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228 VAZQUEZ BLANCO ET AL
AJH–MARCH 2000–VOL. 13, NO. 3, PART 1
ence that was statistically significant (P Ͻ .05) (Table history of hypertension or any other condition that
could increase it. Recently, Degli Esposti et al16 pub-
1).
lished data about preeclamptic patients who had in-
Ventricular Geometric Patterns If we consider the
mean Ϯ 1 SD as the upper normal limit of LVMI and
RWT of NPW (110.4 g/m2 and 0.43, respectively), we
obtained normal geometric values in 26 patients with
PIH (47%), eccentric hypertrophy in 14 (25%), concen-
tric remodeling in 11 (20%), and concentric hypertro-
phy in four (7%), versus 39 (68.4%), eight (14%), eight
(14%), and two (3.5%), respectively, in NPW. However
if we consider the mean Ϯ 2 SD of the LVMI and RWT
as the upper normal limit (130.2 g/m2 and 0.48, re-
spectively), we found a normal geometric pattern in 46
patients (84%), eccentric hypertrophy in four (7%),
concentric remodeling in three (5%), and concentric
hypertrophy in two (4%), versus normal geometric
values in 53 (93%), concentric remodeling in three
(5%), and eccentric hypertrophy in one (2%) in NPW
(Fig. 1). The data for PIH patients compared to data for
NPW were significantly different (P Ͻ .02), and the
risk of having an abnormal geometric pattern was
more than twice as high in PIH patients compared as
in NPW (odds ratio 2.62, CI 1.13–6.16).
creased left ventricular mass, together with systolic
and diastolic dysfunction, in comparison with normal
pregnant women.
Ventricular Geometry In our study, normal preg-
nant women had an average left ventricular mass
index of 90.6 Ϯ 19.8 g/m2 together with a relative wall
thickness of 0.38 Ϯ 0.05. These results differ from
those reported by Ganau et al,9 who consider 106
g/m2 as the normal upper limit for left ventricular
mass. This figure corresponds to the mean value plus
two standard deviations of normal women. Likewise,
for these authors, the normal upper value of relative
wall thickness was 0.44, which corresponds to the 95th
percentile.
These different results may be due to differences in
the population, because the pregnant patients studied
by us had other hemodynamic modifications that can
produce different changes in the structure and func-
tion of the left ventricle.
Having these limitations in mind, we found that if
the mean value plus one standard deviation of normal
pregnant women is considered as a normal limit, we
obtained normal geometric values in 26 of our patients
(47.3%), and abnormal in 29 (52.7%). In 14 hyperten-
sive women (25.4%) eccentric hypertrophy developed,
in 11 (20%) concentric remodeling developed, and in
the last four (7.3%) concentric hypertrophy was ob-
served. But when we considered the mean value plus
two standard deviations as the normal upper limit in
normal pregnant women, we obtained normal geo-
metric values in 46 patients (83.6%), eccentric hyper-
trophy in four (7.3%), concentric remodeling in three
(5.5%), and concentric hypertrophy in two (3.6%). The
data found in our group of patients with pregnancy-
induced hypertension, compared to those in normal
pregnant women, were significantly different.
Ganau et al reported normal geometric values in
52% of patients when considering 106 g/m2 as the
normal upper limit for left ventricular mass and 0.44
as the normal upper limit for relative wall thickness.
These authors found eccentric hypertrophy in 27%,
concentric remodeling in 20%, and concentric hyper-
trophy in 8%.9 These results are similar to ours; how-
ever, despite this, the cause of structural abnormalities
of the left ventricle is different in both situations.
Pregnancy-induced hypertension appears within a
short time, is short lasting, and affects a healthy car-
diovascular system free of previous pathological in-
fluences. Consequently the organism has not enough
time to adapt itself to this pressure overload. On the
other hand, in essential hypertension, the process de-
DISCUSSION
During normal pregnancy a number of hemodynamic
changes take place, such as an increase in blood and
stroke volumes together with heart rate, and a decrease
in peripheral resistance and mean blood pressure.6,7
These changes may be responsible for structural remod-
eling of the left ventricle by themselves13,14
Pregnancy-induced hypertension represents an ad-
equate model to evaluate the consequences of acute
pressure overload on the myocardium during a short
period of time. These patients differ from normal
pregnant women in the fact that peripheral resistance
is increased, and plasma volume may be normal or
decreased.8 The heart must adapt its wall thickness to
this increase in pressure load, to decrease parietal
stress despite the short lasting overload.
In a previous study, Thomson et al15 did not find
significant changes in mass index between normal
pregnant control subjects and pregnancy-induced hy-
pertensive women. The absence of significant differ-
ences between both groups could be explained by the
low number of patients in this study.
On the contrary, in our study, patients with preg-
nancy-induced hypertension had a significant increase
in left ventricular mass, a situation that especially
reflects an increase in septal and posterior wall thick-
ness without changes in left ventricular diastolic di-
ameter. We did not know the left ventricular mass
before the pregnancy; however, it can be assumed that
it was previously normal, because the patients had no velops progressively and the myocardium adapts it-