Efficacy and safety of single antiplatelet therapy with anticoagulation in patients with AMI

Abstract

Background

Dual antiplatelet therapy (DAPT) after percutaneous coronary intervention (PCI) with stenting is standard of care but increases bleeding risk, particularly in patients requiring veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for acute myocardial infarction–cardiogenic shock. Evidence guiding optimal antithrombotic strategies in this high-risk population remains limited.

Methods

We conducted a retrospective observational study at a high-volume ECMO center. From January 2018 to December 2022, 351 VA-ECMO patients were screened, and 72 who underwent PCI immediately prior to or during ECMO were included. Patients were grouped by initial post-PCI antiplatelet strategy: aspirin alone (n = 33), augmented therapy (n = 25), or no antiplatelet therapy (n = 14). The primary objective was to evaluate the safety and efficacy of an aspirin-only strategy for preventing in-stent thrombosis. Efficacy was assessed by the incidence of in-stent thrombosis during ECMO hospitalization, and safety was assessed by the occurrence of major bleeding events.

Results

Groups were similar in age, race, gender, and BMI. No patient developed clinically overt in-stent thrombosis. Major bleeding occurred in 33.3% of aspirin, 48% of augmented, and 50% of no-antiplatelet patients (p = 0.396). Most common bleeding events were hemoptysis, intracranial hemorrhage, and gastrointestinal bleeding.

Conclusions

Among patients undergoing PCI with concurrent VA-ECMO support, no differences in stent thrombosis or major bleeding were observed between aspirin monotherapy, augmented antiplatelet therapy, or no antiplatelet therapy. However, intracranial hemorrhage occurred more frequently in the Augmented AP group. These findings suggest that aspirin monotherapy may provide adequate protection against stent thrombosis while potentially minimizing bleeding risk in this critically ill population.

Keywords

ECMO PCI dual antiplatelet therapy in stent thrombosis

Introduction

Cardiogenic shock (CS) complicates up to 15% of all acute myocardial infarction (AMI) and remains the leading cause of mortality among patients presenting with AMI.¹ Recent evidence supports early employment and escalation of mechanical circulatory support (MCS) to reduce dependency on inotropic agents and support cardiac and non-cardiac organ function.² Among current MCS devices in clinical use, veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is commonly used to provide circulatory and oxygenation support – sometimes in conjunction with axial-flow MCS for concomitant left ventricular unloading.^3,4 Although ECMO was initially introduced in the 1970s, more recent advancements such as percutaneously inserted cannulas and the development of less thrombogenic systems have significantly improved patient outcomes.⁵

The initiation of ECMO exposes blood to artificial surfaces, thereby activating the complement system and the contact (extrinsic) coagulation pathway.^6,7 Additionally, the shear stress generated by the pump can induce red blood cell hemolysis, unravel von Willebrand factor (vWF), promote platelet aggregation, and trigger the denaturation of plasma proteins and lipoproteins, all of which contribute to thrombosis.^6,8 In contrast, prolonged exposure of platelets to high shear stress within the pump head predisposes platelets to receptor shedding, impairing their binding capabilities.⁹ Given the complex interactions between the circuit, red blood cells (RBCs), and platelets, the impact of the circuit and anticoagulation on both the patient and the ECMO system is highly variable.^10,11 Current guidelines for ECMO initiation recommend a bolus dose of an anticoagulant followed by ongoing systemic administration of the selected anticoagulant.¹² In comparison, guidelines for preventing stent thrombosis following percutaneous coronary intervention (PCI) suggest a regimen of dual antiplatelet therapy (DAPT) with aspirin (ASA) and a P2Y12 receptor inhibitor – ideally pre-PCI or immediately post-PCI.^13,14 In AMI-shock patients on ECMO, these recommendations are frequently combined, resulting in patients receiving “triple therapy” with therapeutic anticoagulation and dual antiplatelet therapy. Additionally, in AMI-shock patients with impaired gut perfusion and oral medication absorption, intravenous antiplatelet therapies are often preferred.¹⁵

The use of triple therapy increases the risk of bleeding complications such as device associated bleeding or pulmonary, intracranial, and gastrointestinal hemorrhage.¹⁶ The resulting elevated bleeding risk is associated with higher transfusion requirements, which, in turn, may lead to the development of antibodies, volume overload, and renal dysfunction.¹⁷ Contrarily, the use of a single antiplatelet agent (vs standard of care DAPT) with an anticoagulant may carry the risk of stent thrombosis.¹⁸ At present, there is no clinical guidance regarding the optimal approach to combined antithrombotic and antiplatelet therapy in AMI-shock patients requiring VA-ECMO who have undergone or are undergoing PCI. This study aims to evaluate the efficacy and safety of employing a regimen of single antiplatelet therapy (SAPT) with aspirin alone in addition to systemic anticoagulant therapy for patients with AMI-shock requiring ECMO and PCI.

Methods

Study Design and Population

This study presents a retrospective analysis of patients who received VA-ECMO support between January 2018 and December 2022 at a high-volume cardiac care center. Over the 5-year period, 639 patients were supported with ECMO, of whom 351 received VA-ECMO. Within this cohort, 72 patients underwent PCI either immediately prior to or during VA-ECMO support (Figure 1). This study was approved by the Institutional Review Board (#18-832) at Inova Fairfax Hospital. This research did not receive any specific grant funding from agencies in the public, commercial, or not-for-profit sectors.

Figure 1.

Study design and population.

Study measures

Patients were categorized into one of three groups based on the initial antiplatelet strategy employed while on VA-ECMO: (1) patients who received aspirin alone (Aspirin), (2) patients who received a P2Y12 inhibitor or a glycoprotein IIb/IIIa inhibitor with or without aspirin (Augmented AP), or (3) patients who did not receive any antiplatelet therapy (No AP). All three of these groups received a continuous infusion of a therapeutic anticoagulant per institutional protocol. While the institutional protocol has changed slightly over the years, the first line approach has always recommended that patients on VA-ECMO receive a heparin infusion titrated to an anti-Xa goal of 0.2-0.4 IU/mL or 0.3-0.5 IU/mL.

The aim of this study was to assess the efficacy and safety of an antiplatelet minimization strategy, specifically using aspirin alone, in patients supported with VA-ECMO during or immediately after PCI. Efficacy was determined by the incidence of clinically overt stent thrombosis, as evidenced by recurrent MI and/or need for unplanned repeat revascularization during the index hospitalization. Safety was assessed by evaluating the incidence of stroke or major medical bleeding. Major bleeding was defined using a modified version of the ELSO definition including intracranial hemorrhage, pulmonary, or clinically overt gastrointestinal hemorrhage.

Statistical analysis

The distribution of all continuous data was examined for normality using visual inspection and the Shapiro-Wilk test. Characteristics of the groups are presented as the median and interquartile range (IQR) and compared using the Kruskal Wallis test. Categorical data are presented as counts with proportions and compared using the Chi-square test. Survival analysis was performed using the Kaplan-Meier method and the log-rank test was used to compare groups. For evaluation of survival to hospital discharge and survival to decannulation, time to outcome was calculated from the time of initiation of extracorporeal life support. The Cox proportional hazards model was used to calculate hazard ratios (HRs) with their 95% CI to analyze the association of antiplatelet strategy with relevant outcome. Given sample size constraints, no adjustments for confounding factors were performed. The proportional hazard assumption was tested using Schoenfeld residuals and was found to be valid. All relevant statistical tests were two-tailed and a p < 0.05 was considered statistically significant. Statistical analyses were performed using R version 4.1.2 (R Foundation for Statistical Computing, Vienna, Austria).

Results

All patients who received PCI either immediately prior to or during VA-ECMO support between January 2018 and December 2022 were evaluated. Of the 72 patients, 33 (46%) patients received aspirin alone, twenty-five (35%) patients were managed with augmented antiplatelet therapy, and 14 (19%) received no antiplatelet therapy at all while on ECMO (Figure 1). The latter group typically received no antiplatelet therapy at all post-PCI due to active bleeding. Baseline demographic characteristics were comparable between both groups (Table 1). The prevalence of known coronary artery disease (CAD) prior to admission and coronary angiography was highest in the Aspirin (54.5%) and No AP (50.0%) groups compared to patients in the Augmented AP group (24.0%) (p = 0.0495). No statistically significant differences were seen between the groups regarding other comorbid conditions, including hypertension, diabetes, chronic kidney disease, cerebrovascular disease, heart failure with reduced ejection fraction, and bleeding disorders. The incidence of cardiac arrest was similar across both groups as was the use of targeted temperature management.

Table 1.

Baseline characteristics by antiplatelet strategy.

Parameter	Aspirin (N = 33)	Augmented AP (N = 25)	No AP (N = 14)	P-value
Demographic characteristics
Age, median [Q1, Q3]	63.0 [52.0, 68.0]	63.0 [58.0, 70.0]	66.5 [62.3, 71.8]	0.309
Male	25 (75.8%)	23 (92.0%)	11 (78.6%)	0.243
BMI, median [Q1, Q3]	27.9 [24.5, 33.5]	29.9 [25.2, 36.3]	33.0 [26.7, 38.8]	0.316
Comorbidities
Coronary artery disease	18 (54.5%)	6 (24.0%)	7 (50.0%)	0.0495
Cerebrovascular disease	6 (18.2%)	1 (4.0%)	1 (7.1%)	0.235
Hypertension	19 (57.6%)	12 (48.0%)	8 (57.1%)	0.765
Bleeding history	5 (15.2%)	2 (8.0%)	1 (7.1%)	0.699
Diabetes mellitus	10 (30.3%)	9 (36.0%)	6 (42.9%)	0.691
Chronic kidney disease	4 (12.1%)	1 (4.0%)	1 (7.1%)	0.649
Heart failure with EF less than 40%	27 (81.8%)	21 (84.0%)	10 (71.4%)	0.628
Hospital presentation
Cardiac arrest	17 (51.5%)	14 (56%)	8 (57.1%)	0.856
Targeted temperature management	8 (24.2%)	8 (32.0%)	4 (28.6%)	0.787
Length of stay	18 [11, 26]	16 [12, 25]	2 [1, 10]	<0.001

AP: Antiplatelet; BMI: body mass index; EF: ejection fraction.

Patients underwent PCI either immediately prior to ECMO cannulation or while on ECMO. The number of stents, stent type, left main interventions, and other PCI procedural details are shown in Table 2. Importantly, 66.6% percent of patients in the Aspirin group, 76% of patients in the Augmented AP group, and 42.8% of patients in the no AP group received an oral loading dose with a P2Y12 inhibitor. Fifty-seven percent of patients received MCS support with either an intra-aortic balloon pump or a percutaneous ventricular assist device before escalation to ECMO.

Table 2.

PCI course stratified by antiplatelet strategy.

PCI parameter	Aspirin (N = 33)	Augmented AP (N = 25)	No AP (N = 14)	P-value
ACC bleeding risk, median [Q1, Q3]	12.3 [7.40, 22.3]	12.9 [7.60, 22.5]	19.9 [10.2, 32.7]	0.392
Missing	13 (39.4%)	13 (52.0%)	4 (28.6%)
Left main stent	7 (21.2%)	6 (24.0%)	4 (28.6%)
Number of stents	2 [1, 2]	2 [1, 3]	2 [1, 2]	0.768
Drug eluting stent	31 (93.9%)	24 (96.0%)	14 (100%)	1
Number of stents, median [Q1, Q3]	2.00 [1.00, 2.00]	2.00 [1.00, 3.00]	1.00 [1.00, 2.00]	0.077
Bifurcation stenting	3 (9.1%)	2 (8.0%)	1 (7.1%)	1
Access site
Femoral and radial	4 (12.1%)	1 (4.0%)	0 (0%)	0.12
Femoral	13 (39.4%)	5 (20.0%)	8 (57.1%)
Radial	15 (45.5%)	16 (64.0%)	5 (35.7%)
Brachial	0 (0%)	1 (4.0%)	0 (0%)
Missing	1 (3.0%)	2 (8.0%)	1 (7.1%)
Noncompliant balloon post dilation	26 (78.8%)	21 (84.0%)	11 (78.6%)	0.781
Missing	0 (0%)	1 (4.0%)	1 (7.1%)
Atherectomy	7 (21.2%)	3 (12.0%)	2 (14.3%)	0.731
Intravascular imaging	11 (33.3%)	12 (48.0%)	4 (28.6%)	0.266
TIMI flow, median [Q1, Q3]	3.00 [3.00, 3.00]	3.00 [3.00, 3.00]	3.00 [3.00, 3.00]	0.537
Periprocedural medication
Clopidogrel	6 (18.2%)	5 (20.0%)	0 (0%)	0.217
Prasugrel	1 (3.0%)	0 (0%)	0 (0%)
Ticagrelor	7 (21.2%)	6 (24.0%)	2 (14.3%)
Cangrelor	5 (15.2%)	2 (8.0%)	0 (0%)
Tirofiban	2 (6.1%)	3 (12.0%)	3 (21.4%)
Tirofiban + clopidogrel	1 (3.0%)	2 (8.0%)	0 (0%)
Tirofiban + ticagrelor	7 (21.2%)	5 (20.0%)	3 (21.4%)
Tirofiban + prasugrel	0 (0%)	1 (4.0%)	1 (7.1%)
None	1 (3.0%)	0 (0%)	3 (21.4%)
Missing	3 (9.1%)	1 (4.0%)	2 (14.3%)
Heparin dose (units), median [Q1, Q3]	10000 [6500, 17000]	10600 [8250, 15000]	13000 [7000, 14000]	0.97
Stent length (mm), median [Q1, Q3]	38.0 [20.0, 52.0]	50.0 [20.0, 67.0]	29.5 [21.3, 48.5]	0.462
Max ACT, median [Q1, Q3]	279 [254, 304]	287 [248, 306]	246 [235, 249]	0.39
Final ACT, median [Q1, Q3]	267 [250, 289]	247 [226, 283]	246 [235, 249]	0.462
Reduced EF
No	4 (12.1%)	4 (16.0%)	1 (7.1%)	0.902
Yes	25 (75.8%)	17 (68.0%)	8 (57.1%)
Missing	4 (12.1%)	4 (16.0%)	5 (35.7%)
Other MCS inserted	21 (60.6%)	12 (48.0%)	8 (57.1%)	0.682
Type of MCS
IABP	8 (40.0%)	1 (8.3%)	4 (50.0%)	0.0965
Impella CP	12 (60.0%)	11 (91.7%)	5 (50.0%)

AP: Antiplatelet.

Regarding ECMO support, similar rates of cannulation occurred in the operating room versus emergently in the cardiac catheterization lab or bedside in the intensive care unit. All cannulations utilized ultrasound guidance. The median [interquartile range (IQR)] unfractionated heparin dose for cannulation was 5000 [4500, 8000] units in the Aspirin group, 6500 [5000, 10,000] units in the Augmented AP group, and 8000 [5250, 10800] units in the No AP group (p = 0.114). Non-ECMO MCS for left ventricular (LV) venting (80% axial-flow MCS, 12.5% IABP) was similar across groups with 54.5%, 52.0%, and 64.3% in the Aspirin, Augmented AP, and No AP groups, respectively (p = 0.759). The median [IQR] duration of ECMO support was 6 [4, 9] days in the Aspirin group, 7 [5, 10] in the Augmented AP group, and 1.5 [1, 4.5] days in the No AP group (<0.001) (Table 3).

Table 3.

ECMO course stratified by antiplatelet strategy.

Parameter	Aspirin (N = 33)	Augmented AP (N = 25)	No AP (N = 14)	P-value
Cannulation location
Bedside	3 (9.1%)	3 (12.0%)	2 (14.3%)	0.387
Cath lab	4 (12.1%)	7 (28.0%)	4 (28.6%)
Operating room	26 (78.8%)	15 (60.0%)	8 (57.1%)
Heparin dose (units), median [Q1, Q3]	5000 [4750, 8000]	6500 [5000, 10000]	8000 [5250, 10800]	0.114
Intra-ECMO MCS as LV vent	18 (54.5%)	13 (52.0%)	9 (64.3%)	0.759
Post-ECMO MCS	10 (30.3%)	8 (32.0%)	1 (7.1%)	0.307
ECMO duration (days), median [Q1, Q3]	6.00 [4.00, 9.00]	7.00 [5.00, 10.0]	1.50 [1.00, 4.50]	<0.001

AP: Antiplatelet.

No instances of clinically overt stent thrombosis were observed in any patient. The highest rate of ischemic stroke occurred in the Augmented AP group though the rates were statistically similar across groups at 6.1%, 20.0%, and 14.3% for the Aspirin, Augmented AP, and No AP groups (p = 0.326). Similarly, the rate of hemorrhagic stroke was highest in the Augmented AP group though this did not meet statistical significance. The No AP group had the highest rate of gastrointestinal bleeding at 50.0% compared with 9.1% in the Aspirin group and 16.0% in the Augmented AP group (p = 0.004). Minor bleeding was not different between groups. Thrombotic and bleeding events are detailed in Table 4.

Table 4.

Thrombotic and bleeding complications.

Outcomes	Aspirin (N = 33)	Augmented AP (N = 25)	No AP (N = 14)	P-value
Thrombotic complications
Stent thrombosis	0 (0%)	0 (0%)	0 (0%)
Ischemic CVA	2 (6.1%)	5 (20.0%)	2 (14.3%)	0.326
Major bleeding complications	11 (33.3%)	12 (48.0%)	7 (50.0%)	0.396
Intracranial hemorrhage	4 (12.1%)	6 (24.0%)	2 (14.3%)	0.492
Hemoptysis	5 (15.2%)	4 (16.0%)	1 (7.1%)	0.827
Gastrointestinal bleeding	3 (9.1%)	4 (16.0%)	7 (50.0%)	0.004
Minor bleeding complications	18 (54.5%)	9 (36.0%)	7 (50.0%)	0.398
Nasal bleeding	1 (3.0%)	1 (4.0%)	0 (0%)	1
Hematuria	1 (3.0%)	0 (0%)	0 (0%)	1
Cannulation site bleeding	15 (45.5%)	5 (20.0%)	4 (28.6%)	0.111
Other bleeding	3 (9.1%)	5 (20.0%)	3 (21.4%)	0.38

AP: Antiplatelet.

Figures 2 and 3 show patient survival to ECMO decannulation and hospital discharge. Patients in the No AP group were less likely to survive to ECMO decannulation and hospital discharge.

Figure 2.

Survival to ECMO decannulation.

Figure 3.

Survival to hospital discharge.

Discussion

Patients supported on ECMO are at heightened risk of bleeding due to several contributing factors, including disruptions in natural hemostasis, alterations in the coagulation cascade, and the requirement for systemic anticoagulation. This risk is further exacerbated by the use of mechanical circulatory support devices, such as intra-aortic balloon pumps (IABP) or percutaneous ventricular assist devices, both of which have been associated with the development of thrombocytopenia.¹⁹

ECMO has a multifaceted impact on platelet count and function, as well as on the broader coagulation system. The therapy is known to significantly reduce platelet counts through mechanisms such as the release of inflammatory mediators, mechanical fragmentation of blood components, and the interaction of blood with artificial surfaces.¹⁹ A recent translational study demonstrated that ECMO-related thrombocytopenia exhibits both early onset and resolution that was associated with ECMO initiation and discontinuation.²⁰

Moreover, ECMO-induced shear stress can provoke conformational changes in von Willebrand factor (VWF), promoting its binding to the platelet glycoprotein Ibα (GP Ibα) receptor. This interaction can trigger a range of platelet responses, including GP Ibα ectodomain shedding, which may inhibit platelet aggregation and thrombus formation and accelerate platelet clearance. Although these mechanisms contribute to an elevated bleeding risk, they also highlight ECMO’s potential role as an antiplatelet modality in itself.

Stent thrombosis is a significant risk factor for increased mortality within 30 days after percutaneous coronary intervention (PCI).^21–23 In our study, patients were at risk for both acute and subacute stent thrombosis, which accounts for up to 75% of cases.²⁴ Current guidelines recommend the use of aspirin (ASA) along with a second antiplatelet agent to prevent stent thrombosis.²⁵ ASA works by inhibiting thromboxane A2, which reduces platelet activation and aggregation. In fact, after PCI, ASA has been shown to reduce vessel thrombosis rates by nearly 50%, compared to no ASA treatment, according to a retrospective study.²⁶ A Dutch registry study also highlighted that stopping or failing to initiate clopidogrel therapy within the first 30 days post-stent implantation significantly increases the risk of stent thrombosis, contributing to 12% of acute or subacute events.²⁷ In addition, newer agents like ticagrelor and cangrelor have been shown to reduce the risk of both subacute and acute stent thrombosis by 40% and 38%, respectively, compared to clopidogrel.²⁸

The use of heparin with a single antiplatelet agent has not been evaluated in ECMO; however, in the more modern PCI era, the randomized controlled AUGUSTUS trial found no statistical difference in stent thrombosis (0.5% vs 0.9%) when using a single antiplatelet agent and oral anticoagulation 6 days after stent placement.²⁹ A prospective cohort evaluating stent thrombosis in low-risk patients treated with aspirin only and a heparin-coated stent found a 30-days thrombosis rate of only one percent.³⁰ These studies did not include patients on ECMO but further suggest that a single antiplatelet agent, such as ASA only, with use systemic of anticoagulation during ECMO may provide protection against stent thrombosis as seen with our study results.

Retrospective studies evaluating complications, such as abrupt vessel closure, after PCTA found those with lower activated clotting times (ACT) values peri-procedure were more likely to experience a complication or abrupt closure compared to those with higher ACT values.^31,32 At our center, all patients undergoing PCI were monitored with activated clotting time (ACT) to ensure adequate systemic anticoagulation. No significant difference in ACT was observed between the ASA and DAPT groups (279 vs 287, p = 0.8).

Previously published studies examining the safety of antiplatelet therapy in VA-ECMO are limited. Staudacher and colleagues published their experience with 93 VA-ECMO patients and did not find a difference in bleeding rates in patients prescribed DAPT versus no antiplatelet therapy.³³ Their study differed from ours in that patients may or may not have undergone PCI during hospital admission and their median time on ECMO was 37 h. Similarly, a Dutch study of 100 VA-ECMO patients, approximately half of whom received DAPT in addition to unfractionated heparin, found an increased rate of bleeding in patients prescribed DAPT and a lower incidence of clinically or radiographically overt thromboses in the DAPT group. While the No AP group in our study had a short ECMO course of 1.5 [1,4.5] days, the Aspirin and Augmented AP groups had a median ECMO duration of 6 and 7 days, respectively.

Limitations

Our study is unique in highlighting the complex population that undergoes both PCI and ECMO; however, it is limited by its retrospective design. The decision to implement a dual antiplatelet strategy was made by the admitting clinician and the proceduralist. This retrospective nature introduces variability in key factors, such as heparin dosing, timing of ECMO initiation, and anticoagulation management protocols. Another limitation of our study was the inability to obtain comprehensive data from PCIs performed at other centers prior to transfer. Additionally, blood transfusion requirements were not collected for consideration in the analysis of bleeding.

Conclusion

Our study demonstrated that patients who received PCI immediately prior to or during VA ECMO support did not experience any episodes of stent thrombosis during their ECMO hospitalization – regardless of their antiplatelet strategy (no antiplatelet therapy, Aspirin-only SAPT, or augmented antithrombotic with P2Y12 or glycoprotein IIb/IIIa inhibitor). When comparing patients who received ASA only with anticoagulation to those treated with Augmented AP in addition to anticoagulation, there was a numerically higher incidence of major bleeding events in the Augmented AP group. Further research is needed to identify the optimal antiplatelet strategy for this high-risk population. Future efforts should focus on developing individualized treatment regimens that effectively balance the risk of bleeding with the prevention of stent thrombosis and device-related thrombosis. While current guidelines endorse DAPT, ASA alone may be sufficient to prevent stent thrombosis while minimizing bleeding risks. Given that our study did not observe any instances of stent thrombosis with or without antiplatelet therapy (and regardless of SAPT or Augmented AP), and considering the potential antiplatelet effects inherent to ECMO, it may be worthwhile to explore whether ECMO alone could prevent stent thrombosis without the use of antiplatelet therapy.

Footnotes

Author note

The authors report no research grants or conflicts of interest for this study with the exception of those listed below: Disclosures: Dr. Truesdell reports consulting and speaking fees from Abiomed, Getinge, Shockwave, and Zoll. Dr. Vandenbriele reports consulting and speaking fees and research grants from Abiomed.

Acknowledgements

Contributor JC and AT take full responsibility for the content of this paper and act as guarantors for the data. JC, MF, ML, and LA conceived the study design. MG, KY, EF, KB, LC, TL were responsible for data acquisition. AC performed the data analysis. All authors contributed to the interpretation of the findings, critically revised the paper for intellectual content, and approved the final version of the manuscript.

ORCID iD

Junad M Chowdhury

Funding

The authors received no financial support for the research, authorship, and/or publication of this article.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

IRB Approvel

18-83

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Efficacy and safety of single antiplatelet therapy with anticoagulation in patients with AMI–cardiogenic shock requiring VA-ECMO

Abstract

Background

Methods

Results

Conclusions

Keywords

Introduction

Methods

Study Design and Population

Study measures

Statistical analysis

Results

Discussion

Limitations

Conclusion

Footnotes

Author note

Acknowledgements

ORCID iD

Funding

Declaration of conflicting interests

IRB Approvel

References