Heart and Vessels (2021) 36:1275–1282

https://doi.org/10.1007/s00380-021-01815-0

ORIGINAL ARTICLE

The long‑term prognostic factors in hemodialysis patients with acute

coronary syndrome: perspectives from sarcopenia and malnutrition
Hisaya Kobayashi1 · Masao Takahashi1 · Motoki Fukutomi1 · Yusuke Oba1 · Hiroshi Funayama1 · Kazuomi Kario1

Received: 24 November 2020 / Accepted: 19 February 2021 / Published online: 6 March 2021
© Springer Japan KK, part of Springer Nature 2021

Abstract
Hemodialysis (HD) patients tend to have sarcopenia and malnutrition, and both conditions are related to poor prognosis in
the cardiovascular disease that often accompanies HD. However, the impact of sarcopenia or malnutrition on the long-term
prognosis of HD patients undergoing percutaneous coronary intervention (PCI) for acute coronary syndrome (ACS) remains
unclear. We analyzed 1,605 consecutive patients with ACS who had undergone PCI at a single center between January 2009
and December 2014. We evaluated all-cause mortality and prognosis-associated factors, including sarcopenia/malnutrition-
related factors such as the Geriatric Nutritional Risk Index (GNRI), and Skeletal Muscle Mass Index (SMI). After exclusions,
1461 patients were enrolled, and 58 (4.0%) were on HD. The HD group had lower levels of SMI and GNRI than non-HD
group, and had worse in-hospital prognosis. Moreover, HD group had a significant higher mortality in the long-term follow-
up [median follow-up period: 1219 days; Hazard Ratio (HR) = 4.09, p < 0.001]. After adjusting the covariates, SMI and
GNRI were the factors associated with all-cause mortality in all patients [SMI: adjusted HR (aHR) = 2.39, p = 0.036; GNRI:
aHR = 2.21, p = 0.006]; however, these findings were not observed among HD patients with ACS, and only diabetes was
significantly associated with all-cause mortality (diabetes: aHR = 3.50, p = 0.031). HD patients with ACS had a significantly
higher rate of in-hospital and long-term mortality than non-HD patients. Although sarcopenia and malnutrition were related
to mortality and were more common in HD patients, sarcopenia and malnutrition had a lower impact than diabetes on the
long-term prognosis of HD patients with ACS.

Keywords Chronic kidney disease · Geriatric Nutritional Risk Index · Skeletal Muscle Mass Index · Diabetes · PCI

Introduction catastrophic event and is associated with poor long-term sur-

Cardiovascular disease (CVD) is a common comorbidity and
major cause of mortality in hemodialysis (HD) patients. In
the 2018 US. Renal Data System report, the prevalence of
CVD in HD patients was 70.6% and the 2-year survival rate
for HD patients with coronary artery disease was 66.2%.
Moreover, the 2-year survival rate among HD patients
receiving percutaneous coronary intervention (PCI) was
nearly 50% [1]. Cardiovascular mortality in HD patients has
been estimated to be approximately 9% per year, which is
10–20 times higher than in the general population [2]. Acute
coronary syndrome (ACS) in HD patients is a particularly
* Masao Takahashi
masaotakahashi-gi@umin.org
vival [3–6]. The previous study has shown that HD patients
with acute myocardial infarctions (AMI) had overall mortal-
ity rates of 74% and cardiac death of about 52% at 2 years
[5].
Sarcopenia and malnutrition are widespread syndromes
in older people and are associated with an increased risk
of mortality [7, 8]. Both sarcopenia and malnutrition are
common complications in HD patients [9–12]. In addition,
both syndromes are associated with poor prognosis in HD
patients [10–15]. However, the impact of sarcopenia or mal-
nutrition on HD patients with ACS has not been fully evalu-
ated. In this study, therefore, we investigated the long-term
prognostic factors in HD patients with ACS and whether
sarcopenia and malnutrition would have an impact on the
long-term prognosis.

1
Department of Cardiovascular Medicine, Jichi Medical
University School of Medicine, 3311‑1, Yakushiji,
Shimotsuke, Tochigi 329‑0498, Japan

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1276
Materials and methods
Patients
This study is a retrospective analysis of prospectively
collected data on 1605 consecutive patients with ACS
who underwent PCI at Jichi Medical University Hospital
between January 2009 and December 2014. The 1605 ACS
patients consisted of AMI and unstable angina pectoris
(UAP). AMI was diagnosed based on the presence of typi-
cal chest pain with or without ST-segment elevation on
12-lead electrocardiograms and increased serum creatine
kinase levels. UAP was diagnosed based on the presence
of characteristic chest pain symptoms at rest associated
with transient ischemic ST-segment shifts and normal
serum creatine kinase levels [16]. In general, Troponin
levels are useful for diagnosis of AMI, however, troponin
levels measured at admission are frequently elevated
in HD patients.[17] Therefore, we use serum creatine
kinase levels as an indicator of myocardial infarction. We
excluded those patients who did not performed primary
PCI, and who underwent bypass grafting surgery in the
acute setting.
Data collection
Baseline clinical, laboratory, and angiographic findings
were collected from the medical records at Jichi Medical
University Hospital. Information on the clinical status at
the latest clinical follow-up available was collected based
upon clinic visits, telephone interviews and advice from
the referring physicians. This retrospective observational
study protocol, which adhered to the principles of the
Declaration of Helsinki, was approved by the Institutional
Review Board of the Jichi Medical University School of
Medicine and was carried out by the opt-out method via
our hospital’s website.
Definitions and end points
The primary endpoint of this study was all-cause mor-
tality of the patients. We evaluated the in-hospital death,
and long-term prognosis if the patients discharged alive.
The factors associated with long-term prognosis were also
assessed in each group. As indices of sarcopenia and mal-
nutrition, we used the Skeletal Muscle mass Index (SMI)
and Geriatric Nutritional Risk Index (GNRI), respectively.
The GNRI was calculated as follows from the height, body
weight, and serum albumin level on admission:
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Heart and Vessels (2021) 36:1275–1282
GNRI = 14.89 × albumin (g∕dL) + 41.7
× body weight/ideal body weight.
The ideal body weight was calculated from height and a
body mass index (BMI) of 22 kg/m2. The body weight was
measured just after hospitalization. The GNRI defines four
grades of nutrition-related risk: major risk (GNRI < 82),
moderate risk (GNRI 82 to < 92), low risk (GNRI 92–98),
and no risk (GNRI > 98). Based on these grades, we
divided the patients into two groups, a low GNRI group
(GNRI ≦98) and high GNRI group (GNRI > 98) [18]. The
SMI was calculated as the appendicular skeletal muscle
mass (ASM) divided by the height squared. ASM was cal-
culated from each individual’s anthropometric measure-
ments as follows [19]:
ASM = 0.244 × weight + 7.8 × height + 6.6 × sex
− 0.098 × age + race − 3.3[where female = 0
and male = 1; race = − 1.6(Asian)].
The cut-off values for SMI in Asian population by using
dual X-ray absorptiometry were defined as 7.0 kg ­m−2 for
men and 5.4 kg ­m−2 for women (2 standard deviations below
the sex-specific mean for young adults) [20]. World Health
Organization hemoglobin thresholds were used to define ane-
mia as < 13 g/dL for men and < 12 g/dL for women [21].
Statistical analysis
Continuous variables are presented as means ± standard devia-
tion and the between-group differences were compared using
unpaired Student’s t tests, or Mann–Whitney U tests when the
data were not normally distributed. Categorical variables are
presented as frequencies (with percentages) and the between-
group differences were compared using Pearson’s χ2 tests, or
Fisher’s exact tests when Pearson’s chi-square tests were not
applicable owing to the sample size. The statistical tests were
two-tailed and values of p < 0.05 were considered statistically
significant. The all-cause mortality was calculated and ana-
lyzed by the Kaplan–Meier method, and differences in the
parameter were analyzed by the log-rank test.
Cox proportional hazards models were used to identify the
risk factors for mortality. The hazard ratio (HR) and 95% con-
fidence interval (CI) were derived from Cox proportional haz-
ard models. Cox models met the assumption of proportionality
of risks. Significant variables (p < 0.1) in univariate analysis
were selected for multivariate analysis. All statistical analyses
were performed using the IBM SPSS Statistics software pro-
gram, ver. 24 (IBM Corporation, Armonk, NY, USA).
Heart and Vessels (2021) 36:1275–1282 1277

1219 days after admission. The patient background and char-

Fig. 1  Flowchart of this study enrollment. ACS acute coronary syn-
drome, PCI percutaneous coronary intervention, HD hemodialysis
Results
PCI was performed in 1461 patients with ACS, 58 (4.0%)
were receiving HD (Fig. 1). The median follow-up time was
acteristics are shown in Table 1.
Forty-seven percent of the HD patients were diagnosed
with AMI compared to 67% of the non-HD group. Sub-
jects in the HD group were more likely to have a history of
hypertension, to have current diabetes or to have lower levels
of SMI, GNRI and hemoglobin than those in the non-HD
group. Table 2 shows the lesion characteristics, procedure
and in-hospital outcomes for the patients with or without
HD. Patients diagnosed with ST elevated MI were signifi-
cantly more common in non-HD patients, whereas patients
diagnosed with UAP were significantly more common in HD
patients. Patients with HD were more likely to present with
triple vessel disease, and to undergo rotational atherectomy
in PCI compared to those without HD. Regarding in-hospital
outcomes, HD patients had significantly more cardiac death
than the non-HD patients (HD vs. non-HD: 12.1% vs. 3.8%,
p = 0.008; Table 2). The long-term follow-up evaluation

Table 1  Patient risk factors and Variable HD(−) HD(+) p value

presentation characteristics, by n = 1,399 n = 58
hemodialysis status
Age (years) 67.0 ± 12.0 64.5 ± 8.9 0.492
Male, n (%) 1,107 (79.1) 45 (77.6) 0.906
Diabetes, n (%) 455 (40.2) 35 (61.4) 0.002
Hypertension, n (%) 805 (71.1) 49 (86.0) 0.023
Dyslipidemia, n (%) 742 (65.4) 21 (36.8) < 0.001
Family History, n (%) 326 (29.3) 13 (24.5) 0.549
Current-smoking, n (%) 463 (41.1) 11 (20.4) 0.004
History of myocardial infarction, n (%) 121 (8.7) 6 (10.3) 0.858
Height (cm) 163.0 ± 9.5 163.0 ± 8.9 0.803
Weight (kg) 63.0 ± 13.3 60.0 ± 10.1 0.003
BMI 24.1 ± 3.7 22.1 ± 3.0 < 0.001
SMI (kg/m2) 8.6 ± 1.8 8.3 ± 1.6 0.027
Low SMI (kg/m2) 171 (12.3) 12 (21.4) 0.044
Systolic blood pressure (mmHg) 136 ± 28 126 ± 37 0.196
Diastolic blood pressure (mmHg) 80 ± 18 70 ± 17 < 0.001
Heart rate (/min) 76 ± 21 78 ± 19 0.581
C-reactive protein (mg/dl) 0.18 ± 2.95 0.44 ± 3.02 < 0.001
Hemoglobin (g/dl) 13.7 ± 1.9 11.0 ± 1.4 < 0.001
Creatinine (mg/dl) 0.79 ± 0.64 7.75 ± 2.54 < 0.001
Albumin (mg/dl) 4.1 ± 2.9 3.4 ± 0.6 < 0.001
GNRI 104.3 ± 11.2 96.5 ± 1.0 < 0.001
Low GNRI 277 (27.2) 24 (58.5) < 0.001
Statin, n (%) 1167 (83.4) 22 (37.9) < 0.001
Calcium channel blocker, n (%) 274 (19.6) 21 (36.2) 0.003
RAS inhibitor, n (%) 1075 (76.8) 34 (58.6) 0.002
Beta-blocker, n (%) 1048 (74.9) 35 (60.3) 0.020
Single anti-platelet therapy, n (%) 103 (7.4) 9 (15.5) 0.029
Dual or triple anti-platelet therapy, n (%) 1296 (92.6) 49 (84.5) 0.029
Killip classification > class 2, n (%) 211 (22.5) 10 (35.7) 0.159

HD hemodialysis, MI myocardial infarction, BMI body mass index, SMI skeletal muscle mass index, GNRI
geriatric nutritional risk index, RAS renin-angiotensin system

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1278 Heart and Vessels (2021) 36:1275–1282

Table 2  Lesion characteristics, procedure and in-hospital outcomes,

by hemodialysis status
Variable HD(−) HD(+) p value
n = 1,399 n = 58

Diagnosis
AMI, n (%) 944 (67.5) 27 (46.6) 0.002
STEMI, n (%) 825 (59.0) 24 (41.4) 0.008
NSTEMI, n (%) 119 (8.5) 3 (5.2) 0.268
uAP, n (%) 455 (32.5) 31 (53.4) 0.002
Culprit lesion
RCA, n (%) 481 (34.4) 23 (39.7) 0.307
LAD, n (%) 688 (51.3) 23 (43.4) 0.325
LCx, n (%) 236 (17.6) 13 (24.5) 0.266
LMT, n (%) 67 (5.0) 1 (1.9) 0.513
Successful PCI, n (%) 1227 (88.3) 48 (87.3) 0.821
Drug-eluting stent, n (%) 700 (50.0) 32 (56.1) 0.442
Stent length (mm) 20.0 ± 11.7 21.5 ± 11.2 0.383
Fig. 2  Kaplan–Meier curve for all-cause mortality in patients with
Rotational atherectomy, n (%) 30 (2.1) 9 (15.8) < 0.001
and without HD. HD patients had significantly lower survival rate
PCPS, n (%) 34 (2.4) 0 (0.0) 0.643 than non-HD patients (Log-rank test: p < 0.001)
IABP, n (%) 150 (10.7) 7 (12.1) 0.914
Triple vessel disease, n (%) 165 (12.8) 19 (38.0) < 0.001
Max CPK ≧ 3000 IU/L, n (%) 354 (39.3) 5 (20.0) 0.080
values were significantly higher among the survivor among
Target lesion revascularization, 113 (8.9) 7 (14.9) 0.188
non-HD patients on long-term follow-up, these findings
n (%) were not observed among HD patients.
Target vessel revascularization, 161 (12.6) 11 (23.4) 0.053 After adjusting the covariates, diabetes was the only
n (%) factor associated with all-cause mortality among the HD
Stent thrombosis, n (%) 12 (0.9) 0 (0.0) 1.000 patients, whereas SMI and GNRI were not (diabetes:
PCI within 24 h, n (%) 1292 (92.4) 45 (80.4) 0.004 aHR = 3.50, 95% CI 1.12–10.92, p = 0.031; Table 4). The
Catheter-associated bleeding, 16 (1.1) 1 (1.7) 0.501 long-term follow-up evaluation showed that HD patients
n (%) with diabetes had significantly higher incidence of all-cause
In-hospital cardiac death, n (%) 53 (3.8) 7 (12.1) 0.008 mortality than those without diabetes on Kaplan–Meier anal-
In-hospital non-cardiac death, 6 (0.4) 1 (1.7) 0.248 ysis (HD patients with vs. without diabetes: HR = 3.24, 95%
n (%)
CI 1.13–9.34, p = 0.029; Fig. 3).
AMI acute myocardial infarction, STEMI ST elevated myocardial
infarction, NSTEMI non-ST elevated myocardial infarction, uAP
unstable angina pectoris, RCA​right coronary artery, LAD left anterior
descending artery, LCx left circumflex artery, LMT left main tract,
PCPS percutaneous cardiopulmonary support, IABP intra-aortic bal- Discussion
loon pumping, CPK creatine phosphokinase, PCI percutaneous coro-
nary intervention The major findings of this study are as follows; (1) In-hos-
pital mortality and long-term mortality were significantly
higher in HD patients than non-HD patients. (2) The indices
showed that HD patients had significantly higher incidence of sarcopenia and malnutrition had an impact on long-term
of all-cause mortality on Kaplan–Meier analysis [Hazard mortality in all ACS patients (a low GNRI value showed
Ratio (HR) = 4.09, 95% confidence interval (CI) 2.54–6.59, the strongest association with all-cause mortality). Moreo-
p < 0.001; Fig. 2]. After adjusting the covariates, low GNRI, ver, HD patients with ACS tended to have sarcopenia and
SMI and advanced age were independent risk factor of all- malnutrition. (3) However, among HD patients with ACS,
cause mortality [SMI: adjusted HR (aHR) = 2.39, 95% CI diabetes was more strongly associated with all-cause mortal-
1.06–5.40, p = 0.036; GNRI: aHR = 2.21, 95% CI 1.25–3.92, ity than SMI and GNRI. These results suggested that atten-
p = 0.006; advanced age: aHR = 1.97, 95% CI 1.11–3.50, tion should be paid to the worse prognosis in patients with
p = 0.021; Table 3]. diabetes more than sarcopenia among HD patients.
We evaluated the impact of GNRI and SMI on all-cause HD patients tend to have a greater number of coronary
mortality in long-term follow-up in patients with or without risk factors such as diabetes, hypertension, and low HDL
HD (Supplemental Fig. 1). Although the GNRI and SMI cholesterol [22], and renal failure itself is also an important

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Heart and Vessels (2021) 36:1275–1282 1279

Table 3  Univariate and Covariate Univariate analysis Multivariate analysis

multivariate analysis of
predictors for all-cause Hazard ratio (95% CI) p value Hazard ratio (95% CI) p value
mortality in all patients
Hemodialysis 4.090 (2.538–6.591) < 0.001 2.430 (0.906–6.518) 0.078
Age ≧ 75 years 3.215 (2.391–4.323) < 0.001 1.970 (1.108–3.504) 0.021
Male 0.746 (0.530–1.049) 0.092 1.723 (0.792–3.749) 0.170
Diabetes 1.344 (0.964–1.873) 0.081 1.360 (0.822–2.251) 0.232
Low hemoglobin 3.887 (2.874–5.258) < 0.001 1.426 (0.793–2.567) 0.236
Low SMI 3.439 (2.473–4.783) < 0.001 2.388 (1.056–5.398) 0.036
Low GNRI 4.717 (3.285–6.773) < 0.001 2.211 (1.249–3.915) 0.006
Killip ≧ class 2 2.735 (1.881–3.977) < 0.001 1.524 (0.876–2.649) 0.136
Max CPK ≧ 3000 0.787 (0.529–1.171) 0.237
3 vessels disease 1.863 (1.264–2.746) 0.002 1.176 (0.645–2.146) 0.597

CI confidence interval, SMI skeletal muscle mass index, GNRI Geriatric nutritional risk index, CPK cre-
atine phosphokinase

Table 4  Univariate and Covariate Univariate analysis Multivariate analysis

multivariate analysis of
predictors for all-cause Hazard ratio (95% CI) p value Hazard ratio (95% CI) p value
mortality in HD patients
Age ≧ 75 years 1.674 (0.546–5.133) 0.368
Male 0.489 (0.251–1.937) 0.697
Diabetes 3.243 (1.126–9.338) 0.029 3.497 (1.120–10.918) 0.031
Low hemoglobin 0.147 (0.018–1.218) 0.076 0.212 (0.025–1.775) 0.152
Low SMI 1.359 (0.488–3.783) 0.557
Low GNRI 1.192 (0.369–3.846) 0.769
Killip ≧ class 2 2.775 (0.684–11.264) 0.153
Max CPK ≧ 3000 0.843 (0.154–4.605) 0.843
3 vessels disease 0.531 (0.173–1.631) 0.269

The abbreviations are the same as in Table 3

coronary risk factor [23]. A previous study reported that HD

Fig. 3  Kaplan–Meier curve for all-cause mortality among 4 groups
(HD −/+ and diabetes −/+). HD patients with diabetes had signifi-
cantly higher incidence of all-cause mortality than without diabetes
(Log-rank test: p = 0.022)
patients was higher incident of heart failure or cardiogenic
shock, therefore the in-hospital prognosis of HD patients
after PCI was worse than that of non-HD patients [24]. The
results of the present analysis were similar: in-hospital mor-
tality was higher among HD patients, and HD patients also
had a higher rate of multi-vessel disease and higher Killip
class than non-HD patients. Meanwhile, our data show that
long-term mortality in HD patents was worse than non-HD
patients, and diabetes was the most important factor in the
long-term prognosis of HD patients. This result is reasonable
because diabetes is a strong contributor of atherosclerosis,
which leads to death through the onset of CVD [25], and it
takes a relatively long time to involve in the events. Although
the present study did not investigate the duration of diabetes
or the cause of HD initiation, most HD patients with diabetes
tend to have a long duration of diabetes meaning that they
would also likely have more severe arteriosclerosis. A large

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1280
cohort study on HD patients with AMI showed that the most
powerful independent predictors of mortality from cardiac
causes were older age and diabetic nephropathy [5]. In addi-
tion, diabetes is not only a risk factor for arteriosclerosis,
but a major prognostic factor for diseases such as infectious
disesase and malignant disease [26, 27].
Sarcopenia has characterized by the loss of fat-free mass,
meaning the loss of skeletal muscle mass [28], and patients
with malnutrition decreased not only skeletal muscle but
also fat mass [29]. A previous study showed that sarcope-
nia and malnutrition share similar etiological factors, such
as reduced food intake, inflammation, hormonal changes,
increased energy requirements, and reduced physical activity
[30]. Some studies have shown that HD patients with ACS
undergoing PCI also had worse long-term prognosis than
non-HD patients [31, 32]. However, these reports did not
evaluate the sarcopenia and malnutrition indexes.
GNRI is more accurate than other nutritional tools for
identifying HD patients at nutritional risk [14]. A previous
study showed that low GNRI was strongly associated with
worse long-term clinical outcomes in patients with CVD
[33] who had undergone PCI [34], though non-HD patients
were also included in this study. In the present study, low
SMI and GNRI among ACS patients undergoing PCI were
independently and significantly associated with all-cause
mortality after adjustment for the covariates. In addition,
a previous report in HD patients after ACS has suggested
that low BMI was associated with poor prognosis [35].
However, in the present study we found that sarcopenia and
malnutrition indexes were not an independent risk factor for
long-term all-cause mortality among HD patients with ACS.
Since sarcopenia and malnutrition were involved in HD and
associated with various factors such as age [36, 37], diabetes
[38, 39], and renal dysfunction [40, 41]; the impact of these
syndromes might be diminished when compared among HD
patients. Indeed, a previous study has reported that diabe-
tes was an independent risk factor for all-cause mortality in
HD patients, but sarcopenia was not [15]. Malnutrition and
sarcopenia are known to contribute to long-term mortality
among HD patients; however, factors related to arterioscle-
rosis such as diabetes, may be more important for long-term
prognosis in HD patients with ACS after PCI.
On the other hand, our results showed that diabetes was
less associated with the long-term prognosis than sarcope-
nia and malnutrition in non-HD patients, and these were
different results in HD patients. Usually, strict secondary
prevention is performed after ACS in contemporary era.
Especially, diabetic patients with dyslipidemia is actively
intervened because these patients tend to develop the
CVD [42]. One of the reasons for the different results of
long-term prognosis factors might be the impact of cardio-
protective drugs such as statin, renin-angiotensin system
inhibitor, and beta-blocker because non-HD patients with
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Heart and Vessels (2021) 36:1275–1282
diabetes tended to use cardioprotective drugs including
statin more frequently than non-HD patients without dia-
betes in this study (Supplemental Table 1).
Although in our study ACS patients with HD had a
significantly higher in-hospital mortality and long-term
mortality than ACS patients without HD, Cox regression
analysis showed HD was not independently associated
with long-term mortality after adjusting for covariates.
One of the possible reasons is that these covariates such
as age, SMI and GNRI were strongly associated with long-
term mortality and may have been loosely associated with
HD (significant collinearity was not recognized).
This study has several limitations. First, because it
involved a single-center analysis, the number of subjects
was quite small. Therefore, the statistical power may have
been somewhat low. Hence, a large-scale, multi-center
study is necessary to confirm the results of this study. Sec-
ond, this registry does not evaluate the frailty scale and/
or exercise tolerance indicator, and therefore, the impact
of these factors on long-term prognosis is not clear in
ACS patients with HD. Third, since both SMI and GNRI,
which are indicators of sarcopenia and malnutrition, are
calculated with body weight, they may include many fac-
tors that body weight relates to. Therefore, we checked
the multicollinearity of the multivariate analysis, and all
variance inflation factors are less than 10.0 on this analy-
sis. Although there is some interaction between GNRI and
SMI on multivariate analysis, we believe that using SMI
and GNRI in multivariate analysis at the same time is rea-
sonable. Fourth, the present study did not fully include
factors related to prognosis of myocardial infarction,
because data collection such as prevalence of peripheral
artery disease, door-to balloon time, and left ventricular
ejection fraction at discharge was insufficient. Finally, only
body weight at admission is available in this study, and
the proper timing of body weight assessment is unknown.
There is also a lack of information on a dry weight of HD
patients. Despite these limitations, the long-term progno-
sis and the prognostic factors in HD patients with ACS
were statistically significant and thus clinically important.
In conclusion, HD patient with ACS had a significantly
higher in-hospital mortality and long-term mortality than
non-HD patients. Although sarcopenia and malnutrition
were related to mortality and were more common in HD
patients, sarcopenia and malnutrition had a lower impact
than diabetes on the long-term prognosis of ACS patients
with HD.
Supplementary Information The online version contains supplemen-
tary material available at https:​ //doi.org/10.1007/s00380​ -021-01815-​ 0.
Acknowledgements This research received no grant from any funding
agency in the public, commercial or not-for-profit sectors.
Heart and Vessels (2021) 36:1275–1282
Author contributions Author contribution is as follows; Conception
and design or analysis and interpretation of data: HK, MT, MF, YO,
and HF. Drafting of the manuscript or revising it critically for impor-
tant intellectual content: HK and MT. Final approval of the manuscript
submitted: KK.
Declarations
Conflict of interest All authors declare no conflicts of interest associ-
ated with this manuscript.
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