Association Between Extracorporeal Cardiopulmonary Resuscitation and Prognosis in the Short and Long Term in Patients With Acute Myocardial Infarction Complicated by Refractory Cardiac Arrest

Abstract

Background: Although extracorporeal cardiopulmonary resuscitation (ECPR) is expected to improve outcomes in patients with cardiac arrest (CA), its impact on prognosis in acute myocardial infarction (MI) patients complicated by CA remains unclear. This study aimed to investigate the short- and long-term effects of ECPR on prognosis in these patients.

Methods and Results: This single-center, retrospective study analyzed consecutive MI patients. Patients were classified into 3 groups: CA requiring ECPR (ECPR group); CA achieving return of spontaneous circulation without ECPR (CCPR group); and without CA (non-CA group). The primary endpoint was 30-day mortality, while long-term all-cause mortality, cardiovascular death, and major adverse cardiovascular events were evaluated among discharged patients. Of the 625 patients analyzed, 57 were in the ECPR group, 104 in the CCPR group, and 464 in the non-CA group. Multivariable analysis revealed that the ECPR group had a significantly higher prevalence of 30-day mortality than the CCPR group (adjusted hazard ratio [HR] 3.99; 95% confidence interval [CI] 2.23–7.13) and the non-CA group (HR 43.48; 95% CI 19.70–95.92). However, there were no significant differences in long-term outcomes among the 3 groups.

Conclusions: The 30-day mortality was worse in the ECPR group than in the CCPR or non-CA groups. In contrast, the long-term prognosis was comparable among discharged patients, regardless of the presence of CA or the need for ECPR.

Cardiac arrest (CA) is a serious complication of acute myocardial infarction (MI). Although the mortality of acute MI has declined in past decades,^1,2 prognosis remains poor when complicated by CA.^3–6 CA due to MI is often not resuscitated until coronary reperfusion is achieved, but revascularization is difficult in the case of sustained CA.

Resuscitation in which circulatory collapse is temporally replaced by venoarterial extracorporeal cardiopulmonary membrane oxygenation (ECMO), that is, extracorporeal cardiopulmonary resuscitation (ECPR), is potentially effective for refractory CA. The benefit of ECPR still remains controversial,⁷ although randomized trials demonstrated that ECPR could improve clinical outcomes compared with conventional cardiopulmonary resuscitation (CCPR).^8,9 ECPR is recommended in a limited manner to be considered as a rescue therapy for CA patients for whom the suspected etiology is potentially reversible.^10,11

Acute MI is recognized as one of the reversible causes of CA and a typical indication for ECPR.^12,13 In contrast, the prognosis of MI patients worsens with increasing reperfusion time.¹⁴ The time loss in establishing extracorporeal circulation may lead to an increase in the extent of irreversible infarction. Furthermore, ECMO increases left ventricular workload and wall stress, which exacerbates ischemia-reperfusion injury and increases infarct size.¹⁵ For these reasons, the use of ECMO for acute MI may cause cardiac dysfunction and impact not only short-term but also long-term outcomes. However, the prognostic impact of ECPR on acute MI has not been fully clarified.

To address this gap in knowledge, the aim of this study was to elucidate the short- and long-term prognosis of acute MI patients complicated by refractory CA who were resuscitated using ECPR.

Methods

Study Patients

This is a single-center, retrospective, observational study. We retrospectively analyzed all consecutive patients who were diagnosed with acute MI using coronary angiography and received revascularization between January 2009 and December 2020 at the Cardiovascular Division, National Hospital Organization Osaka National Hospital. Acute MI was defined according to the fourth universal definition of MI.¹⁶ We divided those patients into 3 groups: acute MI with CA that required ECPR (ECPR group); acute MI with CA that achieved return of spontaneous circulation (ROSC) without ECPR (CCPR group); and acute MI without CA (non-CA group). This study was approved by the Osaka National Hospital Institutional Review Board #2 (approval no. 19097). Informed consent was not required because this study was a retrospective study.

ECPR and Post-Resuscitation Care

Basic selection criteria for ECPR in Osaka National Hospital were witnessed CA patients of age <75 years and an initial rhythm of ventricular fibrillation or pulseless ventricular tachycardia who did not achieve ROSC after CCPR, although the indication was rather expanded by the judgment of board-certified emergency physicians on each case. ECPR was not performed for patients with end-stage diseases. If patients showed no sign of life at all, cardiopulmonary resuscitation (CPR) was terminated in the emergency department without further examinations such as cardiac catheterization. Venoarterial ECMO, that is, percutaneous cardiopulmonary support system (PCPS),³ consists of a centrifugal pump and a circuit with a membrane oxygenator (CAPIOX, Terumo Corporation, Tokyo, Japan; or MERA, Senko medical instrument, Tokyo, Japan). Percutaneous cannulation was performed in the femoral vessels with an 18–20 French arterial cannula and a 20–22 French venous cannula. Coronary angiography was performed immediately after initiation of ECMO. Therapeutic hypothermia was performed in unconscious patients after ROSC (target 34℃ for 24–48 h). In cases with an unstable hemodynamic state or complications of hypothermia, temperature management to 36℃ was allowed instead of 34℃.

Data Collection and Follow up

All patient data, including age, sex, ST-segment elevation MI (STEMI), comorbidities, medications, laboratory data, and angiography data, were retrospectively collected from clinical records. Hypertension was defined as blood pressure >140/90 mmHg or the use of antihypertensive drugs. Hypercholesterolemia was defined as low-density lipoprotein cholesterol >140 mg/dL or the use of cholesterollowering drugs. Diabetes was defined as HbA1c (National Glycohemoglobin Standardization Program [NGSP]) ≥6.5% or the use of oral drugs for diabetes or insulin therapy. In addition, out-of-hospital CA, bystander CPR, and initial rhythm were collected in patients with CA. Low-flow duration, which was defined as the interval from initiation of any CPR to initiation of ECMO, was also collected in patients who received ECPR. Clinical outcomes, including cardiovascular (CV) death, recurrent MI, hospitalization for worsening heart failure, and stroke, were collected from the clinical records up to the last visit within 5 years or the date of death.

Clinical Outcomes

The primary outcome was 30-day mortality. The secondary outcomes included all-cause mortality, CV death, and major adverse cardiovascular events (MACE) within 5 years after discharge. MACE was defined as the composite of CV death, recurrent MI, hospitalization for worsening heart failure, and stroke. CV events were defined according to the previous consensus report on cardiovascular and stroke endpoint.¹⁷

Statistical Analysis

Continuous variables were expressed as median with interquartile range and were analyzed using the Mann-Whitney U-test or the Kruskal-Wallis rank sum test. Categorical variables were expressed as frequency and compared using the chi-square, Fisher’s exact, or Fisher-Freeman-Halton tests. The Kaplan-Meier method was used to estimate the cumulative incidence of events, and differences among the 3 groups were assessed using the log-rank test. Univariable and multivariable Cox proportional hazard models were used to assess the risk of 30-day mortality, as well as long-term mortality, CV death, and MACE after discharge, with results expressed as hazard ratio (HR) and 95% confidence interval (CI). The multivariable model for 30-day mortality was adjusted for relevant variables, including age, sex, hypercholesterolemia, STEMI, and estimated glomerular filtration rate.^18,19 Additionally, the multivariable model for long-term outcomes was adjusted for these variables along with discharge medications (β-blockers, ACE inhibitors/ARBs, and statins).²⁰ All statistical analysis was regarded as significant when the P value was <0.05. Post-hoc multiple comparisons were made using Bonferroni correction. Statistical analysis was performed using IBM SPSS Statistics version 27 software (IBM Corp., Armonk, NY, USA) and R software version 4.4.0 (The R Foundation for Statistical Computing, Vienna, Austria).

Results

Patient Characteristics

Among 641 patients who were confirmed as type I acute MI using coronary angiography during the study period, 625 patients were eligible for our analysis. Of those patients, 161 were complicated by CA, of which 57 required ECPR (ECPR group) and 104 achieved ROSC without ECPR (CCPR group; Figure 1). The clinical characteristics of the study patients are presented in Table 1. Patients in the ECPR and CCPR groups were younger than those in the non-CA group. Renal failure and a culprit lesion in the left main coronary artery were more frequent in the ECPR and CCPR groups than in the non-CA group. STEMI and having a chronic total occlusion in a non-infarct-related artery were more frequent in the ECPR group than in the non-CA group. Peak creatine kinase (CK) and CK-myocardial band fraction were highest in the ECPR group. Overall, door-to-balloon time was the longest in the non-CA group. However, among the STEMI patients, it was longer in the ECPR group (median 118 min) compared with the CCPR (104 min) and non-CA (109 min) groups.

Figure 1.

Flow diagram of study patients. CA, cardiac arrest; CCPR, conventional cardiopulmonary resuscitation; ECPR, extracorporeal cardiopulmonary resuscitation; MI, myocardial infarction; ROSC, return of spontaneous circulation.

Table 1.

Baseline Characteristics at Admission

	ECPR (n=57)	CCPR (n=104)	Non-CA (n=464)	P value
Age (years)	60 [48–68]a	65 [53–71]b	70 [61–79]	<0.001
Sex, male	52 (91)	93 (89)	370 (80)	0.012
STEMI	51 (90)a	78 (75)	326 (70)	0.008
Cardiogenic shock	57 (100)a,c	51 (49)b	27 (6)	<0.001
OHCA	53 (93)	98 (94)	–	0.744
Bystander CPR	38 (67)	66 (64)	–	0.684
Initial rhythm
VT/VF	48 (84)	80 (77)	–	0.273
PEA	7 (12)	18 (17)	–	0.400
Asystole	2 (4)	6 (6)	–	0.713
Low-flow duration (min)	51 [41–64]	–	–	–
Comorbidities
Hypertension	24 (42)a	63 (61)	314 (68)	0.001
Hypercholesterolemia	22 (39)	38 (37)b	246 (53)	0.003
Diabetes	24 (42)	41 (39)	159 (34)	0.358
Current smoking	31 (54)a,c	25 (24)	163 (35)	0.001
Medications on admission
β-blockers	8 (14)	15 (14)	63 (14)	0.973
ACE inhibitors/ARB	19 (33)	30 (29)	165 (36)	0.422
Calcium-channel antagonists	13 (23)a	25 (24)b	190 (41)	<0.001
Statins	11 (19)	22 (21)	133 (29)	0.125
Aspirin	11 (19)	20 (19)	123 (27)	0.184
P2Y12 antagonists	4 (7)	18 (17)	46 (10)	0.056
Oral anticoagulants	4 (7)	6 (6)	22 (5)	0.723
Laboratory data
Hemoglobin (g/dL)	13.8 [12.2–15.4]	13.3 [11.9–15.1]	13.9 [12.3–15.1]	0.490
eGFR (mL/min/1.73 m2)	54 [38–62]a	48 [36–67]b	63 [46–76]	<0.001
HbA1c (%)	6.1 [5.7–6.9]	6.0 [5.6–6.8]	5.9 [5.6–6.6]	0.384
CK on arrival (U/L)	145 [103–233]	144 [85–285]	166 [93–469]	0.173
CK-MB on arrival (U/L)	32 [18–65]a	30 [21–49]b	10 [4–30]	<0.001
Peak CK (U/L)	7,176 [2,169–14,254]a,c	2,019 [827–4,843]b	849 [282–2,213]	<0.001
Peak CK-MB (U/L)	550 [238–1,143]a,c	205 [60–490]b	69 [17–215]	<0.001
Culprit lesion of MI
Left main coronary	9 (16)a	12 (12)b	21 (5)	0.001
Left anterior descending	30 (53)	47 (45)	220 (47)	0.662
Left circumflex	7 (12)	16 (15)	77 (17)	0.691
Right coronary	13 (29)	29 (28)	155 (33)	0.182
Multivessel disease	32 (56)	51 (49)	251 (54)	0.590
Triple vessel disease	12 (21)	28 (27)	98 (21)	0.427
Chronic total occlusion	15 (26)a	18 (17)	43 (9)	<0.001
Successful reperfusion	47 (83)a	96 (92)	440 (95)	0.002
Door-to-balloon time (min)	117 [90–145]a	109 [73–138]b	144 [87–418]	<0.001
Revascularization by PCI	57 (100)	99 (95)b	459 (99)	0.035
Outcomes
30-day mortality	27 (47)a,c	26 (25)b	13 (3)	<0.001
CPC 1 or 2 at 30 days	19 (33)a,c	65 (63)b	451 (97)	<0.001

Values are presented as median [interquartile range] or n (%). ^aP<0.017, ECPR vs. Non-CA. ^bP<0.017, CCPR vs. Non-CA. ^cP<0.017, ECPR vs. CCPR. ACE, angiotensin-converting enzyme; ARB, angiotensin II receptor blockers; CA, cardiac arrest; CCPR, conventional cardiopulmonary resuscitation; CK, creatine kinase; CK-MB, creatine kinase-myocardial band; CPC, Cerebral Performance Category; CPR, cardiopulmonary resuscitation; ECPR, extracorporeal cardiopulmonary resuscitation; eGFR, estimated glomerular filtration rate; HbA1c, glycosylated hemoglobin; MI, myocardial infarction; OHCA, out-of-hospital cardiac arrest; PCI, percutaneous coronary intervention; PEA, pulseless electrical activity; STEMI, ST-segment elevation myocardial infarction; VF, ventricular fibrillation; VT, ventricular tachycardia.

Short-Term Mortality

At 30 days, there was a total of 66 (10.6%) deaths: 27 (47.4%) in the ECPR group; 26 (25.0%) in the CCPR group; and 13 (2.8%) in the non-CA group (Table 1). Figure 2 shows the Kaplan-Meier curves for 30-day mortality. A significant difference in 30-day mortality was observed among the groups (overall P<0.001). In the multivariable analysis, patients in the ECPR group demonstrated a significantly higher prevalence of 30-day mortality compared with those in the non-CA group (adjusted HR 43.48; 95% CI 19.70–95.92; P<0.001) and the CCPR group (HR 3.99; 95% CI 2.23–7.13 ; P<0.001; Table 2).

Figure 2.

Kaplan-Meier analysis of 30-day mortality. The Kaplan-Meier curves for 30-day mortality among the 3 groups are shown. Patients in the extracorporeal cardiopulmonary resuscitation (ECPR) group had significantly worse outcomes than those in the other 2 groups. CA, cardiac arrest; CCPR, conventional cardiopulmonary resuscitation; CI, confidence interval; HR, hazard ratio.

Table 2.

Predictive Factors of 30-Day Mortality

	Univariable analysis		Multivariable analysis
	HR (95% CI)	P value	HR (95% CI)	P value
ECPR
vs. CCPR	2.33 (1.36–3.99)	0.002	3.99 (2.23–7.13)	<0.001
vs. non-CA	23.31 (12.01–45.23)	<0.001	43.48 (19.70–95.92)	<0.001
Age (per 1 year)	1.00 (0.98–1.02)	0.729	1.05 (1.02–1.08)	<0.001
Male	1.58 (0.75–3.31)	0.225	0.95 (0.44–2.09)	0.906
STEMI	1.09 (0.63–1.90)	0.755	0.91 (0.50–1.65)	0.766
Hypercholesterolemia	0.37 (0.22–0.64)	<0.001	0.39 (0.22–0.67)	<0.001
eGFR (per 1 mL/min/1.73 m2)	0.97 (0.96–0.98)	<0.001	0.98 (0.97–0.99)	0.001

CI, confidence interval; HR, hazard ratio. Other abbreviations as in Table 1.

Long-Term Outcomes After Discharge

Clinical characteristics of patients discharged alive are detailed in Table 3. The median follow-up period was 776 days (interquartile range 467–1,677 days). Figure 3 shows the Kaplan-Meier curves for all-cause mortality, CV death, and MACE in patients discharged alive. No significant differences were observed in the cumulative incidences of all-cause mortality (P=0.781), cardiovascular death (P=0.986), or MACE (P=0.882) among the 3 groups. Multivariable analysis indicated that the risk of these outcomes in the ECPR group did not significantly differ from the CCPR group (all-cause death: HR 2.07; 95% CI 0.37–11.75; P=0.411; CV death: HR 1.17; 95% CI 0.12–11.71; P=0.891; MACE: HR 1.64; 95% CI 0.43–6.33; P=0.472) or the non- CA group (all-cause death: HR 2.99; 95% CI 0.62–14.33; P=0.172; CV death: HR 1.46; 95% CI 0.18–11.93; P=0.724; MACE: HR 1.51; 95% CI 0.45–5.06; P=0.508).

Table 3.

Baseline Characteristics at Discharge

	ECPR (n=27)	CCPR (n=77)	Non-CA (n=447)	P value
Age (years)	51 [45–64]	64 [53–70]	70 [60–78]	<0.001
Male sex	25 (93)	67 (87)	357 (80)	0.103
STEMI	26 (96)a	60 (78)	313 (70)	0.006
OHCA	25 (93)	74 (96)	–	0.603
Bystander CPR	15 (56)	49 (64)	–	0.458
Initial rhythm
VT/VF	26 (96)	66 (86)	–	0.178
PEA	1 (4)	9 (12)	–	0.448
Asystole	0 (0)	2 (3)	–	1.000
Comorbidities
Hypertension	12 (44)a	45 (58)	304 (68)	0.016
Hypercholesterolemia	14 (52)	28 (36)b	244 (55)	0.013
Diabetes	11 (41)	26 (34)	151 (34)	0.758
Current smoking	19 (70)a,c	19 (25)	158 (35)	<0.001
Medications at discharge
β-blockers	17 (63)	57 (74)	283 (63)	0.188
ACE inhibitors/ARB	17 (63)	56 (73)	321 (72)	0.593
Calcium-channel antagonists	3 (11)	6 (8)b	98 (22)	0.008
Statins	18 (67)	46 (60)b	361 (81)	<0.001
Aspirin	26 (96)	74 (96)	433 (97)	0.694
P2Y12 antagonists	26 (96)	71 (92)	430 (96)	0.249
Oral anticoagulants	2 (7)	10 (13)	49 (11)	0.719
Laboratory data
eGFR (mL/min/1.73 m2)	57 [46–64]	53 [40–70]b	63 [46–76]	0.012
Peak CK (U/L)	4,279 [2,094–11,410]a,c	1,443 [528–4,311]b	828 [275–1,983]	<0.001
Peak CK-MB (U/L)	402 [237–822]a,c	108 [43–420]b	64 [15–211]	<0.001
Culprit lesion of MI
Left main coronary	2 (7)	6 (8)	17 (4)	0.136
Left anterior descending	13 (48)	38 (49)	214 (48)	0.972
Left circumflex	3 (11)	11 (14)	73 (16)	0.714
Right coronary	9 (33)	21 (27)	151 (34)	0.531
Multivessel disease	14 (52)	35 (46)	238 (53)	0.450
Triple vessel disease	3 (11)	18 (23)	92 (21)	0.396
Chronic total occlusion	5 (19)	10 (13)	39 (9)	0.150
Successful reperfusion	25 (93)	72 (94)	426 (95)	0.486
Door-to-balloon time (min)	118 [90–143]	101 [72–129]b	146 [87–422]	<0.001
Revascularization by PCI	27 (100)	73 (95)b	442 (99)	0.049

Values are presented as median [interquartile range] or n (%). ^aP<0.017, ECPR vs. Non-CA. ^bP<0.017, CCPR vs. Non-CA. ^cP<0.017, ECPR vs. CCPR. Abbreviations as in Table 1.

Figure 3.

Kaplan-Meier analysis of all-cause mortality and cardiovascular events after discharge. The Kaplan-Meier curves for (A) all-cause mortality, (B) cardiovascular death, and (C) major adverse cardiovascular events (MACE) in patients discharged alive are shown. There were no significant differences among the 3 groups. CA, cardiac arrest; CCPR, conventional cardiopulmonary resuscitation; CI, confidence interval; ECPR, extracorporeal cardiopulmonary resuscitation; HR, hazard ratio.

Discussion

The present study revealed that acute MI patients who required ECPR had inferior 30-day outcomes compared with those who achieved ROSC without ECPR or those without CA. However, there was no significant difference in the long-term outcomes for patients discharged alive, regardless of whether they experienced CA or received ECPR.

The short-term mortality in patients with acute MI complicated by CA have been previously reported as 31–38%,^4–6 which is consistent with the rate observed in the present study (33%). However, the 30-day mortality of acute MI patients with CA who required ECPR was found to be 47%, significantly higher than the 25% mortality in those who did not require ECPR. Cardiogenic shock is a crucial prognostic factor in patients with acute MI complicated by CA,²¹ and the need for ECPR is classified as the most severe grade of cardiogenic shock.²² In this regard, the worse outcome of patients in the present study requiring ECPR is reasonable. Conversely, previous studies have documented short-term mortality rates of 77–79% in all patients with cardiogenic CA requiring ECPR.^23–25 These percentages were notably higher than those observed in acute MI patients necessitating ECPR, as evidenced in the present study. This discrepancy suggests that CA due to acute MI may be associated with a better prognosis and that patients may deliver greater benefit from ECPR than those with CA from other causes. The cause of CA in acute MI patients is acute myocardial ischemia, which can often be rapidly resolved through coronary intervention.²⁶ If the perfusion of systemic organs, particularly of the brain, can be maintained by extracorporeal life support during the coronary intervention, the risk of irreversible damage to these organs may be minimized, thus enhancing the prognosis for acute MI patients with refractory CA.

Acute MI patients complicated by CA have concerns about long-term prognosis, even if discharged alive. These patients often have large infarct size, advanced coronary stenosis including the left main coronary lesion or chronic total occlusion, and comorbidities such as renal dysfunction.³ The use of ECMO also increases left ventricular workload and wall stress, which leads to exacerbation of ischemia-reperfusion injury and enlargement of the infarct size.¹⁵ Indeed, the patients in the ECPR group had the largest infarct size among the 3 groups. Nevertheless, we found that the long-term prognosis for ECPR patients was comparable not only to that of CCPR patients but also to that of non-CA patients, even after adjusting for confounding factors. This finding contradicts previous reports linking infarct size to worse long-term outcomes.²⁷ A possible explanation for this discrepancy is that patients who had relatively smaller infarct sizes may have been more likely to be discharged alive. Our analysis indicated that patients who survived to discharge had lower peak CK levels compared with those who died in hospital, suggesting that their infarct size, as estimated from those peak CK levels,²⁸ may not have been sufficiently large to have a significant prognostic impact. Although the delay in coronary reperfusion due to the establishment of extracorporeal circulation may exacerbate myocardial injury in patients undergoing ECPR, the door-to-balloon time in these patients was actually shorter than that in non-CA patients in this study. This may be partly attributed to the higher proportion of non-STEMI cases among the non-CA patients. While ECPR patients had the longest door-to-balloon time among STEMI patients, the delay was unlikely to have significantly impacted clinical outcomes. Additionally, refractory CA patients requiring ECPR tend to undergo minimal testing and treatment in the emergency room, allowing for a more rapid transition to catheterization. Consequently, the impact of ECMO insertion on reperfusion time delay may have been minimal. Although limited studies have examined the influence of ECMO on long-term prognosis in acute MI patients, 1 study using ECMO for cardiogenic shock reported favorable long-term outcomes for those discharged alive.²⁹ Our findings suggest that patients who need ECPR, but are discharged alive, may experience favorable long-term prognoses, providing encouragement for the use of ECPR in treating acute MI patients complicated by CA.

To our knowledge, no study has specifically investigated the prognosis of acute MI patients undergoing ECPR. This study is of great importance in elucidating the efficacy and limitations of ECPR for CA due to acute MI. Given that ECPR is an invasive and resource-intensive treatment, careful patient selection is critical to identify those most likely to benefit. Further research is needed to refine the indications for ECPR and improve in-hospital outcomes in patients with MI complicated by CA.

Study Limitations

First, this is a retrospective, observational, single-center study, which may introduce selection bias into the study population for the following reasons. The number of patients complicated by CA in our cohort was relatively larger than in a previous Japanese multicenter registry-based study,²¹ likely due to our hospital’s designation as a tertiary emergency center. There may also be inter-institutional differences in the indication for ECPR and primary PCI in CA patients. The final decision to perform ECPR and angiography was left to emergency physicians in each case. From these perspectives, a multicenter study design may be more effective in addressing these issues. Second, the sample size may be insufficient for adequately assessing long-term prognosis. Additionally, the long study period with a relatively small sample size was also a limitation of this study because devices, medications, and the indication and strategy for primary PCI have changed over time. Third, the medications administered after hospital discharge could significantly influence long-term prognosis, but it was difficult to collect comprehensive information regarding post-discharge medication use. Fourth, the absence of imaging findings, such as echocardiography or magnetic resonance imaging, related to cardiac function or infarct size poses a limitation. Further prospective studies, including imaging data, will be needed.

Conclusions

Patients with acute MI complicated by refractory CA who received ECPR exhibited a worse short-term prognosis compared with those who achieved ROSC without ECPR or those without CA. However, among patients discharged alive, the long-term prognosis was comparable, regardless of whether they experienced CA or received ECPR.

Disclosures

Y.U. received research grants from Abbott, OrbusNeich, Janssen, Eli Lilly, MSD, and Novartis, and lecture fees from Nipro, and Amgen. H.A. received research grant from Boehringer Ingelheim. Y.U., K.I. are members of Circulation Reports’ Editorial Team. The other authors declare no conflicts of interest.

Sources of Funding

There is no funding for this study.

IRB Information

Osaka National Hospital Institutional Review Board #2 (approval no. 19097).

Data Availability

Because of Institutional Review Board restrictions, the study data will not be made available to other researchers for the purpose of reproducing the results.

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