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Cardioembolic stroke in Chagas cardiomyopathy: the interplay between apical aneurysm, left ventricular thrombus and
Julia Teixeira Tupinambás1, Manoel Otavio C Rocha1,2, Thais Aparecida R Lage1
1Post Graduation Program in Infectious Diseases and Tropical Medicine, School of Medicine, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Insights
In Chagas cardiomyopathy (CCM), apical aneurysms increase stroke risk primarily through left ventricular thrombus formation. Prior cardioembolic stroke indicates a higher risk of recurrence, guiding targeted prevention strategies.
Area of Science:
- Cardiology
- Neurology
- Infectious Diseases
Background:
- Apical aneurysm is a known complication of Chagas cardiomyopathy (CCM).
- The independent contribution of apical aneurysm to cardioembolic (CE) stroke and its underlying mechanisms in CCM are not fully understood.
- Understanding these associations is crucial for effective stroke prevention in CCM patients.
Purpose of the Study:
- To evaluate the association between apical aneurysm and CE stroke in patients with CCM.
- To assess the prognostic implications of CE stroke in this population.
- To elucidate the mechanisms linking apical aneurysm to CE stroke.
Main Methods:
- Prospective cohort study of 518 CCM patients.
- Baseline assessments included clinical, electrocardiographic, and echocardiographic evaluations.
- Logistic regression, genetic matching, and causal mediation analyses were used to assess stroke associations and the role of left ventricular (LV) thrombus.
Main Results:
- Apical aneurysm was significantly associated with CE stroke when using genetic matching, with 63.3% of this association mediated by LV thrombus.
- Prior CE stroke and LV thrombus were independent predictors of prior CE stroke.
- Neither prior CE stroke nor apical aneurysm predicted mortality or heart transplantation, but incident CE stroke was linked to prior CE stroke and LV thrombus.
Conclusions:
- Cardioembolic stroke in CCM is predominantly driven by LV thrombus formation.
- Apical aneurysm contributes to embolic risk primarily by promoting thrombus formation.
- Identifying LV thrombus and implementing anticoagulation are key for targeted stroke prevention in CCM.
Objective:
Apical aneurysm is a hallmark of Chagas cardiomyopathy (CCM) and has long been implicated in thromboembolic complications. However, its independent contribution to cardioembolic (CE) stroke and the mechanisms underlying this association remain incompletely understood. This study evaluated the association between apical aneurysm and CE stroke and assessed the prognostic implications of CE stroke in patients with CCM.
Methods:
In this prospective cohort study, 518 patients with confirmed CCM were enrolled at a tertiary referral centre between 2007 and 2022. Baseline evaluation included clinical assessment, electrocardiography and echocardiography. Ischaemic stroke subtype was classified using the Causative Classification System. Logistic regression analyses examined factors associated with CE stroke. Genetic matching was used to assess the association between apical aneurysm and CE stroke while causal mediation analysis evaluated the contribution of left ventricular (LV) thrombus. Cox proportional hazards models assessed factors associated with all-cause mortality or heart transplantation.
Results:
At enrolment, 73 patients (14.1%) had a history of CE stroke. In multivariable analyses, New York Heart Association (NYHA) functional class III/IV, lower LV ejection fraction and LV thrombus were independently associated with prior CE stroke, whereas apical aneurysm was not. However, matched analyses demonstrated a significant association between apical aneurysm and CE stroke, of which 63.3% was mediated through LV thrombus formation. During a mean follow-up of 4.9 years, 174 patients died and 22 underwent heart transplantation. NYHA functional class III/IV, right-sided heart failure, left atrial enlargement and lower LV ejection fraction were independently associated with the composite outcome of death or heart transplantation, whereas neither prior CE stroke nor apical aneurysm was associated with adverse outcomes. Incident CE stroke occurred in 41 patients (9%) and was independently associated with prior CE stroke and LV thrombus.
Conclusion:
In CCM, CE stroke is primarily driven by LV thrombus formation. Apical aneurysm increases embolic risk mainly through thrombus mediation, while prior CE stroke identifies patients at increased risk for recurrence. These findings support targeted stroke prevention strategies focused on thrombus detection and anticoagulation.
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