The SA Journal Diabetes & Vascular Disease Vol 15 No 1 (July 2018)

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SA JOURNAL OF DIABETES & VASCULAR DISEASE RESEARCH ARTICLE
VOLUME 15 NUMBER 1 • JULY 2018 27
study may have been due to the duration of DM2, normal LV filling
pressures determined by E/E’ ratio, and normal LV mass.
We demonstrated that increasing age and BMI had a significant
effect on LA volume. The main difference of our study from previous
ones was the duration of DM2, which was strongy and positively
associated with larger LA diameter and impaired LA function.
CARDIA investigators showed a 20-year follow-up period of diabetes
was associated with indexed LA diameters.19 On the other hand,
Zoppini et al. showed a possible 65% LA enlargement (defined as
indexed Vmax ≥ 34 ml/m ) for each 10 years’ duration of diabetes.14
On the basis of these findings, we speculate that although diabetes
was an independent predictor of LA volume in univariate analysis, in
multivariate analysis, age and BMI were the independent predictors
of LA volume in the early stages of diabetes.
LA function is evaluated and indexed to BSA by calculating
PEV, AEV, TEV and PEF, AEF and TEF from Vmax, Vmin and Volp.
TEV describes the reservoir, PEV describes the conduit, and AEV
describes the pump function of the left atrium. Contrary to current
knowledge, Vmin increases, even in mild LV diastolic dysfunction,
whereas Vmax increases in the later stages, suggesting that
Vmin may be a more sensitive marker of LV diastolic dysfunction.
Moreover, this finding underlines the importance of evaluation of
LA function.22
Based on current knowledge, LA reservoir function is associated
with worsening LV diastolic function.7 Graca et al. showed that
LA reservoir and conduit function were reduced in asymptomatic
DM2 patients.23 The same study also demonstrated that DM2 was
independently associated with LA reservoir function, but not with
conduit function.23
Mondillo et al. investigated only diabetic patients with norma LA
size and did not find any difference in conduit and pump function.
However, they showed LA deformation was impaired in diabetics
even if LA volumes were similar between the groups.24 Murakana
et al. showed decreased LA reservoir and conduit functions in
patients with DM2 even in the absence of LA dilatation.5 Huang et
al. demonstrated, with 2D echocardiographic evaluation, increased
reservoir and pump function and reduced conduit function in
patients with DM2.6
Recently, Atas et al. reported depressed reservoir and pump
function with similar conduit function in patients with DM2
compared to the control group.8
In our study, in accordance with the study of Huang et al.,
we found reduced conduit, and increased pump and reservoir
function in diabetic patients compared with the controls. The
possibly inconsistent results with previous studies may have been
due to different cardiovascular imaging techiques used for the
determination of LA function, small sample sizes, different baseline
characteristics, and different diabetes durations of the study
populations.
There are some limitations to our study. As this was a cross-
sectional study, follow up of the patients for clinical endpoints such
as AF and heart failure could not be done. Therefore, our study
results cannot be used to direct standard clinical care. Moreover,
as the population size was relatively small, our study does not permit
any causal inferences and analysis on the effect of medications on
LA volume and function. For this reason, long-term follow up and
large-scale prospective studies are needed to determine the clinical
predictive value of early LA functional impairment in this population.
Evaluation of LA volume and function with 2D echocardiography
was an additional limitation of our study.
Conclusion
The results of our study showed impaired LA functionmay be present
in patients with DM2 with a disease duration of a maximum of
six months. BMI and increased age caused LA enlargement and
LA volumes that were independent of the effects of hypertension
and DM2. Further studies with larger sample sizes are needed to
better define the underlying mechanisms.
Acknowledgements
The authors thank Arzu Baygul from MedStats Consulting and Prof
Sule Oktay, MD, PhD from Kappa Consulting, Traning and Limited
Research Ltd for statistical analysis and interpretation of the results.
References
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2. Freire CM, Moura AL, Barbosa Mde M, et al. Left ventricule diastolic dysfunction
in diabetes: an update. Arq Bras Endocrinol Metab 2007; 51(2): 168–175.
3. Poulsen MK, Henriksen JE, Dahl J, et al . Left ventricular diastolic function in type
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disease. Circ Cardiovasc Imag 2010; 3: 24–31.
4. Kadappu KK, Boyd A, Eshoo S, et al. Changes in left atrial volume in diabetes
mellitus: more than diastolic dysfunction. Eur Heart J 2010; 13: 1016–1023.
5. Muranaka A, Yuda S, Tsuchihashi K, et al. Quantative assessment of left
ventricular and left atrial functions by strain rate imaging in diabetic patients with
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6. Huang G, Zhang L, Xie M, Fu M, Huang J, Lv Q. Assessment of left atrial function
in diabetes mellitus by left atrial volume tracking method. J Huazhong Univ Sci
Technol 2010; 30: 819–823.
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