S. Perlini et al., Midwall mechanics are improved after regression of hypertensive left ventricular hypertrophy and normalization of chamber geometry, CIRCULATION, 103(5), 2001, pp. 678-683
Citations number
45
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Background-It is still unclear whether substantial regression of hypertensi
ve left ventricular hypertrophy (LVH) and normalization of chamber geometry
are associated with improved left ventricular (LV) myocardial function.
Methods and Results-Midwall mechanics were evaluated in 152 patients underg
oing 1 year of effective antihypertensive treatment. Two-dimensionally dire
cted M-mode echocardiography was performed as follows: (1) after a 4-week p
lacebo "run-in" period, (2) after 1 year of treatment with 20 mg/d lisinopr
il (alone or associated with 12.5 to 25 mg/d hydrochlorothiazide), and (3)
after a final 1-month placebo period to allow blood pressure (24-hour avera
ge ambulatory monitoring) to return to pretreatment levels. Treatment-induc
ed reductions in blood pressure (from 149+/-16/95+/-11 to 31+/-12/83+/-10 m
m Hg, P<0.05) and circumferential end-systolic wall stress (from 84+/-22 to
72+/-19 g/cm(2), P<0.05) were associated with a marked reduction in LV mas
s index (from 159+/-30 to 133+/-26 g/m(2), P<0.05). LVH regression was acco
mpanied by an increase in midwall fractional shortening (from 19.7+/-2.7% t
o 20.9+/-2.7%, P<0.05) and by a decrease in relative wall thickness (from 4
8.2+/-7.7% to 44.1+/-6.7%, P<0.05). The improvement in midwall function ass
ociated with afterload reduction and substantial LVH regression persisted a
fter antihypertensive therapy withdrawal and restoration of the hypertensiv
e state. Despite a significant increase in end-systolic wall stress, furthe
r LV chamber remodeling did not occur. The preservation of relative wall th
ickness was associated with a persistent improvement in midwall systolic fu
nction.
Conclusions-Regression of concentric LVH is associated with an improvement
of midwall systolic function, which is more dependent on the normalization
of LV geometry than on the reduction in LV systolic stress.