CARDIOVASCULAR JOURNAL OF AFRICA • Vol 21, No 2, March/April 2010
84
AFRICA
is also in keeping with our findings. Major predictors of LVM
in our model included LV wall tension, left atrial size, LV wall
stress, LV end-diastolic diameter, diastolic BP, family history of
hypertension and alcohol consumption.
Parameters that cause the left ventricle to remodel can be
categorised as those that affect the external or internal LV loads.
To date, it is still unclear how many vascular parameters affect
cardiac load. The vascular or haemodynamic parameters may
affect blood pressure, properties of the arterial wall, or size of the
arteries. For example, systolic blood pressure imposes external
load on the left ventricle. It is a reflection of the ejection force of
the heart and is influenced by factors such as arterial wall stiff-
ness and transmission speed.
On the other hand, diastolic blood pressure determines the
LV end-diastolic pressure, which is the pressure required for
the aortic valve to open. It affects the internal load of the left
ventricle. In our model, diastolic blood pressure was found to be
an independent determinant of LV mass. Its role as a predictor of
LVM stems from the fact that stretch on the cardiac myocytes is
a stimulant for cardiac hypertrophy. It causes activation of intra-
cellular messengers, changes in ionic homeostasis, and increased
synthesis of various proteins as well as growth factors.
32
All these
can result in cardiac muscle hypertrophy. The same applies to
the role of LV wall tension and wall stress as a predictor of LV
mass.
The association between alcohol consumption and LV mass
is not well established. A previous report on a Caucasians popu-
lation has shown that heavy drinking has a positive but weak
association with LV mass.
33
On the contrary, Sax
et al
.
34
did not
observe any relationship between alcohol consumption and LVM.
Our finding that a family history of hypertension is a strong
predictor of LV mass corroborates the report of other workers.
It has been demonstrated that LV mass is significantly elevated
in normotensive offspring of hypertensive parents, and siblings
of people with LVH.
35
Moreover, studies on twins have shown
some influence of genetics on LV mass, which was independ-
ent of other factors.
36
This may not be unconnected with higher
ambulatory blood pressure loads.
Negative observations
We did not observe the independent relationship between body
mass index and LVM previously reported by other workers.
37,38
BMI showed a weak correlation with LVM in the univariate
regression analysis. On the other hand, there was a strong asso-
ciation between BSA and LV mass in this study as reported by
some workers, but not an independent determinant.
This study did not find age as an independent determinant of
LVM as previously reported.
24,39
Its correlation with LV mass was
also weak in the univariate analysis (
r
=
0.061).
There was little gender difference in the echocardiographic
parameters. Gender also correlated weakly with LV mass. Two
possible reasons are that (1) the influence of gender on LV mass
could have been accounted for by other factors such as height,
weight and body surface area; (2) the choice of a non-gender-
specific partition value for the definition of LVH in this study
could have obliterated any gender difference. Some workers have
reported gender as a determinant of LV mass.
40,41
Aortic root diameter did not enter our model as a predictor
of LVM. The study by Chan
et al
.
31
has reported aortic root
diameter as one of the five strongest determinants of LV mass in
their subjects, apart from stroke volume, systolic BP, BMI and
end-systolic meridional stress-to-volume ratio.
Although total peripheral resistance showed a strong relation-
ship with LVM in the univariate analysis, it was not an inde-
pendent predictor of LVM. This corroborates some studies that
showed that vascular resistance is not a good index of haemody-
namic loading.
42
We also confirmed the rather surprising, inap-
propriate and negative relationship between LV mass and indexes
of arterial stiffness noted earlier by Chan
et al
.
31
Limitations of the study
The first limitation of the study was the fact that it was retrospec-
tive and cross-sectional. It can only claim association but not
causality. Secondly, clinic or casual blood pressure was measured
in the subjects. Many studies have shown that ambulatory blood
pressure is more closely associated with LV mass than clinic
blood pressure.
Thirdly, other variables such as insulin resistance, blood
viscosity, and carotid intima–media thickness that have been
documented as determinants of LV mass were not assessed in this
study. Fourthly, this study did not correlate ECG findings with
ECHO findings. The authors will explore this in future research.
Lastly, there may be concern about the independence of the
haemodynamic parameters, which were derived from some
M-mode measurements also used in the calculation of LV mass.
This concern has been addressed in the recent report by Chan
et
al
.
31
They tested the reliability of M-mode parameters by compar-
ing them with those obtained with the two-dimensional echocar-
diographic truncated ellipsoid formula, which were devoid of
M-mode-derived parameters in 1 238 subjects. They noted a
lower overall model variance (0.59 vs 0.74) but with the same top
predictors of LV mass contributing to 98% of the total variance.
Conclusion
This study found that the most important determinants of LV
mass were LV wall tension, left atrial size, LV wall stress, diasto-
lic BP, a family history of hypertension, and alcohol consump-
tion. These factors appeared to explain about 95% of the variabil-
ity in LV mass in hypertensive Nigerians seen at the University
College Hospital, Ibadan. Mechanical or haemodynamic factors,
possibly interacting with genetic and social factors are the likely
determinants of LV mass in Nigerian hypertensive men and
women. Therefore modulation of these factors pharmacologi-
cally or non-pharmacologically will be of benefit in the manage-
ment and control of hypertension in this population.
The implications of this study are that measures that effec-
tively modulate wall stress and wall tension as well as blood
pressure control, for example antihypertensive therapy, can cause
early regression of LVH. Early screening of relatives of hyper-
tensive subjects may provide an effective blood pressure-control
programme. Non-pharmacological treatment such as avoidance
of excessive alcohol consumption may be an effective tool in a
blood pressure-control programme.
However, based on the recent findings by the LIFE study,
10-12
which showed a correlation between ECG and ECHO findings,
as well as the recommendation of the World Heart Organisation,
‘echocardiography in hypertensive patients in sub-SaharanAfrica
should be used only for research purposes and is not cost effec-
tive in resource-poor countries’.
