Abstract
Although in cross-sectional studies left ventricular mass (LVM), which exceeds that predicted by workload (inappropriate LVM [LVM(inappr)]) but not absolute LVM or LVM index (LVMI), is inversely related to LV ejection fraction (EF), whether on-treatment decreases in LVM(inappr) (%observed/predicted LVM) account for increases in EF beyond LVM or LVMI is unclear. Echocardiography was performed in 168 mild-to-moderate hypertensives treated for 4 months. Although in patients with an LVMI >51 g/m(2.7) (n=112; change in LVMI, -13.7±14.0 g/m(2.7); P<0.0001) but not in patients with an LVMI ≤51 g/m(2.7) (n=56; change in LVMI, 1.3±9.3 g/m(2.7)) LVMI decreased with treatment, treatment failed to increase EF in either group (1.2±10.8% and 2.7±10.7%, respectively). In contrast, in patients with inappropriate LV hypertrophy (LVM(inappr) >150%; n=33) LVM(inappr) decreased (-32±27%; P<0.0001) and EF increased (5.0±10.3%; P<0.05) after treatment, whereas in patients with an LVM(inappr) ≤150% (n=135), neither LVM(inappr) (-0.5±23%) nor EF (0.9±10.3%) changed with therapy. With adjustments for circumferential LV wall stress and other confounders, whereas on-treatment decreases in LVM or LVMI were weakly related to an attenuated EF (partial r=0.17; P<0.05), on-treatment decreases in LVM(inappr) were strongly related to increases in EF even after further adjustments for LVM or LVMI (partial r=-0.63 [CI, -0.71 to -0.52]; P<0.0001). In conclusion, decreases in LVM(inappr) are strongly related to on-treatment increases in EF beyond changes in LVM and LVMI. LV hypertrophy can, therefore, be viewed as a compensatory change that preserves EF, but when in excess of that predicted by stroke work, it can be viewed as a pathophysiological process accounting for a reduced EF.
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