Retinal ischemic perivascular lesions in cortical cerebral infarction: a comparison against controls
摘要
Retinal ischemic perivascular lesions (RIPLs), identified on optical coherence tomography (OCT) imaging, represent focal retinal infarcts. RIPLs have been linked to stroke, but not specifically cortical ischemic infarctions. Main study questions: Do RIPL counts differ among controls, pre-stroke patients, and post-stroke patients?
Subjects/MethodsRetrospective, cross-sectional, single institution study of 65 identified patients consenting for research who had both high-quality, bilateral, 6 mm × 6 mm macular optical coherence tomography (OCT) imaging performed within five years of cortical ischemic infarction occurrence and 65 controls who had a coronary artery calcium (CAC) score of 0 within 1 year following baseline OCT. The differences in mean total RIPLs among pre-stroke, post-stroke, and controls groups were assessed, as were differences by stroke circulation (anterior vs. posterior) and laterality (ipsilateral vs. contralateral eye). The effects of potential confounders (known cardiovascular risk factors) were examined with multivariate analysis.
Results129 patients [controls:65; pre-stroke:27; post-stroke:37 (anterior:17; posterior:20)] were included. Pre-stroke and post-stroke patients have significantly higher RIPL counts compared to controls (mean ± std: controls, 2.05 ± 2.41; pre-stroke, 3.39 ± 3.55; post-stroke, 3.62 ± 4.14; p = 0.03). No differences were identified between pre- and post-stroke patients, anterior and posterior circulation, and ipsilateral and contralateral eyes. Multivariate analyses identified no statistically significant association between RIPL counts and post-stroke patients compared to controls.
ConclusionsPre- and post-stroke patients exhibit higher RIPL counts versus controls, without differences between anterior- and posterior-circulation strokes or ipsilateral and contralateral eyes. In cortical stroke, RIPLs likely indicate chronic microvascular dysfunction from baseline cardiovascular risk factors, not acute stroke-associated changes.