Background Left ventricular (LV) torsion resulting from apical and basal rotation in opposite direction is an important contributor to LV function. Apical hypertrophic cardiomyopathy (aHCM) is a benign, primary myocardial disorder. We hypothesized that end-systolic luminal obliteration in aHCM might affect the LV torsion given the higher contribution of apex on LV torsion. We also evaluated the relation between apical myocardial function and torsion.
Methods Twenty patients with apical HCM and normal control (n=20) were consecutively enrolled. None of aHCM patients showed basal segmental hypertrophy. All were in sinus rhythm with neither significant valvular disease nor LV systolic dysfunction. LV torsion was calculated by deducting basal rotation value from that of apex with 2D speckle tracking echocardiography.
Results Torsion was significantly decreased in aHCM patients compared to the control group (17.5짹5.7 vs. 24.0짹8.4 degree, p=0.008). Apical rotation was significantly decreased in aHCM patients (11.5짹5.8 vs. 19.5짹4.5 degree, p<0.001), but basal rotation value was comparable between the 2 groups. LV torsion was mainly determined by apical rotation (r=0.78, p<0.001) than basal rotation. Early diastolic torsional rate was decreased in aHCM patients with borderline significance (p=0.049). Time from QRS onset to peak systolic and early diastolic torsion rate was significantly shortened in aHCM (p<0.001). Radial and circumferential peak strains of apical segments were not correlated with apical rotation or torsion; however time to peak strain was significantly correlated with torsion or torsional rate (r=0.63, p=0.007) and was related to apical cavitary obstruction, which possibly limits the rotation of apical myocardium in aHCM patients.
Conclusions Patients with aHCM showed a reduction in LV torsion, which was related to shortened time to peak torsion. Apical cavitary obliteration in aHCM is a plausible mechanism explaining a reduction in LV torsion