DOI: 10.1093/eurheartj/ehag785.2370 ISSN: 0195-668X

Heterogeneous left atrial strain trajectories during mavacamten therapy in obstructive hypertrophic cardiomyopathy

D Jensen, T G Donati, M Gonzalez del Hoyo, F C Tanner, C Gruner

Abstract

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.

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