Published online before print May 22, 2003, doi: 10.1161/01.STR.0000076521.37285.31
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(Stroke. 2003;34:1409.)
© 2003 American Heart Association, Inc.
Original Contributions |
Editorial Comment: The Fall and Rise of Lacunar Infarction With Carotid Stenosis
Department of Neurology, Lausanne-CH, Lausanne, Switzerland
Lacunar infarction (LI) is one of the most common subtypes of ischemic stroke.1 Introduced by Fisher,2 the term lacunar infarction is now established in the literature. However, the concept of LI remains a subject of debate,3 since lacunar syndromes were not found to be exclusively pathognomonic of small-artery disease.
In this issue of Stroke, Tejada et al4 address the potential relationship between LI and the presence of an internal carotid artery stenosis (ICAS). Whether this finding is causative or coincidental is debatable. Previous studies5–7 have already investigated the question with opposite opinions.8–14 In the ECST study, patients with LI had less severe ICAS, leading to the hypothesis that severe ICAS in patients with LI may just be coincidental.9 Recently, studies using carotid and transcranial ultrasound15,16 have revisited this question. In the study of Cupini et al,15 the intima-media thickness (IMT) of carotids as measured by ultrasound was significantly higher in patients with nonlacunar infarction (NLI) versus both those with LI and controls. The IMT, considered as an early marker of atherosclerosis when increased, may have a predictive value to separate LI versus NLI. However, another study17 also using the IMT did not find a difference between LI and NLI. Mead et al16 studied patients with recent LI and compared the results of carotid and middle cerebral artery (MCA) ultrasound. The authors16 could not find a difference between patients with LI and those with NLI for either carotid or MCA disease. They concluded that ICA stenosis in patients with LI may be coincidental.
In this debate, the article by Tejada et al4 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 al4 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 al4 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,18 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.
Nevertheless, the study of Tejada et al4 is a new cornerstone illustrating the controversy about LI. For instance, we19 have demonstrated that atrial fibrillation is not always coincidental in patients with subcortical infarcts and a lacunar stroke. We also suggested that some clinical and radiological characteristics were different between patients with subcortical infarcts and cardioembolism versus patients with subcortical infarcts due to small-artery disease. New neuroimaging has shown DWI to be a highly sensitive and specific diagnostic tool for acute small-vessel infarction. These studies7,20–22 accepted the concept that LI may occasionally be associated with ICAS. In addition, an animal model of stroke23 has demonstrated lacunes in the brain of normotensive rats after nonocclusive thrombus in the carotid. DWI-MRI performed in acute lacunar syndrome24 showed that there may a variety of brain lesions and locations. Another DWI study25 reported that almost 1 in every 6 patients presenting with a classical lacunar syndrome had multiple infarcts, including cortical lesions. A recent study26 showed that MCA stenosis should also be found in patients with LI. DWI combined to PWI27 altered the final diagnosis of infarct pathogenesis from small-vessel disease to large-artery embolism in 13 of 19 patients with LI.
The study of Tejada et al4 suggests that lacunar syndromes are not indicative of a single underlying mechanism of stroke. However, further studies using a large number of patients and modern diagnostic tools (DWI and PWI MRI) are needed before altering the current management28 of lacunar infarction.
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