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To the Editor: We read with interest the paper by Simpson and colleagues describing a reduction in left ventricular (LV) mass among predominantly hypertensive subjects with left ventricular hypertrophy (LVH) despite blood pressure being within the normal range on entry.1 Further lowering of systolic blood pressure (SBP) by 9.3 (8.6) mmHg resulted in a reduction of LV mass index by 4.7 (7.3) g. We have recently demonstrated a comparable drop in LV mass in normotensive (<130/80 mmHg) patients with early chronic kidney disease and normal LV mass at baseline following treatment with spironolactone in addition to angiotensin blockade.2 Compared to placebo, treatment with spironolactone for 40 weeks altered LV mass by −14 (13) g versus +3 (11) g (p<0.01) in association with a mean drop in SBP of 11 mmHg. Our data confirm the findings of Simpson and colleagues that in normotensives, LV mass falls in response to further blood pressure lowering but also that this occurs even when baseline LV mass is within normal limits; thus, any reductions in LV mass occur independently of baseline LV mass.
The presence of LVH is consistently associated with increased cardiovascular and total mortality.3 Although LVH has traditionally been considered a dichotomous variable, there is good evidence of a continuous linear relationship between LV mass and risk of cardiovascular disease. This relationship extends to values of LV mass currently considered “within the normal range.”4 Regression of electrocardiographic markers of LVH has been associated with a reduction in events in those with hypertension.5 Although there are preliminary data suggesting that a reduction in LV mass irrespective of the presence of LVH at baseline is associated with fewer non-fatal cardiovascular events,6 large-scale clinical trials are necessary to confirm this and to demonstrate a significant mortality benefit.
Finally, we agree with Simpson and colleagues that it is clear that while blood pressure reduction is an effective method of reducing LV mass, hypertension is not the only cause of LVH. The variations in response to different anti-hypertensive agents suggest that blood pressure-independent mechanisms are involved in the regulation of LV mass.7 In particular, the influence of arterial stiffness and its modulation by the renin–angiotensin–aldosterone system is likely to be of high importance.8 Such a hypothesis was supported by our work, which found that treatment with spironolactone resulted in additional significant reductions in aortic pulse wave velocity, augmentation index and aortic distensibility, suggesting that the fall in LV mass in normotensive subjects was driven by a reduction in aortic stiffness.