-14%, p=0.023) and LA stiffness index (-20%, p=0.002). In contrast, LA strain values did not improve in the overall cohort. However, patients with baseline left atrial reservoir strain (LARS) below median demonstrated increases in LARS from 15.3 ± 3.5% to 18.2 ± 6.3%, LA pump strain (LAPS) from 6.1 ± 3.4% to 6.6 ± 5.7%, and LA conduit strain (LACS) from 9.1 ± 3.6% to 11.6 ± 4.0%. Conversely, patients with baseline LARS above median exhibited reductions in all LA strain components with significant between-group differences (LARS p=0.006; LAPS p=0.033; LACS p=0.009). Conclusion LA mechanical adaptation to mavacamten therapy in oHCM follows heterogeneous trajectories determined by baseline atrial function. Higher baseline LA strain likely reflects an adaptive state to high LV filling pressure that regresses after LV unloading, whereas lower baseline LA strain identifies advanced atrial dysfunction with partial recovery.
No takes yet. Share an insight, caveat, or question.
Jensen et al. (2026) conducted an observational in Obstructive hypertrophic cardiomyopathy (oHCM) (n=38). Mavacamten vs. Baseline (pre-treatment) and stratification by baseline median left atrial reservoir strain (LARS) was evaluated on Left atrial (LA) strain adaptation (reservoir [LARS], pump [LAPS], and conduit [LACS] strain) (p=0.006). Mavacamten in oHCM reduced resting LVOT gradient by 81.3% (p<0.001) and increased LA reservoir strain in patients below baseline median (15.3% to 18.2%, between-group p=0.006).
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: