Editorial Comment: The Fall and Rise of Lacunar Infarction With Carotid Stenosis

Editorial Comment: The Fall and Rise of Lacunar Infarction With Carotid Stenosis: 

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Tejada J, Díez-Tejedor E, Hernández-Echebarría L, Balboa O. Does a relationship exist between carotid stenosis and lacunar infarction? Stroke.2003; 34: 1404–1409.

In this issue of Stroke, Tejada et al address the potential relationship between LI and the presence of an internal carotid artery stenosis (ICAS). The article investigates the relationship between LI and ICAS in a large prospective study of 330 patients, including 205 with LI and 125 with NLI. 

The authors draw 4 interesting conclusions: First, even if the presence of significant (>50%) ICAS is lower in LI compared with NLI, the probability of carotid disease increases when LI is present in the ipsilateral carotid territory. Second, ICAS without contralateral ICAS was reported in 73% of the cases, suggesting that ICAS is indeed a marker of ipsilateral LI. Third, logistic regression analysis in “pure” LI associated with ICAS >50% showed that peripheral artery disease was the only significant factor associated with stroke. Fourth, the combined presence of a left ventricular hypertrophy (LVH) with ICAS >70% determined predominance of LI in 1 hemisphere, suggesting a role of ICAS. Multivariate analysis showed that only 2 factors predicted unilateral LI:LVH and ICAS >75%. Tejada et al conclude that moderate ICAS may appear in an appreciable percentage of LI in the ipsilateral territory and that severe ICAS is related to multiple LI. 

The main message of the report is the identification of the need to search for large-artery disease as the cause of LI. The question raised is whether the etiological association between ICAS and LI should be accepted as a final evidence. 

The study of Tejada et al presents some limitations: 

First, authors used only clinical examination and CT scan (not MRI) to diagnose LI. Cortical small infarcts may mimic LI and inversely, so that MRI with DWI is currently the “gold standard” to investigate an isolated and “active” lacune. Second, because of possible differences between the 2 centers for grading the degree of ICAS, it is reasonable to assume that some ipsilateral or contralateral ICA stenoses were overestimated. Indeed, only 34.5% of cases had radiological examination (DSA or MRA) to confirm ultrasound. In this series, 73% of ipsilateral ICAS were not associated with contralateral ICAS, which is very high. The problem is that criteria to grade ICAS and the technique used, either DSA or ultrasound or MRA, limit the comparisons with other studies. Third, as seen in the article’s Tables 1 and 3, there are no precise data on potential cardiac sources of embolism and the type of echocardiography used. Moreover, as the neuroimaging used to diagnose LI was CT scan, some LI located in the brainstem may have been considered as hemispheric LI ipsilateral to ICAS. 

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