# Comparative efficacy and safety of anticoagulant, combination, and antiplatelet therapies in patients with intracardiac thrombus: a real-world retrospective study

**Authors:** Chenxiao Jiang, Xinyu Wang, Baoyan Wang, Xin Chen, Biao Xu, Jie Ni, Dujuan Sha

PMC · DOI: 10.3389/fmed.2026.1723890 · Frontiers in Medicine · 2026-02-18

## TL;DR

This study compares anticoagulant, combination, and antiplatelet therapies for intracardiac thrombus, finding anticoagulant therapy reduces mortality more than antiplatelet therapy.

## Contribution

The study provides real-world evidence on the comparative efficacy and safety of antithrombotic therapies for intracardiac thrombus.

## Key findings

- Anticoagulant therapy was associated with significantly lower one-year all-cause mortality compared to antiplatelet therapy.
- Combination therapy did not show additional efficacy or safety benefits over monotherapies.

## Abstract

Intracardiac thrombus is associated with significant morbidity and mortality; however, optimal antithrombotic strategies remain uncertain.

To evaluate the efficacy and safety of different antithrombotic regimens in patients with intracardiac thrombus.

In this retrospective study, patients with intracardiac thrombus were enrolled at Nanjing Drum Tower Hospital. Logistic regression assessed the association between antithrombotic therapies and thrombus dissolution, while Cox regression evaluated the association with all-cause mortality. Thromboembolic events and clinically related major bleeding (CRMB) events were compared across treatment groups using chi-square or Fisher’s exact tests. Kaplan–Meier curves depicted one-year cumulative incidence, with subgroup analyses presented using forest plots.

A total of 214 patients were included, of whom 26 received antiplatelet therapy, 118 anticoagulant therapy, and 70 combination therapy. Compared with antiplatelet therapy, anticoagulant therapy was associated with a significantly higher likelihood of thrombus dissolution in the Model 1 (aOR 3.56, 95% CI 1.16–11.20), although this association was attenyated in Model 2 (aOR 2.52, 95% CI: 0.72–9.01). Combination therapy showed a non-significant trend toward improved thrombus dissolution in both Models 1 (aOR 2.40, 95% CI 0.77–7.37) and Model 2 (aOR 2.12, 95% CI 0.66–6.66). For all-cause mortality, anticoagulant therapy was consistently associated with a significantly lower risk compared with antiplatelet therapy in both adjusted models (Model 1: aHR 0.20, 95% CI 0.05–0.79; Model 2: aHR 0.16, 95% CI 0.03–0.78). Compared with antiplatelet therapy, combination therapy was associated with reduced all-cause mortality in the Model 1 (aHR 0.16, 95% CI 0.03–0.90) but not Model 2 (aHR 0.34, 95% CI 0.06–1.75). Combination therapy showed a non-significant trend toward improved thrombus dissolution or all-cause mortality compared with anticoagulant therapy.

In patients with intracardiac thrombus, anticoagulant monotherapy was associated with a significantly lower one-year all-cause mortality compared with antiplatelet therapy, whereas its effect on thrombus dissolution was attenuated after full adjustment, potentially reflecting thrombus-related heterogeneity. Combination therapy did not confer additional efficacy or safety benefits over antiplatelet or anticoagulant monotherapy.

## Full-text entities

- **Genes:** MPL (MPL proto-oncogene, thrombopoietin receptor) [NCBI Gene 4352] {aka C-MPL, CD110, MPLV, THCYT2, THPOR, TPOR}, FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** SAPT (MESH:D012640), bleeding (MESH:D006470), organ dysfunctions (MESH:D009102), ST-segment elevation myocardial infarction (MESH:D000072657), LA (MESH:C535395), myocardial injury (MESH:D009202), blood stasis (MESH:D014647), stroke (MESH:D020521), hypercoagulability (MESH:D019851), renal insufficiency (MESH:D051437), malignancy (MESH:D009369), ischemic (MESH:D002545), inflammatory (MESH:D007249), atherothrombotic disease (MESH:D004194), CHD (MESH:D003327), OACs (MESH:C536683), arterial thrombosis (MESH:D002341), hyperuricemia (MESH:D033461), atherosclerotic plaque (MESH:D058226), Intracardiac (MESH:C538262), necrosis (MESH:D009336), appendage (MESH:D018280), LAA (MESH:D059446), embolic events (MESH:D004617), HF (MESH:D006333), DD (MESH:C538319), Thromboembolic (MESH:D013923), cardiac mass lesion (MESH:D006331), coagulation (MESH:D001778), cardiovascular death (MESH:D002318), DCM (MESH:D002311), MI (MESH:D009203), ischemic stroke (MESH:D002544), AF (MESH:D001281), thrombocytopenia (MESH:D013921), compartment syndrome (MESH:D003161), venous thrombotic (MESH:D020246), endothelial injury (MESH:D057772), LAA thrombus (MESH:D013927), VTE (MESH:D054556), death (MESH:D003643), blood (MESH:D006402), CRMB (MESH:D004830), atherosclerotic (MESH:D050197)
- **Chemicals:** cholesterol (MESH:D002784), aspirin (MESH:D001241), edoxaban (MESH:C552171), TG (MESH:D014280), warfarin (MESH:D014859), creatinine (MESH:D003404), rivaroxaban (MESH:D000069552), Cr (MESH:D002857), dabigatran (MESH:D000069604), clopidogrel (MESH:D000077144), DOACs (-), ticagrelor (MESH:D000077486)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12956654/full.md

## References

38 references — full list in the complete paper: https://tomesphere.com/paper/PMC12956654/full.md

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Source: https://tomesphere.com/paper/PMC12956654