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Association between left atrial enlargement and poor cerebral collaterals in large vessel occlusion
Md Manjurul Islam Shourav1, Bhrugun Anisetti1, Raja R Godasi1
1Department of Neurology, Mayo Clinic, Jacksonville, Florida, United States.
Insights
Left atrial enlargement (LAE) is linked to poor cerebral collaterals in large vessel occlusion (LVO) stroke patients. This finding suggests a heart-brain connection that may influence stroke outcomes.
Area of Science:
- Cardiology
- Neurology
- Radiology
Background:
- Left atrial enlargement (LAE) is a risk factor for atrial fibrillation, a cause of large vessel occlusion (LVO) stroke.
- Cerebral collaterals are crucial for protecting brain tissue during ischemic events.
- The impact of structural heart disease, like LAE, on cerebral collateral circulation is not well understood.
Purpose of the Study:
- To investigate the association between left atrial enlargement (LAE) and cerebral collateral status.
- To determine if LAE is independently related to poor cerebral collaterals in patients with acute LVO stroke.
Main Methods:
- Retrospective analysis of 235 patients with LVO stroke undergoing endovascular thrombectomy (EVT).
- Echocardiography and computed tomography angiography (CTA) were used to assess LAE and cerebral collaterals.
- Multivariate logistic regression adjusted for demographics and vascular risk factors.
Main Results:
- 37.9% of patients had LAE, and 44.7% had poor collaterals.
- Patients with LAE showed a significantly higher prevalence of poor collaterals (58.4% vs. 36.3%, P=0.001).
- LAE was independently associated with poor cerebral collaterals (adjusted OR, 1.84; P=0.048).
Conclusions:
- A significant association exists between LAE and poor cerebral collaterals in LVO stroke patients.
- Further research is needed to explore shared mechanisms, such as endothelial dysfunction, linking heart and brain health.
Objectives:
Left atrial enlargement (LAE) is a known risk factor for atrial fibrillation, a common cause of large vessel occlusion (LVO) leading to ischemic stroke. While robust cerebral collaterals protect penumbral tissue from infarction, the effect of structural heart disease on cerebral collaterals remains uncertain. This study aims to investigate the association between LAE and cerebral collaterals in patients with acute LVO stroke.
Materials And Methods:
We conducted a retrospective study of consecutive patients with middle cerebral and/or internal carotid LVO who underwent endovascular thrombectomy (EVT) between 2012 to 2020. Consecutive patients with echocardiography and computed tomography angiography (CTA) of the head were included. Multivariate logistic regression analysis was performed to evaluate the relationship between LAE and poor cerebral collaterals, adjusting for demographics (age, sex, race) and vascular risk factors (hypertension, diabetes and smoking).
Results:
The study included 235 patients with mean age of 69±15 years and an initial mean National Institutes of Health Stroke Scale score of 18. Of these, 89 (37.9 %) had LAE, and 105 (44.7 %) had poor collaterals. Patients with LAE were more likely to have poor collaterals compared to those without LAE (58.4 % vs 36.3 %, P = 0.001). LAE was independently associated with higher odds of poor collaterals (odds ratio, 2.47; P = 0.001), even after adjusting for covariables (odds ratio 1.84, P = 0.048).
Conclusions:
Our study demonstrated a significant association between LAE and poor cerebral collaterals in patients with LVO stroke undergoing EVT. Further research is warranted to explore potential shared mechanisms, such as endothelial dysfunction, underlying this heart-brain association.
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