Guideline-Directed Medical Therapy for Elderly Patients With Acute Myocardial Infarction Who Undergo Percutaneous Coronary Intervention　― Insights From a Retrospective Observational Study ―

Abstract

Background: The efficacy of guideline-directed medical therapy (GDMT) in the elderly remains unclear. This study evaluated the impact of GDMT (aspirin or a P2Y₁₂ inhibitor, angiotensin-converting enzyme inhibitor or angiotensin receptor blocker, β-blocker, and statin) at discharge on long-term mortality in elderly patients with acute myocardial infarction (AMI) who had undergone percutaneous coronary intervention (PCI).

Methods and Results: Of 2,547 consecutive patients with AMI undergoing PCI in 2009–2020, we retrospectively analyzed 573 patients aged ≥80 years. The median follow-up period was 1,140 days. GDMT was prescribed to 192 (33.5%) patients at discharge. Compared with patients without GDMT, those with GDMT were younger and had higher rates of ST-segment elevation myocardial infarction and left anterior descending artery culprit lesion, higher peak creatine phosphokinase concentration, and lower left ventricular ejection fraction (LVEF). After adjusting for confounders, GDMT was independently associated with a lower cardiovascular death rate (hazard ratio [HR] 0.35; 95% confidence interval [CI] 0.16–0.81), but not with all-cause mortality (HR 0.77; 95% CI 0.50–1.18). In the subgroup analysis, the favorable impact of GDMT on cardiovascular death was significant in patients aged 80–89 years, with LVEF <50%, or with an estimated glomerular filtration rate ≥30 mL/min/1.73 m².

Conclusions: GDMT in patients with AMI aged ≥80 years undergoing PCI was associated with a lower cardiovascular death rate but not all-cause mortality.

Guideline-directed medical therapy (GDMT) for secondary prevention improves clinical outcomes in patients with acute myocardial infarction (AMI).^1–4 With an aging population, percutaneous coronary intervention (PCI) is being performed more often even in elderly patients with AMI,^5–8 and subsequent management of these patients has received increased attention. However, the effect of GDMT at discharge on mortality in elderly patients with AMI who undergo emergency PCI remains unclear because cardiovascular trials rarely include elderly patients, and guidelines are often based on the extrapolation of data from a substantially younger population.^5,9 Consequently, elderly patients are less likely to receive GDMT than younger patients.⁵ Japan, a rapidly aging society, has a large number of elderly patients with coronary artery disease.^6–8,10 Comprehensive information from Japan will be beneficial for developing perspectives on the use of GDMT in other countries.

Therefore, in the present study we investigated the impact of GDMT, which is a combination of aspirin or a P2Y₁₂ inhibitor, angiotensin-converting enzyme inhibitor (ACEi) or angiotensin receptor blocker (ARB), β-blocker, and statin, at discharge on long-term mortality in patients with AMI aged ≥80 years who underwent emergency PCI.

Methods

Study Population

This study was a retrospective single-center observational study in a tertiary hospital. Initially, 2,547 consecutive patients with Type 1 myocardial infarction (MI) who underwent emergency PCI at Miyazaki Medical Association Hospital between January 2009 and June 2020 were enrolled. AMI was diagnosed based on the universal definition of myocardial infarction (MI) recommended by the European Society of Cardiology (ESC) and the American College of Cardiology (ACC)/American Heart Association (AHA).¹¹ Emergency PCI was defined as procedures performed within 24 h after symptom onset. In this study, 1,906 patients aged <80 years and 68 patients who died during hospitalization were excluded; consequently, the study population consisted of 573 patients (Figure 1). Follow-up information was obtained from hospital charts or by contacting patients, family members, or referring physicians for up to 5 years. The median length of follow-up was 1,140 days (interquartile range [IQR] 544–1,733 days).

Figure 1.

Study flow chart. AMI, acute myocardial infarction; GDMT, guideline-directed medical therapy; PCI, percutaneous coronary intervention.

This study was conducted in accordance with the tenets of the Declaration of Helsinki and was approved by the Institutional Review Board of Miyazaki Medical Association Hospital (2020-16, 2022-51). The need to obtain written informed consent from study participants was waived because of the retrospective observational nature of this registry. However, details of the study were posted to inform the patients and to ensure that they had the opportunity to opt-out of the study.

Endpoints and Definitions

The primary outcomes of the study were all-cause mortality and cardiovascular death. GDMT for patients with AMI was defined according to the following 4 classes of drugs based on the recommendation of the ESC, ACC/AHA, and the Japanese Circulation Society guidelines: aspirin or a P2Y₁₂ inhibitor, ACEi or ARB, β-blocker, and statin.^1–4,12 These 4 classes of drugs were selected for GDMT because there were no major revisions to the guideline recommendations during the patient enrollment period.^1–4,12,13 Patients prescribed all 4 classes of drugs were then defined as receiving GDMT. The decision to prescribe GDMT was left to the discretion of each attending physician. Frailty at discharge was classified on the basis of impairments in walking, cognition, and basic activities of daily living, as reported previously.^14,15 Dual antiplatelet therapy was defined as the administration of 2 classes of antiplatelet drugs: aspirin, a P2Y₁₂ inhibitor, or other antiplatelet drugs, such as cilostazol.

Statistical Analysis

Categorical variables are presented as numbers and percentages. Continuous variables are presented as the median and IQR. Categorical variables were analyzed using the Chi-squared test or Fisher’s exact test as appropriate. Continuous variables were compared using the Mann-Whitney U test or Kruskal-Wallis test as appropriate. We used the Kaplan-Meier method to estimate the cumulative incidence of outcomes and assessed the difference between groups with the log-rank test. In addition, in order to avoid the selection bias of prescribing medicines by each attending physician, we used 2 multilevel mixed-effects multivariable Cox proportional hazards models using each physician as a random intercept to compare outcomes between the groups, with the results expressed as hazard ratios (HRs) with 95% confidence intervals (CIs). Model 1 was adjusted for variables with P<0.05 in Table 1; Model 2 was adjusted for clinically relevant variables (age, sex, estimated glomerular filtration rate [eGFR] <30 mL/min/1.73 m², peak creatine phosphokinase [CPK], and left ventricular ejection fraction [LVEF] at discharge).

Table 1.

Patient Characteristics

	Overall (n=573)	Non-GDMT (n=381; 66.5%)	GDMT (n=192; 33.5%)	P value
Baseline characteristics
Age (years)	85 [82–88]	85 [82–88]	83 [82–87]	0.014
Age ≥90 years	78 (13.6)	56 (14.7)	22 (11.5)	0.286
Male sex	275 (48.0)	184 (48.3)	91 (47.4)	0.839
Body weight (kg)	51.3 [45.0–58.9] (n=572)	50.5 [45.0–58.0] (n=380)	52.9 [47.0–60.0] (n=192)	0.080
Hypertension	465 (81.2)	311 (81.6)	154 (80.2)	0.682
Diabetes	150 (26.2)	102 (26.8)	48 (25.0)	0.649
Dyslipidemia	240 (41.9)	160 (42.0)	80 (41.7)	0.940
Previous MI	68 (11.9)	46 (12.1)	22 (11.5)	0.830
Previous stroke	76 (13.3)	55 (14.4)	21 (10.9)	0.244
eGFR (mL/min/1.73 m2)	51.7 [40.2–62.8]	50.6 [39.5–61.9]	53.1 [44.2–64.2]	0.062
eGFR <30 mL/min/1.73 m2	66 (11.5)	50 (13.1)	16 (8.3)	0.090
Peak CPK (IU/L)	883 [213–2,028] (n=570)	670 [189–2,022] (n=378)	1,102.5 [353–2,079.5] (n=192)	0.005
Peak CK-MB (IU/L)	91 [22–217] (n=553)	64 [20–222] (n=363)	120 [34– 217] (n=190)	0.010
BNP (pg/mL)	160.8 [61.3–530.5] (n=531)	175.6 [68.9–507.9] (n=344)	137.5 [48.0–563.3] (n=187)	0.400
STEMI	360 (62.8)	214 (56.2)	146 (76.0)	<0.001
Killip class 2/3/4	140 (24.4)	93 (24.4)	47 (24.5)	0.985
GRACE risk score	178 [158–198]	178 [158–198]	179 [159–198]	0.714
LVEF at discharge (%)	54.0 [45.8–62.4] (n=541)	55.2 [46.1–64.0] (n=353)	53.0 [45.0–59.6] (n=188)	0.026
Frailty at discharge	218 (38.0)	151 (39.6)	67 (34.9)	0.270
Angiographic characteristics
Infarct-related artery location				0.008
Right coronary artery	180 (31.4)	123 (32.3)	57 (29.7)
Left main coronary artery	23 (4.0)	21 (5.5)	2 (1.0)
Left anterior descending artery	287 (50.1)	176 (46.2)	111 (57.8)
Left circumflex	83 (14.5)	61 (16.0)	22 (11.5)
3-vessel disease	119 (20.8)	88 (23.1)	31 (16.1)	0.053
Stent use	526 (91.8)	350 (91.9)	176 (91.7)	0.935
Final TIMI flow grade 3	532 (92.8)	357 (93.7)	175 (91.1)	0.263
Medication at discharge
Aspirin or P2Y12 inhibitor	570 (99.5)	378 (99.2)	192 (100.0)	0.218
Aspirin	561 (97.9)	371 (97.4)	190 (99.0)	0.212
P2Y12 inhibitor	541 (94.4)	355 (93.2)	186 (96.9)	0.069
Dual antiplatelet therapy	555 (96.9)	367 (96.3)	188 (97.9)	0.303
ACE inhibitor or ARB	376 (65.6)	184 (48.3)	192 (100.0)	<0.001
β-blocker	285 (49.7)	93 (24.4)	192 (100.0)	<0.001
Statin	481 (83.9)	289 (75.9)	192 (100.0)	<0.001
No. guideline-directed medications				<0.001
1	30 (5.2)	30 (7.9)	0 (0.0)
2	139 (24.3)	139 (36.5)	0 (0.0)
3	212 (37.0)	212 (55.6)	0 (0.0)
4	192 (33.5)	0 (0.0)	192 (100.0)

Unless indicated otherwise, data are expressed as n (%) or the median [interquartile range]. ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; BNP, B-type natriuretic peptide; CK-MB, creatine kinase-myocardial band; CPK, creatine phosphokinase; eGFR, estimated glomerular filtration rate; GDMT, guideline-directed medical therapy; GRACE, Global Registry of Acute Coronary Events; LVEF, left ventricular ejection fraction; MI, myocardial infarction; STEMI, ST-segment elevation myocardial infarction; TIMI, Thrombolysis in Myocardial Infarction.

All analyses were performed using STATA 18 (StataCorp LLC, College Station, TX, USA). All tests were 2-tailed, and P<0.05 was considered statistically significant.

Results

Baseline Characteristics

The characteristics of the patients are presented in Table 1. The overall median age of the 573 patients was 85 years (IQR 82–88 years), 275 (48.0%) patients were male, and 360 (62.8%) patients had ST-segment elevation myocardial infarction (STEMI). The median eGFR and LVEF at discharge were 51.7 mL/min/1.73 m² (IQR 40.2–62.8 mL/min/1.73 m²) and 54.0% (IQR 45.8–62.4%), respectively. The prescription rates were 99.5% for aspirin or a P2Y₁₂ inhibitor, 65.6% for an ACEi or ARB, 49.7% for a β-blocker, and 83.9% for a statin.

GDMT was prescribed to 192 (33.5%) patients at discharge (Figure 1; Table 1). Compared with patients not receiving GDMT, those with GDMT were younger and had higher rates of STEMI and left anterior descending artery (LAD) culprit lesion, higher levels of peak CPK and creatine kinase-myocardial band isoenzyme (CK-MB), and lower LVEF. There was no significant difference in B-type natriuretic peptide (BNP) concentrations, eGFR, and frailty status between the 2 groups. Regarding medication at discharge, prescription rates of an ACEi or ARB, β-blocker, and statin were higher in the GDMT than non-GDMT group, but there were no significant differences in the prescription rates of aspirin or a P2Y₁₂ inhibitor (Table 1).

We compared patient characteristics according to the number of medications (1–4) included in GDMT (Supplementary Table). In the 1-drug group, 93.3% of patients received aspirin or a P2Y₁₂ inhibitor. Compared with the other groups, more patients in the 1-drug group had a lower eGFR, higher BNP, frailty, left main coronary artery culprit lesion, and final Thrombolysis in Myocardial Infarction (TIMI) flow grade <3. Concentrations of CPK and CK-MB were higher in the 1- and 4-drug (GDMT) groups, and the rates of STEMI and LAD culprit lesions were higher in the 4-drug (GDMT) group. Age, sex, the Global Registry of Acute Coronary Events (GRACE) risk score, and LVEF did not differ significantly among the 4 groups.

Outcomes

The respective cumulative 5-year incidence rates of all-cause death and cardiovascular death were 27.8% and 11.4% in the overall sample, 22.6% and 5.5% in patients with GDMT, and 30.4% and 14.2% in those without GDMT. The median length of follow-up did not differ significantly between the GDMT and non-GDMT groups (1,138 [IQR 639.5–1,716.5] vs. 1,145 [IQR 523–1,750] days, respectively; P=0.665). Kaplan-Meier analyses showed that the cumulative 5-year incidence of cardiovascular death was significantly lower in the GDMT than non-GDMT group (log-rank P=0.007), but there were no significant differences in all-cause mortality (log-rank P=0.110) and non-cardiovascular death (log-rank P=0.929) between the 2 groups (Figure 2). In addition, the analysis was conducted by the number of drugs included in GDMT. The cumulative 5-year incidence of all-cause mortality (log-rank P<0.001) and cardiovascular death (log-rank P=0.002) decreased as the number of drugs increased (Supplementary Figure 1).

Figure 2.

Kaplan-Meier curves for all-cause mortality, cardiovascular death, and non-cardiovascular death. GDMT, guideline-directed medical therapy.

On multivariable Cox proportional hazards analysis, GDMT was independently associated with a lower cardiovascular death rate (Model 1: adjusted [a] HR 0.35, 95% CI 0.16–0.81; Model 2: aHR 0.36, 95% CI 0.16–0.80), but not with all-cause mortality (Model 1: aHR 0.77, 95% CI 0.50–1.18; Model 2: aHR 0.76, 95% CI 0.50–1.15; Table 2). Moreover, multivariable Cox proportional hazards analysis using the number of drugs as variables also showed that the use of ≥2 drugs was associated with significantly lower all-cause mortality and cardiovascular deaths compared with the use of only 1 drug (Table 2).

Table 2.

Multivariable Cox Proportional Hazards Analyses for All-Cause Mortality and Cardiovascular Death

	Univariate		Model 1A		Model 2B
	HR (95% CI)	P value	HR (95% CI)	P value	HR (95% CI)	P value
All-cause mortality
GDMT (vs. non-GDMT)	0.73 (0.49–1.09)	0.127	0.77 (0.50–1.18)	0.235	0.76 (0.50–1.15)	0.190
No. drugs
1	Reference	–	Reference	–	Reference	–
2 (vs. 1 drug)	0.36 (0.20–0.66)	0.001	0.31 (0.15–0.60)	0.001	0.36 (0.18–0.71)	0.003
3 (vs. 1 drug)	0.25 (0.14–0.46)	<0.001	0.23 (0.12–0.46)	<0.001	0.26 (0.13–0.50)	<0.001
4 (vs. 1 drug)	0.24 (0.13–0.45)	<0.001	0.23 (0.11–0.46)	<0.001	0.25 (0.12–0.49)	<0.001
Cardiovascular death
GDMT (vs. non-GDMT)	0.35 (0.15–0.77)	0.010	0.35 (0.16–0.81)	0.013	0.36 (0.16–0.80)	0.013
No. drugs
1	Reference	–	Reference	–	Reference	–
2 (vs. 1 drug)	0.40 (0.16–0.97)	0.044	0.31 (0.13–0.78)	0.013	0.38 (0.15–0.96)	0.041
3 (vs. 1 drug)	0.26 (0.11–0.63)	0.003	0.18 (0.07–0.45)	<0.001	0.20 (0.08–0.51)	0.001
4 (vs. 1 drug)	0.12 (0.04–0.35)	<0.001	0.09 (0.03–0.28)	<0.001	0.11 (0.04–0.32)	<0.001

^AAdjusted for variables with P<0.05 in Table 1. ^BAdjusted for clinically relevant variables: age, sex, estimated glomerular filtration rate <30 mL/min/1.73 m², peak creatine phosphokinase, and left ventricular ejection fraction at discharge. CI, confidence interval; GDMT, guideline-directed medical therapy; HR, hazard ratio.

We then assessed the effect of each type of medication after discharge. ACEi or ARB (aHR 0.45; 95% CI 0.30–0.67) and statin (aHR 0.57; 95% CI 0.36–0.91) were associated with lower all-cause mortality (Model 1). In addition, aspirin or a P2Y₁₂ inhibitor (aHR 0.12; 95% CI 0.02–0.92), ACEi or ARB (aHR 0.22; 95% CI 0.11–0.41), and statin (aHR 0.38; 95% CI 0.20–0.74) were independently associated with a lower cardiovascular death rate (Model 1; Figure 3).

Figure 3.

Effect of each guideline-directed medication on outcomes. Adjusted for variables with P<0.05 in Table 1 (Model 1). ACEi, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; CI, confidence interval; GDMT, guideline-directed medical therapy; HR, hazard ratio.

Selected Subgroup Analyses

We assessed the consistency of the effect of GDMT on outcomes among 9 subgroups (Figure 4; Supplementary Figure 2). HRs in Figure 4 and Supplementary Figure 2 were adjusted by Models 1 and 2, respectively. The effect of GDMT on cardiovascular death, compared with non-GDMT, was generally consistent. In particular, there was significant protection against cardiovascular death in patients aged 80–89 years, patients with reduced LVEF, eGFR ≥30 mL/min/1.73 m², frailty, or non-3-vessel disease, or patients who were male.

Figure 4.

Subgroup analysis of the effect of guideline-directed medical therapy (GDMT) on outcomes. Adjusted for variables with P<0.05 in Table 1 (Model 1). CI, confidence interval; CPK, creatine phosphokinase; eGFR, estimated glomerular filtration rate; HR, hazard ratio; LAD, left anterior descending artery; LMCA, left main coronary artery; LVEF, left ventricular ejection fraction; STEMI, ST-segment elevation myocardial infarction.

Discussion

The major findings of this study are as follows: (1) among 573 patients with AMI aged ≥80 years discharged after undergoing emergency PCI, 192 (33.5%) patients received GDMT; (2) patients receiving GDMT were younger, had higher rates of STEMI and LAD culprit lesion, had a higher level of peak CPK, and had a lower LVEF; (3) GDMT at discharge was independently associated with a lower cardiovascular death rate but not with decreased all-cause mortality; and (4) the favorable impact of GDMT on cardiovascular death was significant in patients aged 80–89 years, patients with reduced LVEF, high eGFR, frailty, or non-3-vessel disease, or patients who were male.

Several studies have shown that GDMT is associated with low in-hospital mortality and favorable long-term outcomes in patients with AMI.^{1–4,12,16,17} A national cohort study from the UK also demonstrated that quality indicators, including prescription rates of GDMT, are associated with mortality rates.¹⁸ Thus, GDMT (aspirin, β-blocker, ACEi/ARB, and high-intensity statin at discharge) is included in the quality indicators of AHA STEMI-receiving facilities.⁴ Meanwhile, the management of elderly patients with AMI is a topic of interest in this era of worldwide aging populations, and there has clearly been an increase in the number of patients undergoing PCI in recent years.^5–8,19 The care of elderly patients with AMI is complicated by the increased atherothrombotic and thromboembolic risks, as well as the bleeding risk, compared with younger patients, and by the complexity of geriatric syndrome, which involves frailty, multimorbidity, and polypharmacy.^5,20 However, the efficacy of GDMT at discharge for elderly patients with AMI is not well studied because these patients are often excluded from clinical trials due to concerns about comorbidities, functional status, cognition, and limited life expectancy.^5,9,20,21 Consequently, it has been reported that elderly patients, compared with younger patients, do not receive adequate GDMT.^5,19,21 Indeed, only approximately one-third of elderly patients in the present study received GDMT. In the present study, the proportion of patients aged ≥80 years among all patients with AMI who underwent PCI was as high as 25.2%. This proportion is comparable to that of the largest nationwide Japanese AMI registry, in which 23.6% of patients were aged ≥80 years,⁵ suggesting that our data closely reflect the current status of patients with AMI in Japan, a superaging society. This study shows that patients receiving GDMT are younger and have higher rates of STEMI and LAD culprit lesions, a higher level of peak CPK, and a lower LVEF than those not receiving GDMT. In addition, the group receiving only 1 drug had a lower eGFR and more frailty than the other groups. Moreover, the present study also demonstrates that GDMT at discharge is independently associated with a lower cardiovascular death rate, but not with decreased all-cause mortality. In addition, with regard to non-cardiovascular death, there was no significant difference between the GDMT and non-GDMT groups. Our results support those of previous studies^{5,8,9,19–21} and indicate that although pharmacologic management of elderly patients with AMI remains challenging because of the need to consider non-cardiac factors, advanced age alone should not preclude potentially beneficial GDMT.

The benefit of GDMT on cardiovascular death, but not on all-cause mortality, was consistent in the broad population studied other than those aged ≥90 years. In the subgroup analysis of the present study, GDMT was significantly effective in reducing cardiovascular death in patients aged 80–89 years, with lower LVEF, eGFR ≥30 mL/min/1.73 m², frailty, and non-3-vessel disease, and in males. The number and complexity of comorbid conditions commonly increase with advancing age, such that AMI in very elderly adults typically occurs in the context of multimorbidity, which affects mortality.^5,22 We should avoid unnecessary polypharmacy and select elderly patients for whom GDMT is appropriate. The After Eighty study showed that the efficacy of an invasive strategy for elderly patients with non-STEMI or unstable angina is diluted with increasing age and its efficacy is not apparent in those aged ≥90 years.²³ Such age-related dilution of efficacy may also occur in patients aged ≥90 years receiving GDMT. In contrast, GDMT in general is the cornerstone of treatment for patients with AMI with low LVEF and large MI.^1–3,12 A recent study demonstrated that among elderly patients hospitalized with heart failure with reduced ejection fraction, β-blocker and/or renin-angiotensin system inhibitor use at discharge was associated with lower rates of 30-day and 1-year mortality across all age groups.²⁴ Our findings support this evidence and suggest that GDMT is also applicable to elderly patients with AMI with low LVEF. Chronic kidney dysfunction is one of the most common and strongest independent predictors of mortality in all cardiovascular diseases.^5,21,22 A higher eGFR allows for the safe use of ACEi or ARB and reduces the risks of drug interactions, hyperkalemia, and unexpected adverse effects. Meanwhile, because the use of a β-blocker did not independently affect clinical outcomes in the present study, it may be possible to omit this prescription in elderly patients with bradycardia or polypharmacy concerns. Further large-scale studies are needed to clarify which subgroups benefit from GDMT among patients with AMI aged ≥80 years who undergo PCI.

Study Limitations

This study has several limitations. First, this was a retrospective single-center observational study with a relatively small sample size, not a randomized controlled trial. Data on valvular disease were also not available. Therefore, there may be selection bias and unmeasured confounders. The decision to prescribe GDMT was left to the discretion of each attending physician. In fact, several variables were not well balanced between the GDMT and non-GDMT groups. Some patients may not have received GDMT because their condition or comorbidities were too advanced. Second, we evaluated only GDMT at discharge, and data on adherence to GDMT and GDMT in the chronic phase, which may affect outcomes, were not available. Recently, Lee et al reported that adherence to GDMT is associated with a lower incidence of major adverse cardiovascular events during a 3-year follow-up.¹⁶ Third, updates of guidelines for patients with AMI and those with heart failure during this study period may have affected outcomes. Because patients were enrolled through June 2020, we could not assess the effect of newer agents, such as sodium–glucose cotransporter 2 inhibitors and sacubitril/valsartan, recently added to the guidelines for heart failure.²⁵ Finally, we did not evaluate rehospitalization for non-fatal MI or heart failure as an endpoint. Further studies are needed to determine whether GDMT will reduce these adverse events even in elderly patients with AMI.

Conclusions

This study found that GDMT, which is a combination of aspirin or a P2Y₁₂ inhibitor, an ACEi or ARB, a β-blocker, and a statin at discharge, is associated with a lower cardiovascular death rate but not with decreased all-cause mortality in patients with AMI aged ≥80 years who undergo PCI.

Sources of Funding

No funds were received for this study.

Disclosures

None declared.

IRB Information

This study was approved by the Institutional Review Board of Miyazaki Medical Association Hospital (2020-16, 2022-51).

Data Availability

The deidentified participant data will not be shared.

Supplementary Files

Please find supplementary file(s);

https://doi.org/10.1253/circj.CJ-23-0837

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