Persisting LV hypertrophy despite effective antihypertensive therapy

de Simone G, Devereux RB, Izzo R et al.
J Am Heart Assoc. 2013 Jun 6;2(3):e000144. doi: 10.1161/JAHA.113.000144.

Background

Clinical trials have indicated that reduction of hypertensive left ventricular mass (LVM) can be achieved during antihypertensive management [1-5] and that results in fewer cardiovascular events [6,7]. It is as yet unknown whether similar reductions can be obtained in a free-living population in clinical practice, as were seen in the standardized trial environment. This study was therefore set up to compare changes in LVM over a 4-year follow-up in the unselected cohort of treated hypertensive participants in the longitudinal population-based Strong Heart Study (SHS)[8] and to identify predictors of modifications in LVM. 851 American Indians from 13 communities in the USA were included in this analysis, 488 (57%) of whom were women. The fourth SHS examination was considered the baseline exam [9,10].

Main results

• As compared to the baseline exam, systolic BP decreased in 343 (40%) participants, increased in 270 (32%) and remained unchanged in 238 (28%).
• In comparison to the moment of the baseline exam, only 3% of men and 10% of women had clear LV hypertrophy (LVH) regression (P<0.0001 between genders). 14% of men and 15% of women who did not have LVH at the baseline exam had developed LVH during follow-up.
• On average, the LVM index (LVMi: normalised for height to linearise the curvilinear relation between LVM and height across a wide age range, in g/m^2.7) increased during the follow-up time, from 43.8+9.9 g/m^2.7 at baseline to 44.9+10.5 g/m^2.7, P=0.0001). This change depended most on changes in men. Percent change of LVMi was weakly related to percent change of SBP (r=0.18), and follow-up SBP (r=0.19) and DBP (r=0.14, all P<0.01).
• Lack of decrease in LVMi was not related to use of a certain class of medication used at baseline. In a multivariable, multistep logistic regression analysis, it was however related to initially higher BMI and urinary albumin/creatinine excretion. These effects were independent of other significant effects of older age, male gender and change in BP over time.
  Analysis of a subpopulation with target BP at follow-up, but baseline LVH and no regression of LVH, yielded the same pattern of risk (high baseline BMI: OR: 1.08, 95%CI: 1.04-1.12, P<0.0001) and log10 urinary albumin/creatinine (OR: 1.78, 95%CI: 1.23-2.56, P<0.002).

Conclusion

This analysis of a sample of free-living hypertensive adults with high prevalence of obesity and diabetes, suggests that antihypertensive management may not effectively decrease LVM in daily clinical care programs. Obesity appears to hamper attempts to reduce LVM in real life. Lack of reduction is at least partially independent of BP control and types of antihypertensive treatment. Therefore, results of clinical trials on regression of LVH cannot be automatically extrapolated to unselected free-living populations enrolled in standard care programs of primary cardiovascular prevention.  

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