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Similarities to Large Artery Vs Small Artery Disease

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Similarities to Large Artery Vs Small Artery Disease ORIGINAL CONTRIBUTION The Course of Patients With Lacunar Infarcts and a Parent Arterial Lesion Similarities to Large Artery vs Small Artery Disease Oh Young Bang, MD, PhD; Sung Yeol Joo, MD; Phil Hyu Lee, MD; Uk Shik Joo, MD; Jae Hyuk Lee, MD; In Soo Joo, MD; Kyoon Huh, MD Background: The significance of occlusive lesions of Main Outcome Measures: Recurrent strokes and the the parent artery in patients with lacunar syndrome (LS) prognosis were registered for 1 year, and the outcome and small deep infarcts (SDIs) on diffusion-weighted im- of the PAD group was compared with that of the SAD aging remains unclear. and LAD groups. Objective: To compare the recurrence of stroke in pa- Results: During follow-up, there were 9 deaths (6 vas- tients with LS and SDIs between those with vs without a cular) and 18 recurrent strokes. The recurrence rate in parent arterial lesion. the PAD group (16%) was significantly higher than that in the SAD group (1%) (P=.01) but similar to that in the Design: Analysis of data from a prospective acute stroke LAD group (17%) (P=.87). The presence of the parent registry. arterial lesion was the only independent predictor of stroke recurrence in patients with LS and SDIs (odds ratio, 13.8; Setting: University hospital. 95% confidence interval, 1.5-123.9; P=.02). Patients: Using clinical syndrome, diffusion-weighted Conclusions: Although LS on examination, SDIs on dif- imaging, and vascular studies, we divided 173 patients fusion-weighted imaging, and a stable hospital course sug- into 3 groups: (1) parent arterial disease occluding deep gest lacunar stroke of benign course, our results indicate perforators (PAD), LS with SDIs, and a parent arterial le- that the PAD group represents an intracranial type of LAD. sion (n=32); (2) small artery disease (SAD) (n=70); and (3) large artery disease (LAD) (n=71). Arch Neurol. 2004;61:514-519 ACUNAR STROKES, THAT IS, LA- However, middle cerebral artery cunar syndrome (LS) with (MCA) stenosis is recognized increas- symptomatic small deep in- ingly in patients with SDIs.10,11 Previ- farcts (SDIs) on neuroimag- ously, Madden et al12 reported that ap- ing, are associated with low proximately one third of patients who were Lmortality rates and low stroke recur- initially diagnosed as having small artery rence rates in hospital- and community- disease (SAD), based on clinical features based studies.1-7 Moreover, intracranial ste- and baseline computed tomographic find- nosis has been reported to be a negligible ings, had abnormalities on diagnostic study cause of SDI.8 For these reasons, physi- and suggested that a careful evaluation of cians treating patients with LS and SDIs the etiology is justified in all patients with are apt to be negligent in investigating the stroke, regardless of the presumed sub- underlying cause, such as parent arterial type. In a previous study by our group,13 disease (PAD). In fact, in the TOAST (Trial we recently found that atherosclerotic of ORG 10172 in Acute Stroke Treat- MCA lesions were a common cause of ment) criteria, a widely used classifica- striatocapsular SDIs in Asian patients, and tion scheme for ischemic stroke sub- it was reported14,15 that approximately half types, patients with traditional LS and of the patients with MCA stenosis also had ipsilateral intracranial stenosis are classi- SDIs. Owing to the high risk of stroke if fied as having “2 or more causes identi- occlusive lesions are present,10 the prog- From the Department of fied” and are lumped together with pa- nosis or recurrence rate in patients with Neurology, School of Medicine, tients with an “incomplete or negative LS and SDIs might depend on the exis- Ajou University, Suwon, evaluation” as having so-called ischemic tence of a parent arterial lesion. How- South Korea. stroke of unknown cause.9 ever, no long-term follow-up data on pa- (REPRINTED) ARCH NEUROL / VOL 61, APR 2004 WWW.ARCHNEUROL.COM 514 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 396 Patients Admitted During the Study NE 24 Excluded DWI 13 Had Subacute/Chronic Infarction 11 Had No Relevant Lesion on DWI 372 Randomized 136 Patients With Lacunar SD (LS) 236 Patients With Non-LS and SDIs on DWI and Larger Lesions on DWI • Workup 34 Excluded 165 Excluded 4 Had a Cardioembolic Source Vascular, Cardiologic Laboratory 36 Had a Cardioembolic Source 4 Had Another Determined Cause 19 Had Undetermined Etiology • Follow-up 8 Had Incomplete Workup 41 Had No Determined Etiology 18 Were Lost to Follow-up mRS Barthel Index 13 Had Another Determined Etiology 19 Had Incomplete Workup 37 Were Lost to Follow-up SAD Group PAD Group LAD Group n = 70 n = 32 n = 71 Figure 1. Selection and grouping of the patients. NE indicates neurologic examination; DWI, diffusion-weighted image; SDI, small deep infarct; SD, syndrome; LS, lacunar syndrome; mRS, modified Rankin Scale; SAD, small artery disease; PAD, parent arterial disease; LAD, large artery disease. tients with occlusive lesions of the parent artery, such of prothrombic tendency, including protein C, protein S, an- as the MCA or the basilar artery (BA), are available. tithrombin III, and antiphospholipid antibodies (lupus anti- We hypothesized that the course of patients with coagulant and anticardiolipin IgG and IgM) were checked in lacunar stroke (with LS and SDIs on neuroimaging) all patients younger than 50 years. and an occlusive lesion of the parent artery is similar PATIENT SELECTION to that of large artery disease (LAD) rather than that of SAD. Therefore, we compared the long-term prognosis During the study, 396 consecutive patients with symptomatic of patients with LS and SDIs in terms of the stroke ischemic stroke were admitted to the Department of Neurol- recurrence rate, type of recurrent stroke, and progno- ogy at Ajou University Hospital (Figure 1). The group in- sis and its relation to possible clinical prognostic fac- cluded 136 patients with acute symptomatic lacunar infarcts. tors and the existence of a relevant large arterial Patients with acute symptomatic lacunar infarcts were defined lesion. Furthermore, we compared these patients with as those who were examined within a week of symptom onset those with non-LS. who showed focal neurologic deficits lasting longer than 24 hours that were consistent with LS and those who had rel- METHODS evant small deep lesions on DWI. All patients provided in- formed consent to participate in this study. Between December 1, 2000, and May 23, 2002, we prospec- Digital subtraction or magnetic resonance angiography, tively studied consecutive patients with ischemic stroke, who electrocardiography, and transthoracic echocardiography were had been examined within a week of symptom onset, and those performed in all patients, and transesophageal echocardiogra- who had a relevant lesion on diffusion-weighted imaging (DWI). phy and Holter monitoring were performed in selected pa- tients, especially when the possibility of a cardioembolic source RISK FACTORS AND LABORATORY WORKUP was suggested or when no other cause of stroke was found. Pa- tients with potential sources of cardioembolism (atrial fibril- Patients were evaluated according to a protocol that included lation, mitral stenosis, prosthetic valve, myocardial infarction demographic data, medical history, vascular risk factors, and within 6 weeks, intracardiac clot, ventricular aneurysm, and the National Institutes of Health Stroke Scale at days 0 to 7.16 bacterial endocarditis)20 were excluded from the study (n=4) We used the same criteria for vascular risk factors as in our pre- because a stenotic lesion of an intracranial artery on digital sub- vious study17: hypertension, diabetes mellitus, hypercholester- traction or magnetic resonance angiography might represent a olemia, and smoking. On day 7 after hospital admission, all the partially recanalized clot rather than an atherosclerotic lesion. patients were evaluated according to the National Institutes of We also excluded (1) patients with other determined causes, Health Stroke Scale, the modified Rankin Scale,18 and the Bar- such as carotid dissection, hypercoagulable state, vasculitis, and thel Index.19 Laboratory tests included brain magnetic reso- complicated migraine (n=4); (2) those who did not undergo a nance imaging (1.5 T), vascular study, echocardiography, elec- complete workup (n=8); and (3) those who were not fol- trocardiography, and routine blood testing. Hemostatic markers lowed up for 1 year after the index stroke (n=18). (REPRINTED) ARCH NEUROL / VOL 61, APR 2004 WWW.ARCHNEUROL.COM 515 ©2004 American Medical Association. All rights reserved. Downloaded From: https://jamanetwork.com/ on 10/01/2021 3-month intervals for up to 12 months after stroke onset. Dur- Table 1. Clinical Characteristics of 173 Patients ing 1-year follow-up, information on the attainment of end points was obtained through direct clinical examination and through SAD Group PAD Group LAD Group information given by family members in cases of death (n=4). Characteristic (n = 70) (n = 32) (n = 71) Recurrent stroke was defined as a focal neurologic deficit oc- Age, mean ± SD, y 58 ± 12 60 ± 12 64 ± 13 curring suddenly in a vascular territory, lasting more than 24 Male sex, No. (%) 43 (61) 22 (69) 42 (59) hours, and occurring at any time after the acute phase of the 7,26 Territory, No. (%)* index stroke. The type of recurrent stroke was based on clini- Carotid 55 (79) 25 (78) 56 (79) cal and magnetic resonance imaging findings. To define the out- Vertebrobasilar 15 (21) 7 (22) 15 (21) come of patients with stroke, Barthel Index scores during fol- Lacunar syndrome, No. (%) low-up after the index stroke were divided into 2 classes at a Pure motor hemiplegia 45 (64) 24 (75) 0 cutoff value of 60, and the modified Rankin Scale scores were Sensory-motor stroke 12 (17) 6 (19) 0 divided at a cutoff value of 3.27 Pure sensory stroke 8 (11) 1 (3) 0 Dysarthria–clumsy hand 4 (6) 0 0 STATISTICAL ANALYSIS syndrome Ataxic-hemiparesis 1 (1) 1 (3) 0 Between-group differences were examined using the ␹2 test, Severity of stroke, Fisher exact test, unpaired t test, or 1-way analysis of vari- mean ± SD score† ance with post hoc analysis.
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