Adaptative or maladaptative hypertrophy, different spatial distribution of myocardial contraction

Left ventricular hypertrophy (LVH) may be an adaptative remodelling process induced by physical training, or result from pathological stimuli. We hypothesized that different LVH aetiology could lead to dissimilar spatial distribution left ventricular (LV) contraction, and compared different components of LV contraction using 2-dimensional (2-D) speckle tracking derived strain in subjects with adaptative hypertrophy (endurance athletes), maladaptative hypertrophy (hypertensive patients) and healthy controls.

We enrolled 22 patients with essential hypertension, 50 endurance athletes and 24 healthy controls. All subjects underwent traditional echocardiography and 2-D strain evaluation of LV longitudinal, circumferential and radial function. LV basal and apical rotation and their net difference, defined as LV torsion, were evaluated.

LV wall thicknesses, LV mass and left atrium diameter were comparable between hypertensive group and athletes. LV longitudinal strain was reduced only in hypertensive patients (P < 0.05). LV apex circumferential strain was higher in hypertensive patients than in other groups (P < 0.001), LV basal circumferential strain, although slightly increased, did not reach significant difference. Hypertensive patients showed significantly increased rotation and torsion (P < 0.001), while no differences were observed between athletes and control.

In patients with pathological LVH, LV longitudinal strain was reduced, while circumferential deformation and torsion were increased. No differences were observed in LV contractile function between subjects with adaptative LVH and controls. In pathological LVH, increasing torsion could be considered a compensatory mechanism to counterbalance contraction and relaxation abnormalities to maintain a normal LV output.