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Hemodialysis International 2016; 20:564–572
Hemodialysis-induced regional left
ventricular systolic dysfunction
Yuxin NIE,1,2 Zhen ZHANG,1,2 Jianzhou ZOU,1,2,3 Yixiu LIANG,4 Xuesen CAO,1,2
Zhonghua LIU,1,2 Bo SHEN,1,2 Xiaohong CHEN,1,2 Xiaoqiang DING1,2,3
1
Division of Nephrology, Zhongshan Hospital, Fudan University, Shanghai, P. R. China; 2Shanghai
Institute of Kidney Disease and Dialysis, Shanghai, P. R. China; 3Key Laboratory of Kidney and Blood
Purification of Shanghai, Zhongshan Hospital, Fudan University, Shanghai, P. R. China; 4Division of
Cardiology, Zhongshan Hospital, Fudan University, Shanghai, P. R. China
Abstract
Introduction Hemodialysis (HD) patients are under observably elevated cardiovascular mortality.
Cardiac dysfunction is closely related to death caused by cardiovascular diseases (CVD). In the general population, repetitive myocardial ischemia induced left ventricular (LV) dysfunction may progress to irreversible loss of contraction step by step, and finally lead to cardiac death. In HD
patients, to remove water and solute accumulated from 48 or 72 hours of interdialysis period in a
4-hour HD session will induce myocardial ischemia. In this study, we evaluated the prevalence and
potential risk factors associated with HD-induced LV systolic dysfunction and provide some evidences for clinical strategies. Methods We recruited 31 standard HD patients for this study from
Fudan University Zhongshan hospital. Echocardiography was performed predialysis, at peak stress
during HD (15 minutes prior to the end of dialysis), and 30 minutes after HD. Auto functional imaging (AFI) was used to assess the incidence and persistence of HD-induced regional wall motion
abnormalities (RWMAs). Blood samples were drawn to measure biochemical variables.
Findings Among totally 527 segments of 31 patients, 93.54% (29/31) patients and 51.40% (276/
527) segments were diagnosed as RWMAs. Higher cTnT (0.060 6 0.030 vs. 0.048 6 0.015 ng/mL,
P 5 0.023), phosphate (2.07 6 0.50 vs. 1.49 6 0.96 mmol/L, P 5 0.001), UFR (11.00 6 3.89 vs.
8.30 6 2.66 mL/Kg/h, P 5 0.039) and lower albumin (37.83 6 4.48 vs. 38.38 6 2.53 g/L, P 5 0.050)
were found in patients with severe RWMAs (RWMAs in more than 50% segments). After univariate
and multivariate analysis, interdialytic weight gain (IDWG) was found as independent risk factor of
severe RWMAs (OR 5 1.047, 95%CI 1.155–4.732, P 5 0.038). Discussion LV systolic dysfunction
induced by HD is prevalent in conventional HD patients and should be paid attention to. Patients
would benefit from better weight control during interdialytic period to reduce ultrafiltration rate.
Key words: Hemodialysis, left ventricle, systolic dysfunction, myocardial injury, myocardial
stunning
INTRODUCTION
Correspondence to: X. Ding, MD, 180 Fenglin Road,
Shanghai, 200032, P. R. China, E-mail: ding.xiaoqiang@
zs-hospital.sh.cn
Conflict of Interest: The authors declare that they have no
conflict of interests.
Disclosure of grants or other funding: The authors declare that
they have no grants or other funding.
Among Hemodialysis (HD) patients, prevalence of CVD
and cardiovascular mortality is observably elevated. According to the USRDS annual data report 2015, more than 60%
of death were caused by CVD, such as chronic heart failure
(CHF), arrhythmia, cardiac arrest, and so forth.1 It is as 30
times higher than the general population at the same age.2
One important reason that may lead to cardiac death is LV
C 2016 International Society for Hemodialysis
V
DOI:10.1111/hdi.12434
564
HD-induced LV systolic dysfunction
dysfunction, which is extremely prevalent in HD patients,1
and always represents poor prognosis.
In nondialysis patients, cardiac systolic dysfunction
caused by transient subclinical myocardial ischemia may
persist for a period even perfusion has returned to normal. This delayed recovery of LV function is defined as
myocardial stunning.3 Recurrent episodes of stunning are
cumulative and contribute to the pathophysiology of heart
failure.4 In HD patients, because of the intermittent blood
volume reduction due to fluid removal, systemic hypoperfusion, and cardiac ischemia is quite common represented
by intradialytic hypotension (IDH).5 This ischemic effect,
though transient, could potentially cause myocardial
fibrosis in the long term and the subsequent LV kinetic
dysregulation.6 The combination of coronary hypoperfusion and resultant myocardial dysfunction culminates in
an elevated mortality in chronic HD patients.
In this study, we tried to explore the prevalence and
risk factors of HD-induced LV systolic dysfunction in HD
patients.
The study adhered to the Declaration of Helsinki and
was approved by the Ethical Committee, Zhongshan Hospital, Fudan University
HD parameters
Dialysis was conducted using GAMBRO (AK200S, Sweden) with low-flux hollow polysulfone membrane dialyzers, surface area either 1.4 or 1.6 m2, prescriptions
depend on patients individually. Dialysate composition
was Na1 138 mmol/L, K1 2 mmol/L, Ca21 1.25 mmol/L,
Mg21 0.5 mmol/L, and bicarbonate 32 mmol/L. The dialysate flow was set at 500 mL/minutes, and dialysate temperature was set at 378C. Ultrafiltration volume (UF) was
set individually according to their IDWG. Blood pump
was set at a range from 200 to 250 mL/minutes depends
on the patient’s access. Blood pressure (BP) was recorded
before the start of dialysis and then per hour during HD
session. All HD sessions were 4 hours. Low molecular
weight heparin was used for anticoagulation.
Echocardiography assessment
MATERIALS AND METHODS
Patient population
Thirty-one standard HD patients agreed to participate in
this study from Fudan University Zhongshan hospital
hemodialysis unit from November 2014 to April 2015.
Patients are dialyzed three times a week for 4-hours per
session. Patients with following situations were excluded:
(a) Left ventricular ejection fraction (LVEF) < 55% or
NYHA class III or IV; (b) Myocardial infarction within last
6 months; (c) Dialysis vintage <3 months; (d) Cancer.
Echocardiographs and blood samples were conducted at
the end of the longest interdialytic period, since most cardiovascular events occur after the long interdialytic break.
Venous blood samples were drawn by phlebotomy immediately before and after each dialysis session. All biochemical analyses including serum albumin, prealbumin,
hemoglobin, serum creatinine (SCr), blood urea nitrogen
(BUN), uric acid (UA), sodium (Na1), potassium(K1),
calcium (Ca21), phosphate, magnesium (Mg21), and ferritin were measured using an automatic analyzer in clinical laboratories. The concentration of high-sensitivity
cardiac troponin T (hs-cTnT) was determined using
immunoturbidimetry assay. N-terminal proBNP was
assessed using enzyme-linked immunosorbent assay
(ELISA).
Hemodialysis International 2016; 20:564–572
Apical two-dimensional echocardiography was conducted
before the start of HD, at peak stress during HD (15
minutes before the end of dialysis) and 30 minutes after
the end of HD (GE medical systems, Germany) by a single
doctor, who is blinded to the patients’ other clinical
results. Images were digitally recorded for subsequent offline analysis (EchoPAC Clinical Workstation Software,
GE, Germany). At least three stable consecutive cardiac
cycles were recorded for analyze using AFI technic, which
can track the wall motion by detect the endocardial borders semiautomatically.
Each ventricular was divided into 17 segments as
shown in Figure 1.7 All segments were analyzed for their
percentage of peak systolic strain (%PSS). Segments those
showed reductions of % PSS more than 20% comparing
to baseline were defined as RWMAs. HD-induced regional
LV systolic dysfunction was defined as new occurrences
of RWMAs in at least two LV segments at any time point
after the beginning of HD session.8 Wall motion score
index (WMSI) was calculated for each patient as well.
Statistical analysis
SPSS (version 20.0) was used for statistical analysis. Statistical significance level was defined as 0.05. Data were
expressed as counts/percentages for discrete variables or
as means 6 SDs for continuous variables. Comparison
between patients with and without HD-induced LV systolic dysfunction was made by a chi-square test for
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Nie et al.
Comparison between patients with/
without severe RWMAs
Figure 1 Left ventricular segmentation. Numbers in the figure represents: 1. Basal anterior; 2. Basal anteroseptal; 3.
Basal inferoseptal; 4. Basal inferior; 5. Basal inferolateral; 6.
Basal anterolateral; 7. Mid anterior; 8. Mid anteroseptal; 9.
Mid inferoseptal; 10. Mid inferior; 11. Mid inferolateral; 12.
Mid anterolateral; 13. Apical anterior; 14. Apical septal; 15.
Apical inferior; 16. Apical lateral; 17. Apex.
categorical variables. For normally distributed continuous
variables and non–normally distributed continuous variables, we chose a t test or a Mann–Whitney test, respectively. The Pearson correlation was used to assess linear
relationships. Univariate and multivariate logistic regression were used to figure out the risk factors for HDinduced myocardial stunning. Multivariate analysis
involved variables showed statistical differences in univariate analysis.
We defined RWMAs occurred in more than 50% segments as severe RWMAs. When comparing patients with
and without severe RWMAs, we found significant differences of serum phosphate level before dialysis, hs-cTnT
and ultrafiltration rate (UFR) between two groups
(P 5 0.001, 0.023, 0.039, respectively). What’s more,
patients with severe RWMAs showed higher WMSI than
another group (1.04 6 0.05 vs. 1.00 6 0.02, P 5 0.021).
However, there’s no significant difference of baseline
LVEF and other LV structures between two groups (supporting Information Table 2). Serum albumin showed a
higher trend in patients without severe RWMAs, although
not reaching statistical significance (P 5 0.050; Figure 3).
There is no difference of age, gender, history of diabetes
and CVD, dialysis vintage, dialysis access, dry weight
(DW), IDWG, serum Ca21, serum K1, NT-proBNP level,
reduction of mean artery pressure (MAP).
Association of candidate predictors with
severe RWMAs
Using Pearson rank correlation analysis, serum cTnT
before hemodialysis (r 5 0.437, P 5 0.014), IDWG
(r 5 0.372, P 5 0.039), UF (r 5 0.357, P 5 0.049), UFR
(r 5 0.368, P 5 0.042) were positive related with number
of RWMAs segments. In univariate regression analysis,
IDWG (OR 5 1.047, 95%CI 1.155–4.732, P 5 0.038),
RESULTS
Characteristics of study participants
Of the total 31 patients, there are 19 males and 12
females, with a mean age at 60 years old. The baseline
characteristics are listed in supporting Information
Table 1.
Among totally 527 segments of 31 patients, 93.54%
(29/31) patients and 51.40% (276/527) segments were
diagnosed as RWMAs. Basal anterior (22/276), apical septal (20/276), apical lateral (20/276) and mid anterior (19/
276) were the most likely influenced segments. Meanwhile, basal inferoseptal (12/276), mid inferoseptal (13/
276), mid inferior (13/276) and mid inferolateral (14/
276) were segments not influenced so much (Figure 2).
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Figure 2 Distribution of HD-induced RWMAs regions.
Numbers in the vertical axis represents: 1. Basal anterior; 2.
Basal anteroseptal; 3. Basal inferoseptal; 4. Basal inferior; 5.
Basal inferolateral; 6. Basal anterolateral; 7. Mid anterior; 8.
Mid anteroseptal; 9. Mid inferoseptal; 10. Mid inferior; 11.
Mid inferolateral; 12. Mid anterolateral; 13. Apical anterior;
14. Apical septal; 15. Apical inferior; 16. Apical lateral; 17.
Apex.
Hemodialysis International 2016; 20:564–572
HD-induced LV systolic dysfunction
Figure 3 Comparison between patients with/without severe RWMAs. Due to the wide range of variables’ values (five orders
of magnitude difference), the figure is presented by Logarithmic scale axis. Blue bar represents patients with RWMAs less
than 50% (n 5 13). Red bar represents patients with RWMAs equals to or more than 50% (n 5 18).
Table 1 Detection of hemodialysis-induced myocardial stunning in univariate and multivariate regression analyses
Predictor
Univariable analysis
IDWG (for every additional percentage)
UFR (for every additional liter per hour)
Phosphorus (for every additional mmol/L)
WBC (for every additional count of 109)
Multivariable analysis
IDWG (for every additional percentage)
Odds Ratio (95% CI)
1.047
66.627
3.070
2.177
(1.155–4.732)
(1.186–3746.760)
(0.091–9.505)
(1.095–4.329)
1.047 (1.155–4.732)
P value
0.038
0.041
0.052
0.026
0.038
CI 5 Confidence interval; IDWG 5 interdialytic weight gain; UFR 5 Ultrafiltration rate; WBC 5 White blood cell count.
UFR (OR 5 1.004, 95%CI 1.001–1.008, P 5 0.041) were
risk factors of severe RWMAs. Then we toke covariables
associated with outcome with P < 0.1, after multivariate
logistic regression, only IDWG remained as independent
risk factor (Table 1).
Figure 4 Sensitivity analysis using different methods to
define RWMAs. WMSI 5 Wall motion score index;
WMS 5 Wall motion score; SF 5 Shortening fraction.
Hemodialysis International 2016; 20:564–572
DISCUSSION
HD-induced LV systolic dysfunction is quite prevalent in
maintenance HD patients. In our study, about 90%
patients and more than half segments were diagnosed as
RWMAs. However, the percentage of RWMAs varies quite
different from study to study. The widely range is mainly
due to different methods used in different studies. Burton
et al evaluated RWMAs by shortening fraction (SF), and
defined RWMA as the region showed a decline in SF
more than 20% from baseline, and the prevalence of
RWMAs in his study was 74%;9 Assa et al defined
RWMA as region showed an increase in WMSI, and
reported the prevalence of RWMAs in at least 2 out of 17
LV regions as 29%;8 while Dubin et al defined RWMA as
an increase of sum of wall motion score (WMS) in all LV
segments, and they found the prevalence of RWMAs as
23%.10 When we used the other three methods mentioned above for a sensitivity analysis, the results varied
from 30% to 90%, as shown in Figure 4. Comparing to
these methods, the region was defined as RWMA as long as
it showed a decline of %PSS more than 20% from baseline
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Nie et al.
according to the AFI method (strain echocardiography)
used in our study. Sometimes the systolic function is still
within the normal range even after the decline. At this time,
the region is defined as RWMA if using “strain” method,
but non-RWMA if using WMS or WMSI. Similarly, when
comparing methods using %PSS and %SF, the latter one
only represents global LV systolic function, while %PSS
could represents regional segment function. If a heart
shows changes of %PSS in a few LV segment with preserved global systolic function, it is defined as RWMA if
using %PSS, but non-RWMA if using %SF. As a result, it
leads to a higher prevalence of RWMAs when choosing
strain echocardiography than choosing WMS or %SF.
Since there is no standard criterion for HD-induced LV systolic dysfunction yet, it is hard to judge which method is
better than others. Strain echocardiography is more sensitive to detect early stage reduction of cardiac function.
What is more, it has been proved that even among patients
with reserved LV functions, strain echocardiography is still
reliable and powerful.11
Some researchers found that patients with HD-induced
cardiac dysfunction were under worse baseline cardiac
functions.8,10 In our study, the baselines LVEFs for
patients without and with severe RWMAs were 63.46% 6
7.38% and 64.59% 6 5.83%, respectively (P 5 0.979),
and WMSI were 1.00 6 0.02 and 1.04 6 0.05, respectively (P 5 0.021). There’s just a slightly higher WMSI
with similar LVEF in patients with severe RWMAs. The
reason why we failed to find association between baseline
cardiac function and occurrence of RWMAs may be due
to the different study population. In Assa’s study, 35.2%
patients have baseline LVEF<50%, and 40% patients
have WMSI > 1. Similarly, in Dubin’s study, 12.5%
patients had heart failure with average baseline LVEF of
40%, and some degrees of diastolic dysfunction. While in
our study, we excluded patients with LVEF<55%, and
our baseline LVEF was 64%, with only 25% patients had
WMSI>1, which means our study’s population was
under a better baseline cardiac function. As a result, there
showed no significant differences of LVEF between
patients with and without severe RWMAs. Further studies
including patients with worse heart functions would be
more comprehensive and representative, and should be
considered for a better illustration.
Besides systolic function, diastolic function is an important part of the cardiac function as well, which represents
the ability of the heart to expand and refill the ventricles.
It was determined by the intrinsic ventricular properties,
such as stiffness and relaxation. When the ventricles systole, the cardiac muscles both contract and twist, the circumferential muscles distort to the helical orientation,
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which varies from endocardium to epicardium by 1608.12
During this process, elastic energy is stored in myocytes.13
When diastolic period starts, the stored energy is released
to “untwist” the ventricles, and create suction pressures,
which initiate the ventricles filling.14,15 In the general
population, studies showed that the ischemia and periischemia regions caused by coronary artery occlusion represented ischemia-induced diastolic dysfunction, which
could be relieved after a period of reperfusion.16,17 Similarly, during HD sessions, diastolic dysfunction caused by
HD-induced ischemia has been proved using conventional echocardiography and Tissue Doppler Imaging
(TDI) methods.18–20 What is more, diastolic dysfunction
has been proved closely related with poor outcome, even
in patients with preserved systolic function.21 However,
as HD patients are usually with rapidly blood volume
changes during HD sessions, evaluate the diastolic function by conventional methods, such as early mitral flow
velocity and atrial filling, might not be accurate.22 AFI
conducted by two-dimensional speckle tracking echocardiography (STE) is a more sensitive and reliable method
to measure diastolic function.23,24 Further research focus
on diastolic strain abnormalities should be considered for
the assessment of HD-induced diastolic dysfunction.
According to our results, we found that segments with
single coronary artery blood supply were more prone to
be impacted during HD, such as basal anterior, apical
septal, apical lateral, and mid anterior segments. In a
recent study, Huang et al also found that apical inferior,
mid anterior, basal anterior and basal lateral segments
showed a trend toward higher strain value at peak dialysis
compared with it before dialysis.25 Since in Huang’s
study, the author divided LV chamber into 12 segments,
while we divided it into 17 segments, although the names
of influenced segments are not exactly the same, they
showed highly similar distribution in a bulls-eye display.
What is more, Huang et al also found that the segmental
longitudinal strains (SLS) of the mid septal and apical septal segments, as well as apical, inferior and septal arears
were associated with survival outcome. The authors
attributed the anatomically vulnerable regions to the mismatch of perfusion/ischemia. McIntyre et al reported that
when using H2-15O positron emission tomography to
assess myocardial blood flow (MBF), LV segments dysfunction could be induced by decline of MBF.26 However,
the reason why some segments are more “fragile” than
others is remain unclear. It has been reported that there is
a reduction of the number of capillaries per volume
among HD patients due to the uremic toxins and cardiac
structural abnormal.27,28 As a result, it shows a mismatch
of myocytes and capillaries.22 Besides that the increased
Hemodialysis International 2016; 20:564–572
HD-induced LV systolic dysfunction
vascular calcification and arterial stiffness29 result impaired
microperfusion of the heart. Thus, the ability to adapt the
hemodynamic pressure induced by HD is decreased. It has
been widely recognized that IDH plays an important role in
elevated CV mortality in HD patients. Beyond the fluid
removal during HD sessions, another hypothesis for IDH is
defective vasoregulation.22 Several risk factors may contribute to this deficiency. Chesterton et al reported impaired
baroreflex sensitivity due to autonomic dysfunction in HD
patients.30 Meanwhile, endothelium as the key regulator of
vascular function was damaged as a consequence of the
combination of inflammation,31,32 endotoxins,33 and oxidative stresses.34 Eventually, multiple factors lead to abnormal perfusion of the end organs and vulnerable vascular
beds, especially when under increasing circulatory stress
induced by HD.22
In the general population, the most popular hypothesis
about the mechanisms of ischemia induced cardiac dysfunction is “Oxyradical Hypothesis.”35 Thus, it mostly
occurs during the first few minutes of reperfusion with
arterial blood.35,36 However, according to our study and
some other research,9,37 HD-induced LV systolic dysfunction mostly happens during the dialysis session (before
the end of dialysis session) instead of the period of reperfusion (after the end of dialysis session). This might in
some levels explain the increased risk of sudden cardiac
death during and immediately after hemodialysis.38 Different occurrence times imply that cardiac dysfunction in
HD patients might have different mechanisms from general population, which are still not well demonstrated and
needs further research.
When comparing patients without severe RWMAs, hscTnT is statistically higher in patients with severe RWMAs.
Higher hs-cTnT as a biomarker represents severer myocardial injury, so even there is neither symptom, such as chest
pain; nor difference of basic cardiac structures and functions between two groups, potential insufficiency of coronary artery blood reserve and subclinical myocardial injury
may already exists. During HD, because of the quick
removal of fluid and instable of hemodynamics, myocardial
dysfunction was induced.
Higher UFR is a risk factor of HD-induced RWMAs.
During dialysis session, overload volume accumulated in
two to three interdialytic days is removed in 4 hours.
Consequently, it brings strong stress to the heart. Previous
studies demonstrated that both larger IDWG39 and higher
UFR40 were associated with poor survival. HD-induced
cardiac dysfunction may present a new idea to explain
why this would happen. When giving more frequent or
extended HD treatments, the dysfunction could be lessened by the reduction of UFR, which provides further eviHemodialysis International 2016; 20:564–572
dences for it.41 According to this finding, personalized
dialysis target to minimize UFR either by more frequent
dialysis scheduling or by extended dialysis should be considered, to prevent HD-induced RWMAs and improve
long-term cardiovascular outcomes.
Albumin is in a lower lever in patients with severe
RWMAs, although not meeting a statistical significance
(P 5 0.05). This might because of the limit of sample size.
Lower albumin represents of malnutrition status and
inflammation, which have been well demonstrated with
atherosclerosis and poor survival.42 More inflammatory
markers such as C-reactive protein, IL-6 and IL-33 and so
on could provide more clues about inflammation and
HD-induced cardiac dysfunction. In clinical practice,
maintaining albumin level at an appropriate range should
always be highly focused.
In patients with severe RWMAs, they were found under
a higher serum phosphate level. Elevated phosphate level
is well known associated with adverse cardiovascular outcomes. Suzuki and his coworkers found that in spontaneously hypertensive rats, high phosphate and zinc-free diet
markedly reduced their left ventricular systolic and diastolic function and cause severe myocardial fibrosis histopathologically.43 Liu et al. described that high phosphate
level is related with increased secretion of ANP and BNP
in cardiac myoblast.44 Hyperphosphate may cause cardiomyocytes abnormalities both in structural and functional.
When during HD, under stresses caused by changes in
electrolytes, acid-base balance, and blood volume on a
heart that is already in a nonhealthy state, myocardial dysfunction is induced.
It has been well illustrated that HD-induced regional
LV systolic dysfunction is closely related to a poor longterm cardiac function and an elevated mortality rate.8,9,11
Thus, strategies to prevent the occurrence of HD-induced
cardiac injuries could contribute to a better survival. The
protective effects of cooler dialysate on cardiac have been
well studied by many researchers. Selby et al reported
that when comparing patients using dialysate with temperatures of 37 (HD [37]) and 35 (HD [35]) degree centigrade, less regional LV systolic dysfunction was induced
during HD session with more stable hemodynamic parameters in patients with HD (37).37 Further study attributes the
protective effect of cool dialysate to the improvement of baroreflex variability.45 Although, the effectiveness of cool dialysate has been acknowledged, the intolerable temperature is
still a big problem. As a result, individualized cool dialysate
was demonstrated. Jefferies et al proved that dialysate with
the temperature 0.58 lower than the patients’ core temperature was as effective as HD (35), and without compromising
tolerability.46 A most recently randomized controlled trial
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involved 73 incident HD patients with 12 months followup, and evaluated the patients’ systolic and diastolic function
by cardiac magnetic resonance imaging, and left ventricular
mass as well. It confirmed the benefit of individualized cool
dialysate for cardiac protection over a 12-month period.47
Beyond the cardio-protection, the strategy of individualized
cool dialysate also represents multi end organs protection.48
Using individualized cooled dialysate is an effective intervention with no additional cost, and is easy to accept and
widely use.
An alternative option to reduce HD-induced cardiac
dysfunction is to minimize the UFR by more frequent HD
scheduling. A cross-sectional study has proved the effectiveness of this strategy to reduce HD-induced cardiac
injury.41 Besides that patients undergoing frequent HD,
such as daily HD or nocturnal dialysis, may also benefit
from better clearance of endotoxin.49,50 However, frequent HD may leads to additional cost and inconvenience, which limits its utilization. It also has been
reported that the blood flow of arteriovenous fistula
(AVF) is associated with HD-induced cardiac injury. In
patients with higher AVF flow, both the number of
regions of RWMAs and the severity of RWMAs were significantly less than patients with lower AVF flow.51 The
benefit of high AVF flows maybe due to better distal
microcirculation, and lead to a remote preconditioning.
Beyond these strategies, the Sodium Lowering in Dialysate
(SoLID) trial is a multicenter, randomized, controlled 3year trial in New Zealand, which is still keep going to
clarify the effect of dialysate sodium concentration on the
cardiovascular risks among HD patients. We look forward
to the information and results brought by this trial.52
HD-induced myocardial dysfunction is common in HD
patients, especially in those with higher hs-cTnT, serum
phosphate, and UFR, and lower albumin level patients.
Transient myocardial ischemia caused by HD can lead to
temporary LV dysfunction and stunning, and repeat episodes of stunning may lead to structural and functional
abnormalities, and eventually heart failure.
There are some limitations. First of all, we performed
echocardiography at three time points: predialysis, at
peak stress during HD (15 minutes before the end of dialysis) and 30 minutes into the recovery period, so we were
lack of data when RWMAs were exactly happened, and
when were fully recovered. Second, because of the sample
size, our ability to reach statistical significance is limited,
for example, albumin level. Third, we did not include
evaluation of diastolic function, which is also a key component of cardiac function and prognosis. Further study
including the assessment of diastolic function should be
considered.
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CONCLUSIONS
HD-induced myocardial regional systolic dysfunction is a
common phenomenon among conventional HD patients,
which may lead to poor survival and quality of life and
should be paid attention to. Better control of weight gains
during interdialytic period to reduce UFR might be benefit to patients. Maintain phosphate and albumin level at
an appropriate range would also be helpful. More frequent HD scheduling, extended HD, and individualized
dialysate temperature setting are indicators of personalized treatments for better organ protection.
ACKNOWLEDGMENTS
The authors are grateful to all of the staff at the Blood Purification Center, Zhongshan Hospital, Fudan University.
Manuscript received December 2015; revised March
2016.
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SUPPORTING INFORMATION
Additional Supporting Information may be found in the
online version of this article.
Supplement Table 1 Baseline characteristics.
Supplement Table 2 Baseline LV structure and function.
Hemodialysis International 2016; 20:564–572
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