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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 29, No 4, July/August 2018
234
AFRICA
patients with hypertrophy, 96% (22 patients) were concentric
in pattern and 4% had eccentric hypertrophy (one patient). As
expected, patients had diastolic dysfunction with significantly
greater indices of elevated filling pressure [E/E
′
and left atrial
(LA) volume index] pre-dialysis compared to the normal control
group.
During dialysis, CKD patients were ultra-filtrated a mean of
2.2
±
0.9 litres, with a mean change in weight of 2.2
±
1.0 kg.
As a result, there was a significant difference in pre- and post-
dialysis weights (Table 1). No statistically significant differences
between systolic, diastolic, mean arterial pressure and heart rate
were found.
There was a significant decrease in LVEDV, LVESV, E/E
′
and
LA volume index (LAVI) after dialysis whereas a significant
increment in EF was noted compared to pre-dialysis values
(Table 2). However, the stroke volume and PP/SV did not change.
At baseline, there was no difference in net speckle-tracking
twist and basal rotation between controls compared to CKD
patients prior to their dialysis session. However, there was a
significant decrease in apical rotation between the control and
pre-dialysis group (6.3
±
1.6 vs 4.8
±
2.3°;
p
=
0.01). There was
no statistically significant difference when comparing net twist,
basal rotation or apical rotation in CKD patients before and
after dialysis (Table 3).
In the univariate linear regression analysis of twist, the
presence of hypertension, diabetes, the use of ACE inhibitor
or angiotensin receptor blocker (ARB), and change in weight
before and after dialysis were compared against the difference
in apical, basal and net twist before and after dialysis. These
variables showed a trend towards statistical significance with an
independent association between hypertension and the difference
in apical twist (regression coefficient of 0.34;
p
=
0.088), and in
the use of an ACE inhibitor or ARB versus net twist (regression
coefficient of 0.34;
p
=
0.09). A significant association was
demonstrated between the differences in systolic and diastolic
blood pressure versus basal twist post-dialysis (
p
=
0.02 and
p
=
0.006, respectively), and the difference in diastolic blood pressure
and apical twist post-dialysis (
p
=
0.04).
Discussion
The major findings of this study are (1) apical rotation appears
to be reduced in patients on chronic haemodialysis with net
twist remaining unchanged; and (2) LV twist is less susceptible
to haemodynamic fluctuations associated with dialysis than EF.
The use of EF as a measure of systolic function in CKD
is suboptimal because of the variable load changes and the
effects of uraemic metabolites during dialysis. According to
the ‘Starling effect’, LV function is determined by load, with
increasing preload resulting in improved LV function, and vice
versa. Similarly, systolic function is inversely related to afterload.
However, it is not only load changes that play a role in systolic
function in CKD patients on dialysis. An additional possibility
is that the removal of negatively inotropic uraemic toxins during
haemodialysis improves cardiac function.
7,11,36
In clinical practice,
trying to predict the relative interplay of load changes and
uraemia on EF is extremely complex.
7
In this study, CKD patients had similar EF to the control
participants at baseline, which is not surprising since systolic
dysfunction is seen in only 15% of CKD patients.
37
During
dialysis, there was a significant reduction in preload (LVEDV,
LVESV, LAVI and E/Ea ratios), but no significant change in
afterload (MAP and PP/SV ratios).
31
Therefore, it would be
reasonable to postulate that the EF should have been reduced,
according to Starling. Since EF increased after dialysis, the
removal of uraemic metabolites during haemodialysis may have
been responsible for the improvement.
7
Considering these changes, one might suppose that if apical,
basal and net twist were subject to load changes, any or all of
these parameters would decrease with reduced preload. These
measures of rotation did not change with dialysis. This lack of
significant change after dialysis implies that the components of
myocardial rotation: apical rotation, basal rotation and net LV
twist are relatively load independent, but whether they are also
relatively immune to the acute metabolic changes of uraemia
requires further study.
The key to understanding LV twist and its contribution to
cardiac systolic function is in understanding the arrangement of
myocardial fibres in a ‘left-handed’ helix sub-endocardially with
clockwise rotation, and a ‘right-handed’ helix sub-epicardially
with counter-clockwise rotation (Fig. 4). In normal cardiac
physiology, apical rotation provides the greater contribution to net
twist because of the larger radius of rotation of its sub-epicardial
predominant fibres compared to the sub-endocardial
predominant base. For example, conditions that are known to
affect mainly the sub-endocardial layer of the myocardium,
such as hypertensive LVH,
38
aortic stenosis,
39
hypertrophic
cardiomyopathy,
39
amyloidosis
40
and early myocardial ischaemia
41
have been shown to cause apical hyper-rotation through the
relatively unopposed sub-epicardial muscle fibres. This may be a
compensatory function to preserve systolic function, with many
of these conditions showing increase in net LV twist despite a
Table 3. Speckle-tracking characteristics
Characteristics
Control
(
n
=
26)
Pre-dialysis
(
n
=
26)
Post-dialysis
(
n
=
26)
Apical rotation (°)
6.3
±
1.6
4.8
±
2.3*
5.5
±
3.6
Basal rotation (°)
–3.3
±
1
–3.4
±
1.9
–3.3
±
1.9
Net twist (°)
9.6
±
1.9
8.2
±
3.1
8.8
±
4.1
*
p
-value < 0.05 vs control group.
Table 2. Echocardiographic characteristics
Characteristics
Control
(
n
=
26)
Pre-dialysis
(
n
=
26)
Post-dialysis
(
n
=
26)
LV end-diastolic volume (ml)
71.0
±
9.8 97.9
±
39.2* 83.5
±
23.9
†
LV end-systolic volume (ml)
30.6
±
7.6 41.1
±
23.7 35.2
±
20.3
†
Stroke volume (ml)
40.5
±
10.2 57.4
±
28.3* 49.3
±
16.5
LV end-diastolic diameter (mm)
44.9
±
0.3 45.8
±
0.7 45.3
±
0.6
LV end-systolic diameter (mm)
28.8
±
0.4 32 .0
±
0.6* 29.7
±
0.6
Interventricular septal diameter
(mm)
10.0
±
0.2 14.1
±
0.3*
14.0
±
0.3
Posterior wall thickness (mm)
9 .0
±
0.1 13.5
±
0.3* 13.2
±
0.3
Relative wall thickness (mm)
0.4
±
0.04 0.6
±
0.1* 0.6
±
0.1
Ejection fraction (%)
61.7
±
6.2 58.8
±
13.7 61.2
±
13.6
†
LV mass index (g/m
2
)
84.5
±
18.9 156.1
±
61.9* 152.7
±
62
Left atrial volume index(ml)
25.8
±
5.6 33.4
±
15.2 * 27.8
±
15.6
†
Mitral E/A (ratio)
1.2
±
0.4
1.1
±
0.4
1.1
±
0.7
E/E
′
(ratio)
9.8
±
2.4 15.2
±
5.2* 13.0
±
5.8
†
Pulse pressure/stroke volume
(mmHg/ml)
1.3
±
0.8
1.4
±
0.9
1.3
±
0.8
*
p
-value < 0.05 vs control group, †
p
-value < 0.05 vs pre-dialysis group
‡