Abstract
Background
Lacunar infarcts are small, deep brain infarctions traditionally attributed to intrinsic small vessel disease, such as lipohyalinosis and microatheroma formation. However, emerging evidence suggests that a subset of lacunar strokes may result from embolic occlusions originating from proximal large arteries or the heart. Identifying the underlying etiology is crucial for optimizing secondary prevention strategies, as embolic strokes require different management approaches compared to non-embolic small vessel disease.
Objective
This study aims to evaluate the prevalence of proximal embolic sources in patients with lacunar infarcts and assess their clinical and imaging characteristics to determine whether embolism plays a significant role in their pathogenesis.
Methods
In this prospective observational study over 18 months at a tertiary care hospital, 337 ischemic stroke patients were screened. Sixty patients (17.8%) with radiologically confirmed lacunar infarcts were enrolled. Demographic data, vascular risk factors, and clinical presentations were recorded. Investigations included computed tomography (CT) angiography to assess large-artery pathology, 2D echocardiography to identify cardiac embolic sources, and 72-h Holter monitoring to detect atrial fibrillation or other arrhythmias. Stroke severity was evaluated using the National Institutes of Health Stroke Scale (NIHSS), and functional outcomes were assessed using the modified Rankin scale (MRS).
Results
The prevalence of lacunar strokes was 17.8%, with the majority (60%) occurring in individuals aged 41-60 years. Hypertension was the most common risk factor (45%), followed by diabetes mellitus (31.67%) and dyslipidemia (41%). Proximal embolic sources were identified in 36.6% of patients based on CT angiography, with the most common sites being the internal carotid artery (40.9%) and the middle cerebral artery (13.6%). Cardiac abnormalities were detected in 18.3% of cases on echocardiography, and Holter monitoring identified atrial fibrillation in 3.3%. Functional outcomes showed moderate to severe disability (MRS 3-5) in 43.34% of patients, with neurological deterioration occurring in 40% within the first week.
Conclusion
This study suggests that embolic mechanisms contribute to a significant proportion of lacunar infarcts. Routine vascular and cardiac imaging should be considered in lacunar stroke patients to identify potential embolic sources, which may necessitate anticoagulation for secondary stroke prevention. Further research is needed to refine diagnostic criteria and optimize treatment strategies for embolic versus non-embolic lacunar strokes.
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