CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 1, January/February 2020
AFRICA
45
of hypertension. Results from the study by Dewland
et al.
suggest that LA diameter is significantly greater in whites than
blacks.
19
Severe hypertension in hospitalised patients recruited by
Sun
et al.
would have had a greater effect on LA size compared
to patients with mild hypertension in this study.
It should be noted that the LA is not shaped symmetrically
and LA enlargement does not occur uniformly. Expansion of
the LA is constrained by the thoracic cavity, aortic root, right
ventricular outflow tract and the rigid trachea bifurcation. With
the above in mind, changes in LA size therefore preferentially
occur in the superior–inferior axis (longitudinal diameter).
20
Consequently, all the morphological changes in LA size
only become prominent with age and duration of hypertension.
Therefore, the aforementioned anatomical factors, coupled with
severity of hypertension accounted for the differences observed
between our findings and those of Sun
et al
.
12
Our analysis
supports the fact that estimation of LA changes by surface and
volume will be more relevant and accurate in the clinical setting
than anterior–posterior and transverse dimensions.
Up to a quarter of the hypertensive patients in our study had
LA enlargement. This is considerable and is a call for concern,
given the fact that LA enlargement increases the risk of stroke
and is associated with poor cardiovascular outcomes. Our
findings are in agreement with of those of Cuspidi
et al.
in Italy.
21
However, we had a lower proportion of participants with LA
enlargement relative to those found by Chen
et al.
22
in Japan and
Milan
et al.
in Italy.
23
Possible explanations for the variations lie in differences in
study designs, presence of concomitant pathologies in their
subjects, and different diagnostic cut-off values used to define
LA enlargement. In these studies, co-morbidities included atrial
fibrillation, diabetes mellitus and obesity, among others. In the
study by Chen
et al.,
mean age was 69
±
10 years and diagnostic
cut-off for LA enlargement was LAVI
>
32 ml/m
2
. In the study by
Milan
et al.,
23
the mean age was 50.7
±
12.2 years with duration
of hypertension ranging from 11–120 months and diagnostic
cut-off for LA enlargement was LAVI
>
22 ml/m
2
. Finally, in the
study by Cuspidi
et al.
,
21
mean age was 58.3
±
16 years, with the
elderly patients above 65 years making up 41% of patients.
The observation that a large proportion of hypertensive
patients had LA changes in the early phase of high blood
pressure has important prognostic and diagnostic implications.
This highlights the fact that structural changes may occur early
in these patients therefore early screening for diagnosis may
prevent future cardiovascular events.
Factors that correlated with LA volume were BMI, DBP and
diastolic dysfunction. An association between increasing body
mass and LA volume has been shown in previous studies by
Adebayo
et al
.
18
Although the mechanism is not well understood,
obesity is linked with increased stoke volume, which causes
cardiac alterations.
Contrary to previous studies, ours did not show any
relationship between LAR and LVM and age. Our patients
were mostly newly diagnosed and relatively young hypertensive
patients, which could explain the differences. In our final analysis,
LV diastolic dysfunction was the only predictor of LA size. A
clear relationship has been reported by Matsuda
et al.
24
This
strengthens the fact that, in the absence of other pathological
disease, hypertension leads to impaired LV relaxation and
reduced expandability of the left ventricle. The end result is
increased atrial filling pressures and subsequent LA enlargement.
Our study was limited in that we had a small sample size and
therefore the resultant loss of power could lead to decreased
chances of finding associations (type II error). Second, we
worked on both treated and untreated hypertensive patients,
which could have modulated changes in LA size. However,
there was a significant number of hypertensive patients with
increase in LA size compared to the controls, indicating that
the blood pressure medication had very little or no effect on LA
size. We also believe that the short duration of treatment might
have had little or no effect on LA size. Lastly, the case–control
design limited this study with regard to establishing a temporal
relationship.
The strength of this study is based on the fact that we used
newly diagnosed hypertensive patients and/or those with a short
duration of hypertension from diagnosis. This makes our finding
more relevant in enhancing management.
Conclusion
This study shows that that there was a significant proportion
of patients with hypertension who had LA remodelling, even
early at diagnosis, and hence there could be early cardiac
morphological modifications in these patients. Also, LA size
increased disproportionately with a significant increase in the
length, surface area and volume.
LA volume measurements should be assessed routinely in
order to identify early morphological changes in hypertensive
heart disease, and not lay emphasis only on traditional parameters
of the left ventricle. Future studies are warranted to better
elucidate the biological mechanisms underlying linking of the
early phase of hypertension with LAR as well as its prognostic
implications in our population.
This study was funded by Clinical Research Education Networking and
Consultancy (CRENC). The abstract has been published in
Archives
of
Cardiovascular Disease
2018;
10
(suppl): 110–111. Poster 420 Echography: JESFC.
We thank the Douala General Hospital and Deido District Hospital and
all cardiologists and personnel who helped in the realisation of this work. We
are grateful to patients who agreed to participate in our study.
References
1.
Fezeu L, Kengne A-P, Balkau B, Awah PK, Mbanya J-C. Ten-year
change in blood pressure levels and prevalence of hypertension in urban
and rural Cameroon.
J Epidemiol Commun Health
2010;
64
(4): 360–365.
2.
Ataklte F, Erqou S, Kaptoge S, Taye B, Echouffo-Tcheugui JB, Kengne
AP. Burden of undiagnosed hypertension in sub-Saharan Africa: a
Table 6. Multivariate linear regression analysis for independent
predictors of left atrial size
Variable
B
95% CI of the difference
p
-value
BMI
0.300
–0.026 to 0.041
0.300
DBP
–0.280
–0.001 to 0.007
0.330
LVEDD
–0.110
–0.013 to 0.020
0.630
E/A
0.370
0.328 to 1.832
0.003*
E/E
′
0.150
–0.016 to 0.080
0.290
R
2
=
38.3%. *Statistically significant. B, coefficient of regression; CI, confidence
interval, BMI, body mass index, BSA, body surface area; SBP, systolic blood
pressure, DBP, diastolic blood pressure, LVEDD, left ventricular end-diastolic
diameter.