Differentiation of pathologic forms of cardiac hypertrophy from athlete heart by 2D-strain-Doppler echocardiography

Purpose: Assessment of the underlying etiology of left ventricular hypertrophy (LVH) is a challenging clinical problem. In this study we sought to determine whether tissue Doppler imaging (TDI) and speckle tracking imaging (STI) could distinguish between subjects with pathological LVH, such as occurs in hypertensive heart disease, hypertrophic cardiomyopathy (HCM), or aortic stenosis, and those with athletic LVH. Methods: A total of 113 participants were studied, comprising competitive athletes (25), hypertensive heart disease (25), HCM (12), aortic stenosis (21), and healthy volunteers (30). Left ventricular mass index, ejection fraction, end-diastolic, end-systolic and stroke volume index, diastolic wall thickness, wall thickness ratio and diastolic and systolic wall-to-volume ratios were determined. Peak systolic longitudinal strain (e), peak systolic strain rate (SR-S), peak early diastolic strain rate (SR-E), and peak late diastolic strain rate (SR-A) values were measured by TDI in the basal, mid and apical segments in apical 4-chamber view. Averaged LV rotation and rotational velocities from the base and apex were obtained by STI and used for calculation of LV torsion (LVtor). The analysis of strain Doppler parameters and rotation was performed offline using customized computer software (EchoPac, Version 7.0, General Electric). All of the calculations were averaged for at least 3 consecutive beats. Results: Left ventricular (LV) mass indices were similar for all forms of LVH (p..05), which were higher than those obtained in healthy volunteers (p,.05). Athletes had no significant differences in e and SR-E compared with control subjects (p ¼ .16 and .82, respectively). Patients with pathologic LVH had significantly decreased e and SR-E (average septum: 216.8 + 3.2%, and 1.66 + 0.37 s-1, respectively) comparedwith control subjects (221.9 + 3.5%, and 2.44 + 0.45 s-1, respectively; all p,.0005). LVtor increased significantly in pathologic LVH and in athletes compared to normals (p,.005 and .0001, respectively). In pathologic LVH LVtor increased mainly as a result of reduced basal rotation (23.8+1.3 vs 26.1+1.6 degrees, p¼.04). In athletes the LVtor increase was the result of an increase in both basal and apical rotation (basal rotation, 26.1+1.6 vs 28.9+1.8 degrees, p¼.03; apical rotation, 17.2+3.2 vs 25.9+4.6 degrees, p¼.07). Conclusions: Pathologic LVH has significant longitudinal strain and SR-E reduction versus controls and a different pattern of LV torsion compared to athletes. These findings suggest that TDI and STI may have a clinical impact in the assessment of physiologic LVH state.