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Published on: August 28, 2018
The correlation between carotid siphon calcification and lacunar infarction
Nu Rhee Hong1, Hyung Suk Seo, Young Hen Lee
1Department of Radiology, Korea University Ansan Hospital, 516 Gojan1-dong, Danwon-gu, Ansan, Gyeonggi, 425-707, South Korea.
Insights
Carotid siphon (CS) calcification is linked to lacunar infarction, a type of stroke caused by small-vessel disease. Higher CS calcification scores indicate a greater risk of developing lacunar infarction.
Area of Science:
- Neurology
- Radiology
- Vascular Medicine
Background:
- Small-vessel disease is a common cause of lacunar infarction.
- Carotid siphon (CS) calcification is a potential indicator of cerebrovascular disease.
Purpose of the Study:
- To investigate the correlation between carotid siphon calcification and lacunar infarction.
- To determine if CS calcification can predict the occurrence of lacunar infarction.
Main Methods:
- Retrospective study of 445 patients over 40 years old.
- Classification into groups based on lacunar infarction count (0, 1-3, 4+).
- Evaluation of CS calcification severity using CT scans and a five-point scale; statistical analysis with ANOVA and logistic regression.
Main Results:
- Significant differences in CS calcification scores were found among groups with varying lacunar infarction counts (P < 0.05).
- Higher CS calcification scores were associated with increased rates of lacunar infarction.
- CS calcification, age, and hypertension were identified as significant risk factors for lacunar infarction (P < 0.05).
Conclusions:
- Carotid siphon calcification is correlated with the occurrence of lacunar infarction.
- The degree of CS calcification may serve as a predictor for future lacunar infarction.
Introduction:
The aim of this study was to evaluate the correlation between carotid siphon (CS) calcification and lacunar infarction caused by small-vessel disease.
Methods:
This retrospective study included 445 patients (M/F = 256:189) older than 40 years (mean age 60.0 ± 12.3 years, range 41-98 years) without large intracranial lesions who had undergone both brain CT and MRI within an interval of 6 months. The patients were classified into three groups according to the number of lacunar infarctions: group I-zero infarctions (n = 328), group II-one to three infarctions (n = 94), and group III-four or more infarctions (n = 23). The severity of CS calcification was evaluated on CT and scored on a five-point scale (0-none, 1-stippled, 2-thin continuous or thick discontinuous, 3-thick continuous, 4-double tracts), and the calcification scores on both sides were summed. An ANOVA test was used to compare calcification scores among the three groups, and a logistic regression test was used to evaluate the influence of CS calcification and known cerebrovascular risk factors on the occurrence of lacunar infarction.
Results:
On the ANOVA test, total calcification scores were significantly different among the three groups (group I = 1.28 ± 1.99, group II = 3.31 ± 2.39, group III = 4.36 ± 2.08; P < 0.05). Higher rates of lacunar infarction were associated with higher CS calcification scores. On the logistic regression test, CS calcification, age, and hypertension were significant risk factors for lacunar infarction (P < 0.05).
Conclusion:
CS calcification was correlated with the occurrence of lacunar infarction. The degree of CS calcification may be used to predict the possibility of a future lacunar infarction.
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