Relationship between inappropriate left ventricular hypertrophy and ejection fraction independent of absolute or indexed mass in a community sample of black African ancestry.

AIM

We determined whether left ventricular hypertrophy (LVH) which exceeds that predicted from workload [inappropriate LV mass (LVM(inappr))] is associated with reduced left ventricle (LV) systolic chamber function independent of and more closely than absolute or indexed left ventricular mass (LVM).

METHODS

In 626 randomly selected adult participants from a community sample of black Africans, using echocardiography we assessed absolute LVM, LVM indexed to height(2.7) (LVMI), LVM(inappr), LV wall stress, ejection fraction, and midwall fractional shortening (FSmid). LVM(inappr) was determined as percentage of observed/predicted LVM. Predicted LVM was calculated from a previously validated formula that incorporates stroke work. LVMI(inappr) more than 150% was considered to be inappropriate LVH. This threshold was identified from the upper 95% confidence interval for LVMI(inappr) determined in 140 healthy participants.

RESULTS

A total of 21.7% of participants had LVH (LVMI > 51 g/m(2.7)) and 18.5% had inappropriate LVH. With adjustments for LV stress and other confounders there was a strong inverse relationship between LVM(inappr) and ejection fraction (partial r = -0.41, P < 0.0001), whereas only modest inverse relations between LVM or LVMI and ejection fraction were noted (partial r = -0.07 to -0.09, P < 0.05-0.09) (P < 0.0001, comparison of partial r values). The independent relationship between LVM(inappr) and ejection fraction persisted with further adjustments for LVM or LVMI (partial r = -0.52, P < 0.0001). LVM(inappr) and FSmid were similarly inversely related (P < 0.0001) and these relations were also stronger and independent of LVM or LVMI.

CONCLUSION

Inappropriate LVH is strongly and inversely related to variations in ejection fraction independent of and more closely than LVM or LVMI in a community sample of black African ancestry. These data suggest that LVH is a compensatory response to workload, but when exceeding that predicted by workload, is associated with LV systolic chamber decompensation.