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DOI: 10.1055/a-2576-8009
Navigating Anticoagulation in Ischemic Left Ventricular Aneurysms: Lessons from Cardiac Magnetic Resonance Imaging

Left ventricular (LV) systolic dysfunction is associated with increased risk of thromboembolic events.[1] However, clinical trials of routine anticoagulation for patients with depressed LV systolic function have not supported universal anticoagulation in this population,[2] [3] highlighting the need for better risk stratification to guide prophylactic strategies.
Ischemic LV aneurysm commonly occurs in the context of a non-perfused anterior wall ST elevation myocardial infarction (MI) leading to reduced LV systolic function and a hypokinetic, akinetic, or dyskinetic segment of the LV.[4] These aneurysms considerably increase the risk of LV thrombus (LVT) formation.[5] However, not all patients with ischemic LV aneurysm develop LVT and there is no consensus for anticoagulation in this population. Determining the incidence, predictors, and preventative strategies against LVT and systemic embolism in patients with chronic LV aneurysm has remained controversial.[6] In the era of percutaneous coronary interventions, the incidence of post-infarction LVT in patients with ischemic LV aneurysm varies between 5 and 15% when assessed by transthoracic echocardiography and 12 and 27% using cardiac magnetic resonance imaging (CMR).[7] The risk of thromboembolic events such as stroke with LVT can be as high as 11.2% over a median follow-up of 38.7 months[8] with previous observational studies showing annual risk of 10 to 15% in untreated[4] versus 3.7% with majority of patients on anticoagulation.[9] Adding complexity to the issue, LVT in the setting of ischemic aneurysms is both slow to resolve—with one serial CMR surveillance study showing persistent LVT 1 year after proper anticoagulation in 37% of patients—and carries a high recurrence risk even after initial resolution, with discontinuation of anticoagulation acting as a contributing factor.[10]
This variability in the development of LVT and its risk of subsequent embolism suggest that additional factors, such as the morphometric features of the aneurysm, may impact the risk of LVT formation and embolism. In this context, the identification of novel imaging-based risk factors could refine clinical decision-making, helping to determine which patients with LV aneurysms are at greater risk for thrombus formation and might benefit from prophylactic anticoagulation.
In this issue of Thrombosis and Haemostasis, Wu et al[11] offer new insights into this dilemma by identifying novel CMR-based risk factors. In a retrospective analysis of 317 hospitalized patients with ischemic LV aneurysm over 8 years, they examined the characteristics of ischemic left LV associated with thrombus formation using delayed enhancement CMR and compared comorbidities between 88 patients with LVT and 229 without. Patients with LVT had lower LVEF, and greater LV mass and volume. Interestingly neither history of MI nor usage of antiplatelet or anticoagulation therapies was different between the two groups. On CMR, they identified three significant risk factors associated with LVT: Wider aneurysm neck (odds ratio [OR] 1.33 per 5 mm increment in neck size), a higher aneurysm shape index (ratio of maximum length to neck width) (OR 1.63 per 20%, 95% CI 1.23–2.16), and a global late gadolinium enhancement (LGE) extent greater than 50% (OR 6.58, 95% CI 3.04–14.27).
The authors should be congratulated for this timely and important contribution. This study represents the largest CMR-based investigation to date on LVT in ischemic LV aneurysms and highlights the growing role of advanced imaging in risk stratification in addition to diagnosis.
Their findings introduce two key insights: First, the emphasis on aneurysm shape—indicated by a higher shape index—challenges the traditional focus on aneurysm size alone. In addition, a deeper, wider-necked aneurysm was found to correlate more strongly with thrombus formation, suggesting that hemodynamic factors influenced by aneurysm morphology are more critical in thrombus formation than previously recognized. Second, the strong association between extensive LGE—a marker of myocardial fibrosis—and LV thrombus risk, irrespective of LV systolic function. The finding that over half of the LVT cases had a history of remote MI, up to 18 months prior, suggests that fibrosis is a long-term thrombotic risk factor, not just an early post-MI concern. Besides these MRI-based features, clinical correlates, such as history of heart failure, were also more common in those with LVH. This aligns with the AHA Scientific Statement on the Management of Patients at Risk for and with Left Ventricular Thrombus.[4]
Despite these advances, some unresolved issues remain. First, the study findings for CMR features seem somewhat contradictory. On the one hand, a wider aneurysm neck is reported to correlate with greater risk of LVT and yet on the other hand, a smaller neck contributing to a higher shape index is also reported to increase the risk of LVT. The possibilities include model overfitting and, alternatively, a statistical interaction, such that a small neck is only predictive of greater risk in the context of longer aneurysm longitudinal diameter.
Moreover, the study cohort lacks external validation and racial and ethnic diversity, raising concerns about generalizability. This is important given reported ethnic differences in the clinical outcomes of thromboembolism (hence, stroke) and bleeding.[12] [13] Referral bias and variations in imaging protocols, particularly in LGE assessment, may also impact reproducibility across clinical settings. Additionally, although certain clinical characteristics have been linked to LV thrombosis, there is still no structured framework, such as a scoring system, that integrates both imaging data and clinical features. Last but not least, this study does not inform which LVT features directly drive embolic events, which are the most consequential events warranting anticoagulation. Therefore, to bridge this gap and translate these insights to practice, the results of this study need external validation in large inclusive cohorts; a risk score may be needed to identify patients at higher risk per clinical and imaging criteria, and ideally, randomized trials to demonstrate net benefit in those deemed at high risk.
Nevertheless, the current study is a nice addition to the literature. Clinical and imaging criteria can guide risk assessment and serve as a basis for shared decision-making for preventative antithrombotic therapy as we await the generation of further high-quality evidence ([Fig. 1]).


Publication History
Received: 01 April 2025
Accepted: 07 April 2025
Accepted Manuscript online:
08 April 2025
Article published online:
24 April 2025
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