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Left ventricular rotation is physiologically affected by acute changes in preload. We investigated the acute effect of preload changes in chronically underloaded and overloaded left ventricles in children with shunt lesions.
A total of 15 patients with atrial septal defects (Group A: 7.4 ± 4.7 years, 11 females) and 14 patients with patent arterial ducts (Group B: 2.7 ± 3.1 years, 10 females) were investigated using 2D speckle-tracking echocardiography before and after interventional catheterisation. The rotational parameters of the patient group were compared with those of 29 matched healthy children (Group C).
Maximal torsion (A: 2.45 ± 0.9°/cm versus C: 1.8 ± 0.8°/cm, p < 0.05), apical peak systolic rotation (A: 12.6 ± 5.7° versus C: 8.7 ± 3.5°, p < 0.05), and the peak diastolic torsion rate (A: −147 ± 48°/second versus C: −110 ± 31°/second, p < 0.05) were elevated in Group A and dropped immediately to normal values after intervention (maximal torsion 1.5 ± 1.1°/cm, p < 0.05, apical peak systolic rotation 7.2 ± 4.1°, p < 0.05, and peak diastolic torsion rate −106 ± 35°/second, p < 0.05). Patients in Group B had decreased maximal torsion (B: 1.8 ± 1.1°/cm versus C: 3.8 ± 1.4°/cm, p < 0.05) and apical peak systolic rotation (B: 8.3 ± 6.1° versus C: 13.9 ± 4.3°, p < 0.05). Defect closure was followed by an increase in maximal torsion (B: 2.7 ± 1.4°/cm, p < 0.05) and the peak diastolic torsion rate (B: −133 ± 66°/second versus −176 ± 84°/second, p < 0.05).
Patients with chronically underloaded left ventricles compensate with an enhanced apical peak systolic rotation, maximal torsion, and quicker diastolic untwisting to facilitate diastolic filling. In patients with left ventricular dilatation by volume overload, the peak systolic apical rotation and the maximal torsion are decreased. After normalisation of the preload, they immediately return to normal and diastolic untwisting rebounds. These mechanisms are important for understanding the remodelling processes.
To evaluate the role of torsion in hypertrophic cardiomyopathy in children.
A total of 88 children with idiopathic hypertrophic cardiomyopathy (n = 24) and concentric hypertrophy (n = 20) were investigated with speckle-tracking echocardiography and compared with age- and gender-matched healthy controls (n = 44).
In hypertrophic cardiomyopathy, we found increased torsion (2.8 ± 1.6 versus 1.9 ± 1.0°/cm [controls], p < 0.05) because of an increase in clockwise basal rotation (−8.7 ± 4.3° versus −4.9 ± 2.5° [controls], p < 0.001) and prolonged time to peak diastolic untwisting (3.7 ± 2.4% versus 1.7 ± 0.6% [controls] of cardiac cycle, p < 0.01), but no differences in peak untwisting velocities. Hypertrophic cardiomyopathy patients demonstrated a negative correlation between left ventricular muscle mass and torsion (r = −0.7, p < 0.001). In concentric hypertrophy, torsion was elevated because of increased apical rotation (15.1 ± 6.4° versus 10.5 ± 5.5° [controls], p < 0.05) without correlation with muscle mass. Peak untwisting velocities (− 202 ± 88 versus −145 ± 67°/s [controls], p < 0.05) were higher in concentric hypertrophy and time to peak diastolic untwisting was delayed (1.8 ± 0.8% versus 1.2 ± 0.6% [controls], p < 0.05).
In contrast to an increased counterclockwise apical rotation in concentric hypertrophy, hypertrophic cardiomyopathy is characterised by predominantly enhanced systolic basal clockwise rotation. Diastolic untwisting is delayed in both groups. Torsion may be an interesting marker to guide patients with hypertrophic cardiomyopathy.
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