CARDIOVASCULAR JOURNAL OF AFRICA • Vol 23, No 3, April 2012
AFRICA
151
the proportion of patients with a normal LV mass or geometry
did not significantly increase (17.5 to 26%), while 25% remained
with concentric LVH and 25%with eccentric LVH. Moreover, the
proportion of patients with concentric LV remodelling increased
from 12 to 23% (
p
<
0.05). These residual abnormalities in LV
structure were noted even though therapy resulted in a decrease
in LVM and relative wall thickness.
Although a number of studies have demonstrated that
antihypertensive therapy can regress LVH as well as reduce LV
relative wall thickness, few studies have reported on the ability
of therapy to normalise LV structure. In this regard, in contrast
to the outcome of the present study where 25% of patients
remained with concentric LVH and only 26% had a normal LV
structure after one year of therapy, in the LIFE study after one
year of therapy in 853 patients with electrocardiographic LVH
at baseline, the prevalence of residual concentric LVH was 6%
and the proportion of patients with a normal LV structure was
51%.
13
In another study conducted in 182 patients, 30% of whom
had concentric LVH at baseline, only 14% of 182 patients had
concentric LVH after one year of therapy.
14
An explanation for the markedly higher prevalence of residual
concentric LVH and lower prevalence of a normal LV structure
after one year of antihypertensive therapy in our study compared
to previous studies
13,14
is most likely the higher proportion of
patients with an increased baseline concentric LVH. Indeed, in
previous studies,
13,14
the prevalence of concentric LVH at baseline
was approximately 10 to 30%, compared to the approximately
51% of patients with concentric LVH in our study. Moreover,
in previous studies
13,14
mean baseline LV relative wall thickness
ranged from 0.41 to 0.45, while in the present study, mean
baseline LV relative wall thickness was 0.50.
The markedly higher prevalence of concentric LVH (
>
50%)
and mean relative wall thickness values noted in our study,
which was conducted in a group of patients of African descent,
compared to previous studies conducted in patients of European
descent,
13,14
is consistent with ethnic disparities in the extent of
concentric LV remodelling previously reported to exist between
groups of African and European descent.
21
Furthermore, the
markedly higher prevalence of concentric LVH and mean relative
wall thickness values noted in the present compared to previous
studies
13,14
is consistent with the high prevalence of obesity in our
sample. In this regard, we have recently demonstrated a strong
relationship between central obesity and concentric LVH and
remodelling in patients of African descent.
26
The high prevalence of a residual abnormality in LV structure
even after a year of antihypertensive therapy in the present
study is not explained by poor systolic and diastolic BP control.
Neither clinic nor 24 hour systolic/diastolic BP and clinic BP
control was independently associated with residual LV structural
abnormalities. Indeed, in the present study the clinic BP control
rates were 64% compared to 60% in previous studies reporting
on a low prevalence of residual LV structural abnormalities after
one year of therapy.
14
Moreover, unlike in other studies,
13,14
we used ambulatory BP
monitoring to further evaluate the effect of therapy on 24-hour
BP profiles. In this regard, 47% of patients achieved 24-hour BP
values below 130/80 mmHg. Importantly however, in a separate
model, 24-hour PP was independently related to an abnormal
LV structure. In contrast, office PP could not account for the
variability in left ventricular mass or relative wall thickness in
the LIFE study after one year of antihypertensive treatment.
13
Similarly, we were unable to show a relationship between clinic
PP and residual LV structural changes.
The high prevalence of a residual abnormality in LV structure
even after a year of antihypertensive therapy in the present
study is not explained by a poor response of the left ventricle
to therapy. Indeed, in the present study, the mean decrease in
LV relative wall thickness produced by antihypertensive therapy
was similar to that noted in other studies reporting on a low
prevalence of residual LV structural abnormalities after a year
of therapy.
13,14
Although the present study was not designed to
assess the effects of specific drug classes, we were also unable
to identify a relationship between drug class and the LV response
to therapy.
Importantly, of the 51.5% of patients with concentric LVH at
baseline, 28% changed their LV geometric pattern to eccentric
LVH, and 24.5% normalised their LVMI but maintained a
concentric LV geometry, while 34% remained in the concentric
LVH category after 13 months of treatment. Therefore, although
approximately half of these patients no longer remained in the
concentric LVH category, only 13% normalised their geometry
after a year of therapy. These data suggest that, at least in our
population sample, concentric LVH is difficult to normalise. In
this regard, one previous study conducted in patients of European
descent has demonstrated similar outcomes where only 27% of
those with concentric LVH at baseline normalised LV structure.
14
In contrast however, in the LIFE study, 75% of patients with
concentric LVH at baseline normalised LV structure after one
year of therapy.
13
A reason for these discrepancies is not apparent
and further studies are required to address this issue.
The limitations of the present study include the following.
A large proportion of the study group consisted of females
and hence the outcomes may be specific to females. Second,
the patients participating in the trial were recruited from an
urban African community with a high unemployment rate, and
a number of participants relocated to alternate areas where
employment was available. Therefore retention rates at 13
months were low.
23
Third, antihypertensive treatment was based
on drug combinations from a variety of classes to achieve BP
control and therefore we cannot draw conclusions as to whether
the effect noted in our study applies to all antihypertensive
agents. However, the present approach is in line with what is
likely to occur in clinical practice where combination therapy
with different classes of agents is the most likely method of
achieving BP control. Lastly, we did not assess the effect of
treatment beyond 13 months and hence we do not know what
antihypertensive therapy for two to three years may have
achieved. However, we do not believe that further significant
changes in LV structure would have occurred, as maximal
changes were already present at four months of therapy and no
further changes were noted from four to 13 months of therapy.
Conclusion
In this study we show that after more than a year of
antihypertensive therapy in hypertensives of African ancestry,
including combination therapy where required, no significant
change in the proportion of patients with a normal left ventricle
occurred. Twenty-five per cent still had residual concentric LVH,
and a further 25% eccentric LVH, while the proportion with
