What is the clinical evidence from this study?

Study design: Cohort. Population: STEMI and high-risk NSTEMI (n=604). Intervention: Chronic oral anticoagulation (OAC) vs. Non-OAC users. Primary outcome: Long-term all-cause mortality after discharge (HR 0.81, 95% CI 0.47-1.37, p=0.43).

What does this research mean for the field?

Chronic oral anticoagulation use is not an independent predictor of long-term mortality in STEMI and high-risk NSTEMI patients undergoing primary percutaneous coronary intervention after multivariable adjustment, with mortality driven primarily by baseline comorbidity burden. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine whether chronic oral anticoagulation is an independent predictor of mortality and adverse outcomes in patients with STEMI or high-risk NSTEMI undergoing primary PCI.

October 4, 2026Cardiovascular TherapeuticsOpen Access

Is Oral Anticoagulation an Independent Predictor of Mortality in STEMI and High‐Risk NSTEMI Patients After Primary PCI? A Propensity Score‐Matched Retrospective Analysis

Q: What are the key findings of this study?

Chronic oral anticoagulation use was not an independent predictor of long-term mortality (HR 0.81, p=0.43) in STEMI and high-risk NSTEMI patients after primary PCI, with prognosis driven instead by comorbidities.

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Key result

Chronic oral anticoagulation is not associated with long-term mortality after PCI for acute MI.

HR 0.81
95% CI 0.47-1.37
P=0.43
n=604

Why the study?

Managing STEMI and high-risk NSTEMI patients on chronic oral anticoagulation undergoing primary PCI involves competing ischemic and bleeding risks that require evaluation.

Does chronic oral anticoagulation use independently predict long-term mortality in STEMI and high-risk NSTEMI patients after primary PCI?

Key Points

To determine whether chronic oral anticoagulation is an independent predictor of mortality and adverse outcomes in patients with STEMI or high-risk NSTEMI undergoing primary PCI.
Conducted a single-centre retrospective study of 604 consecutive STEMI and high-risk NSTEMI patients treated with primary PCI between 2012 and 2023.
Compared 100 oral anticoagulation users with 203 propensity score-matched non-anticoagulated controls across a mean follow-up of approximately 3 years.
Postdischarge long-term mortality was significantly higher in oral anticoagulation users than in controls (31% vs. 14.8%, p = 0.001), with higher rates of access-site haematoma (8% vs. 2%, p = 0.02) and minor bleeding (7% vs. 1.5%, p = 0.03), while in-hospital mortality was comparable (7% vs. 5.9%, p = 0.80).
Multivariable Cox regression revealed that oral anticoagulation was not an independent predictor of long-term mortality (HR 0.81, 95% CI 0.47–1.37, p = 0.43).
Independent predictors of long-term all-cause mortality were older age (HR 1.06 per year, 95% CI 1.023–1.10, p = 0.001), reduced left ventricular ejection fraction (HR 0.95 per 10% increase, 95% CI 0.93–0.98, p < 0.001), and chronic kidney disease (HR 2.16, 95% CI 1.11–4.23, p = 0.023).

Study Design

Type

Cohort (n=604)

Multicenter

Structured PICO

Does chronic oral anticoagulation use independently predict long-term mortality in STEMI and high-risk NSTEMI patients after primary PCI?

Population

604 consecutive patients with STEMI or high-risk NSTEMI undergoing primary PCI, from which 100 chronic oral anticoagulation users were propensity-matched to 203 controls and followed for a mean of 3 years.

Exposure

Chronic oral anticoagulation (OAC) therapy (warfarin, rivaroxaban, apixaban, dabigatran, or edoxaban) prior to admission, with the majority (67%) discharged on triple antithrombotic therapy (OAC + DAPT).

Comparator

Propensity score-matched non-OAC users, with nearly all (94%) discharged on dual antiplatelet therapy (DAPT) alone.

Outcome

Long-term all-cause mortality after dischargehard clinical

Main Result

Hazard Ratio: 0.81 (95% CI 0.47–1.37)

Absolute Event Rate: 31% vs 14.8%

p-value: p=0.43

Limitations

Retrospective, single-centre design limits generalisability and introduces potential selection and information bias
Residual baseline imbalances remained after propensity score matching, indicating potential residual confounding
Confounding by indication, as OAC use is driven by underlying conditions like atrial fibrillation whose effects cannot be completely separated
Small sample size of the OAC group reduced statistical power for subgroup analyses
Antithrombotic treatment changes during follow-up were not systematically captured, leading to potential time-varying exposure misclassification
Retrospective, single-centre design limits generalisability and introduces selection/information bias
Residual baseline imbalances after propensity score matching (e.g., prior stroke, CAD, smoking)
Confounding by indication (OAC driven by underlying conditions like AF)
Small OAC group size reducing statistical power for subgroup analyses
Antithrombotic treatment changes during follow-up not systematically captured

Implication

OAC should not yet alter post-PCI risk stratification in ACS; leaves open whether comorbidities fully explain excess mortality in retrospective cohorts.

Abstract

BACKGROUND: Managing STEMI and high-risk NSTEMI-equivalent patients on chronic oral anticoagulation (OAC) undergoing primary PCI poses competing ischaemic and bleeding risks. METHODS: This single-centre retrospective study enrolled 604 consecutive STEMI/high-risk NSTEMI patients undergoing primary PCI (2012-2023). OAC users (n = 100) were compared with propensity score-matched controls (n = 203). Primary endpoints included all-cause mortality, bleeding, stroke, recurrent MI and rehospitalisation over a mean 3-year follow-up. RESULTS: OAC users had a higher prevalence of prior ischaemic stroke/TIA (19% vs. 3%, p < 0.001) and known coronary artery disease (33% vs. 20%, p = 0.015). In-hospital mortality was comparable (7% vs. 5.9%, p = 0.80). Postdischarge long-term mortality was significantly higher in OAC users (31% vs. 14.8%, p = 0.001), as were access-site haematoma (8% vs. 2%, p = 0.02) and minor bleeding (7% vs. 1.5%, p = 0.03). On multivariable Cox regression, OAC use was not an independent mortality predictor (HR 0.81, 95% CI 0.47-1.37, p = 0.43); age, reduced ejection fraction and chronic kidney disease were the principal determinants. CONCLUSION: Despite higher postdischarge mortality and bleeding, OAC use was not independently associated with mortality after adjustment. Comorbidity burden drives prognosis, emphasising comprehensive risk stratification in this population.

Discussion

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Published by Cardiovascular Therapeutics · CC BY

Cite This Study

POLAT et al. (2026) conducted a cohort in STEMI and high-risk NSTEMI (n=604). Chronic oral anticoagulation (OAC) vs. Non-OAC users was evaluated on Long-term all-cause mortality after discharge (HR 0.81, 95% CI 0.47-1.37, p=0.43). Chronic oral anticoagulation use was not an independent predictor of long-term mortality (HR 0.81, p=0.43) in STEMI and high-risk NSTEMI patients after primary PCI, with prognosis driven instead by comorbidities.

synapsesocial.com/papers/6ac19d7eaeea5716e8c6c6d2 https://doi.org/10.1155/cdr/1295386

Topics

STEMI management

Percutaneous coronary intervention

Anticoagulation in AF

Chronic total occlusion PCI

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Implication

OAC should not yet alter post-PCI risk stratification in ACS; leaves open whether comorbidities fully explain excess mortality in retrospective cohorts.

Is Oral Anticoagulation an Independent Predictor of Mortality in STEMI and High‐Risk NSTEMI Patients After Primary PCI? A Propensity Score‐Matched Retrospective Analysis

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

Topics

Is Oral Anticoagulation an Independent Predictor of Mortality in STEMI and High‐Risk NSTEMI Patients After Primary PCI? A Propensity Score‐Matched Retrospective Analysis

Key Points

Study Design

Structured PICO

Main Result

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

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