Marked regional left ventricular heterogeneity in hypertensive left ventricular hypertrophy patients

Concentric hypertensive left ventricular (LV) hypertrophy is presumed to be a symmetrical process. Using MRI- derived intramyocardial strain, we sought to determine whether segmental deformation was also symmetrical, as suggested by echocardiography. High echocardiographic LV relative wall thickness in hypertensive LV hypertrophy allows preserved endocardial excursion despite depressed LV midwall shortening ( MWS). Depressed MWS is an adverse prognostic indicator, but whether this is related to global or regional myocardial depression is unknown. We prospectively compared MWS derived from linear echocardiographic dimensions with MR strain(is an element of) in septal and posterior locations in 27 subjects with ECG LV hypertrophy in the Losartan Intervention for Endpoint Reduction in Hypertension Study. Although MRI- derived mass was higher in patients than in normal control subjects ( 124.0 +/- 38.6 versus 60.5 +/- 13.2g/ m(2); P < 0.001), fractional shortening ( 30 +/- 5% versus 33 +/- 3%) and end-systolic stress ( 175 +/- 22 versus 146 +/- 28 g/cm(2)) did not differ between groups. However, mean MR( is an element of) was decreased in patients versus normal control subjects ( 13.9 +/- 6.8% versus 22.4 +/- 3.5%), as was echo MWS ( 13.4 +/- 2.8% versus 18.2 +/- 1.4%; both P < 0.001). For patients versus normal control subjects, posterior wall( is an element of) was not different ( 17.8 +/- 7.1% versus 21.6 +/- 4.0%), whereas septal( is an element of) was markedly depressed ( 10.1 +/- 6.6% versus 23.2 +/- 3.4%; P < 0.001). Although global MWS by echocardiography or MRI is depressed in hypertensive LV hypertrophy, MRI tissue tagging demonstrates substantial regional intramyocardial strain( is an element of) heterogeneity, with most severely depressed strain patterns in the septum. Although posterior wall 2D principal strain was inversely related to radius of curvature, septal strain was not, suggesting that factors other than afterload are responsible for pronounced myocardial strain heterogeneity in concentric hypertrophy.