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Small deep infarction in patients with atrial fibrillation: evidence of lacunar pathogenesis
Yong-shik Park1, Pil-Wook Chung, Yong Bum Kim
1Department of Neurology, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, South Korea.
Insights
In patients with atrial fibrillation (AF), severe white matter lesions (WMLs) and multiple lacunes predict small deep infarcts, suggesting small vessel disease as a cause, not just cardioembolism.
Area of Science:
- Neurology
- Cardiology
- Radiology
Background:
- Distinguishing cardioembolism from small vessel disease in atrial fibrillation (AF) stroke is challenging.
- Preexisting small vessel disease may influence acute infarct patterns in AF patients.
Purpose of the Study:
- To investigate if preexisting small vessel disease differs by infarct pattern in AF patients.
- To identify factors associated with acute single small deep infarction in AF stroke patients.
Main Methods:
- 231 AF stroke patients were categorized into lacunar (n=20) or nonlacunar (n=211) infarct patterns.
- White matter lesions (WMLs) severity (Fazekas scale), multilacunar state, and microbleeds were assessed.
- Demographics, vascular risk factors, and neuroimaging data were compared between groups.
Main Results:
- Lacunar infarct pattern group had significantly more severe WMLs (median total score 2.5 vs. 1.0) and a higher prevalence of multilacunar state (65% vs. 28.9%).
- Microbleed presence did not differ between groups.
- Periventricular WMLs, deep WMLs, and multilacunar state were independent predictors of a lacunar infarct pattern.
Conclusions:
- Severity of WMLs and chronic lacunes are independent predictors of infarct pattern in AF patients.
- Acute single small deep infarction in AF may stem from intrinsic small vessel disease.
Background:
It is difficult to clarify whether small deep infarction is caused by cardioembolism or intrinsic small vessel disease in patients with atrial fibrillation (AF). The purpose of this study was to determine whether preexisting small vessel disease would differ according to the presenting infarct pattern and to determine the factors associated with acute single small deep infarction in stroke patients with AF.
Methods:
Between January 2008 and August 2012, 1,592 consecutive patients with acute ischemic stroke presenting within 7 days of symptom onset were entered in a prospectively maintained stroke registry. For the present study, 231 stroke patients with AF were enrolled irrespective of the stroke subtype. We divided these patients into 2 groups (lacunar infarct pattern, n = 20, vs. nonlacunar infarct pattern, n = 211) according to the acute infarct pattern on diffusion-weighted imaging. Patients with acute single small deep infarction on diffusion-weighted imaging were assigned to the lacunar infarct pattern group. We assessed the severity of preexisting small vessel disease by grading white matter lesions (WMLs) according to the Fazekas scale (periventricular WML score ranging from 0 to 3 and deep WML score ranging from 0 to 3 were added to give a total WML score ranging from 0 to 6), multilacunar state (number of chronic lacunes ≥2) and the presence of microbleeds. Demographic characteristics, vascular risk factors and neuroimaging data were compared between the two groups.
Results:
Patients with a lacunar infarct pattern showed more severe WMLs than those with a nonlacunar pattern [median total WML score 2.5 (range 2-4) vs. 1.0 (0-2); p < 0.001]. A multilacunar state was more prevalent in the lacunar infarct pattern group compared with the nonlacunar pattern group (65 vs. 28.9%; p = 0.001). However, the presence of microbleeds did not differ between the groups. Multiple logistic regression analyses revealed periventricular WMLs [odds ratio (OR) 4.12, 95% confidence interval (CI) 2.14-7.92], deep WMLs (OR 3.42, 95% CI 1.75-6.66) and multilacunar state (OR 7.85, 95% CI 2.45-25.6) as the predictors of a lacunar infarct pattern.
Conclusions:
The severity of WMLs and chronic lacunes were independent predictors of the incident infarct pattern, which suggested that acute single small deep infarction might be caused by intrinsic small vessel disease despite the presence of concomitant AF.
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