Regional Heterogeneity in 3D Myocardial Shortening in Hypertensive Left Ventricular Hypertrophy: A Cardiovascular CMR Tagging Substudy to the Life Study

BACKGROUND Increased relative wall thickness in hypertensive left ventricular hypertrophy (LVH) has been shown by echocardiography to allow preserved shortening at the endocardium despite depressed LV midwall circumferential shortening (MWCS). Depressed MWCS is an adverse prognostic indicator, but whether this finding reflects reduced global or regional LV myocardial function, as assessed by three-dimensional (3D) myocardial strain, is unknown. METHODS AND RESULTS Cardiac Magnetic Resonance (CMR) tissue tagging permits direct evaluation of regional 3D intramyocardial strain, independent of LV geometry. We evaluated 21 hypertensive patients with electrocardiographic LVH in the LIFE study and 8 normal controls using 3D MR tagging and echocardiography. Patients had higher MR LV mass than normals (116 ± 40 versus 63 ± 6 g/m2, P = 0.002). Neither echocardiographic fractional shortening (32 ± 6 versus 33% ± 3%), LVEF (63% versus 64%) or mean end-systolic stress (175 ± 27 versus 146 ± 28 g/cm2) were significantly different, yet global MWCS was decreased by both echocardiography (13.4 ± 2.8 versus 18.2% ± 1.5%, P < 0.001) and MR (16.8 ± 3.6 versus 21.6% ± 3.0%, P < 0.005). 3D MR MWCS was lower at the base versus apex (P = 0.002) in LVH and greater in lateral and anterior regions versus septal and posterior regions (P < 0.001), contributing to the higher mean global MWCS by MR than echo. MR longitudinal strain was severely depressed in LVH patients (11.0 ± 3.3 versus 16.5% ± 2.5%, P < 0.001) and apical twist was increased (17.5 ± 4.3 versus 13.7 ± 3.7, P < 0.05). Importantly, both circumferential and longitudinal shortening correlated with LV relative wall thickness (R > 0.60, P = 0.001 for both). CONCLUSIONS In patients with hypertensive LVH, despite normal LV function via echocardiography or CMR, CMR intramyocardial tagging show depressed global MWCS while 3D MR strain revealed marked underlying regional heterogeneity of LV dysfunction.