Detection of Left Atrial Remodeling by Three-Dimensional Echocardiography in Symptomatic Patients Known to Had Non-Obstructive Hypertrophic Cardiomyopathy

Abstract

Background: Hypertrophic cardiomyopathy (HCM) is one of the most prevalent inherited disorders and a common cause of sudden heart death. Left atrial (LA) dilatation frequently occurs in patients with HCM as a result of impaired left ventricular (LV) relaxation or associated involvement of LA myocardium in HCM.

Methods: We enrolled 170 patients known to had HCM (non-obstructive type) and 30 healthy subjects (control group). All of them underwent two-dimensional (2D) echocardiography to measure LV dimensions, function, LA dimension, LA deformations, pulmonary artery pressure (PAP) and LV global longitudinal strain (LVGLS). LA volumes and mechanics were also measured by three-dimensional (3D) echocardiography.

Results: By 2D echocardiography, patient group revealed significantly lower all LA functions vs. control group including reservoir (26 4 vs. 43 3, P < 0.001), conduit (-14 2 vs. -25 2, P < 0.001), and booster pump functions (-12 2 vs. -18 1, P < 0.001). PAP was significantly higher in patient group (42 7 vs. 27 4 in control group). LVGLS was significantly lower in patient group (-15.4% vs. -23% in control group). Using 3D speckle tracking echocardiography (STE), there were a significantly higher indexed maximum LA volume (Vmax indexed) (43.5 5.6 vs. 28.7 3.7, P < 0.001), but significantly lower left atrial strain at reservoir function (LASr) (24 4 vs. 41 3, P < 0.001), left atrial strain at conduit function (LAScd) (-13 2 vs. -24 2, P < 0.001), and left atrial strain at contractile function (LASct) (-11 2 vs. -18 1, P < 0.001).

Conclusion: Three-dimensional transthoracic echocardiography (TTE) is a feasible method for the assessment of LA remodeling, but there is adverse LA remodeling in patients with long-standing non-obstructive HCM including impaired all LA mechanics and with increased septal thickness, there are more diastolic dysfunction and more reduction of LA mechanics.

Cardiol Res. 2024;15(5):396-403
doi: https://doi.org/10.14740/cr1690