Introduction 1 2 3 4 5 6 7 8 9 10 Patients and methods 11 2DE was undertaken for HCM patients and control subjects with lying in the left lateral decubitus using both apical and parasternal views. 2DE studies were performed using a 3.5 MHz transducer and a commercially available ultrasound system (Philips Sonos 7500, Best, The Netherlands). The following measures were obtained. Left ventricular (LV) function LV fractional shortening and ejection fraction were selected as a marker for systolic function. LV end-diastolic (LV-EDD) and end-systolic (LV-ESD) dimensions were measured using M-mode from parasternal long axis view and thus LV fractional shortening were calculated by the traditional formula: Fractional shortening (%) = [LV-EDD − LV-ESD]/LV-EDD%. LV end-diastolic (LV-EDV) and end-systolic (LV-ESV) volumes were measured by 2D biplane modified Simpson’s method and then ejection fraction was calculated by the formula: Ejection fraction = [LV-EDV−LV-ESV]/LV-EDV. Transmitral E/A ratio was defined by pulsed wave Doppler and used as a marker of LV diastolic function. Mitral regurgitation 2 2 2 12 LA diameter (LAD) 1 Fig. 1 A B c  LA mass 13 3 3 2 Fig. 2 A B  LA volume (LAV) 6 × 1  × 2  1 2 3 V max V min V Pre-A 14 15 Fig. 3 1 2 1  2  V max V min max × V Pre A V min V Pre A × V min × V max V Pre A V max V Pre A V max × LA kinetic energy (LA-KE) 16 × × P × 2 P −3 To characterize the three phases of LA activity, PA-SV and PA-EF were defined as indices for LA conduit function, AA-SV, AA-EF, and LA-KE for LA pump function, and AEI for LA reservoir function. Statistical analysis t t P Results 1 17 P P P Table 1 Baseline clinical and echocardiographic data of HCM patients and controls  N n P Age (yr) 38 ± 15  35 ± 15   Male gender (%) 24 (80%) 18 (60%)  Left ventricular FS (%) 38.4 ± 9.6 30.3 ± 5.4 0.03 Left ventricular EF (%) 71.1 ± 17.7 57.4 ± 1.0 0.001 Peak A velocity (cm/s) 61.5 ± 20.3 39.7 ± 9.9 0.01 Mitral regurgitation     No 5 (20%) 24 (80 %) 0.0001     Mild 15 (60%) 6 (20%)     Moderate-severe 5 (20%) 0 (0%) Antero-posterior LAD (mm) 42.8 ± 5.8 34.1 ± 4.2 0.0001 Medial-lateral LAD (mm) 45.6 ± 9.9  36.2 ± 3.8 0.001 Superior-inferior LAD (mm) 60.8 ± 9.0 44.8 ± 6.7 0.0001 Mean LAD (mm) 49.7 ± 7.2 38.4 ± 4.0 0.0001 Anterior left atrial wall (mm) 3.6 ± 1.0 3.5 ± 1.0 NS Posterior left atrial wall (mm) 3.5 ± 1.2 3.1 ± 1.1 NS Left atrial mass (g) 89.8 ± 37.2 47.8 ± 18.1 0.0001 Abbreviations: FS fractional shortening, EF ejection fraction, and LAD left atrial diameter 1 P P 2 V max V min V Pre-A V max r P Table 2 Left atrial mass and function in non-obstructive HCM and obstructive HCM patients  n n n P     * ** Mean LAD (mm) 38.4 ± 4.0 49.6 ± 7.6 49.9 ± 7.0 0.0001 0.0001 LA mass (g) 47.8 ± 18.1 86.8 ± 41.1 93.9 ± 32.5 0.002 0.001 V max (ml) 38.2 ± 10.7 64.7 ± 26.7 65.9 ± 28.1 0.002 0.009 V min (ml) 17.4 ± 7.6 32.7 ± 22.1 37.1 ± 19.7 0.02 0.008 V pre A (ml) 24.9 ± 7.7 44.7 ± 24.7 48.5 ± 21.5 0.008 0.005 TA-SV (ml) 20.5 ± 6.9 32.0 ± 8.9 28.8 ± 13.1 NS NS TA-EF (%) 54.7 ± 14.2 53.6 ± 13.8 45.4 ± 12.8 NS NS AA-SV (ml) 7.3 ± 4.0 12.0 ± 6.2 11.4 ± 6.5 0.001 0.001 AA-EF (%) 31.4 ± 17.8 29.7 ± 13.5 25.4 ± 12.8 NS NS LA-KE (kdynes.cm) 11.9 ± 7.4 18.3 ± 12.5 a 0.03 0.001 PA-SV (ml) 13.4 ± 5.7 20.0 ± 8.8 17.5 ± 9.8 0.02 NS PA-EF (%) 33.9 ± 10.1 34.0 ± 14.8 27.1 ± 7.0 NS 0.03 AEI (%) 141.7 ± 74.0 134.8 ± 74.4 91.1 ± 39.7 NS 0.02 Abbreviations: see text * P ** P a P LA pump function P P P LA conduit function P P P LA reservoir function P Discussion 18 20 21 22 23 24 10 25 26 27 28 29 In HCM patients, the rate of left ventricular relaxation deteriorates due to markedly thickened and non-compliant left ventricle, which led to deterioration of LA conduit function. This was expressed by reduction in PA-EF in our HCM patients compared to controls. 30 8 Study limitation 18 19 Conclusion Hypertrophic cardiomyopathy is associated with dilated LA and increased LAV that reflects the severity of LA overload. Higher AA-SV and LA-KE in HCM patients especially obstructive type indicates augmented LA pump function to overcome the high left ventricular filling pressure caused by severe left ventricular hypertrophy. Lower PA-EF and AEI in obstructive HCM patients indicate impaired LA reservoir and conduit functions. These findings may have clinical implication for the follow up of HCM patients