Author(s)

C. A. Jackson, A. Hutchison, M. S. Dennis, J. M. Wardlaw, A. Lindgren, B. Norrving, C. S. Anderson, G. J. Hankey, K. Jamrozik, P. Appelros, C. L. M. Sudlow

ISBN

0039-2499

Publication year

2010

Periodical

Stroke

Periodical Number

4

Volume

41

Pages

624-629

Author Address

Sudlow, CLM Western Gen Hosp, Div Clin Neurosci, Edinburgh EH4 2XU, Midlothian, Scotland Univ Edinburgh, Div Clin Neurosci, Edinburgh EH8 9YL, Midlothian, Scotland Univ Lund Hosp, Dept Neurol, S-22185 Lund, Sweden Univ Sydney, George Inst Int Hlth, Sydney, NSW 2006, Australia Royal Perth Hosp, Dept Neurol, Perth, WA, Australia Univ Adelaide, Sch Populat Hlth & Clin Practice, Adelaide, SA 5005, Australia Orebro Univ Hosp, Dept Neurol, Orebro, Sweden Univ Edinburgh, Inst Genet & Mol Med, Edinburgh EH8 9YL, Midlothian, Scotland

Full version

Background and Purpose-Differences in risk factor profiles between lacunar and other ischemic stroke subtypes may provide evidence for a distinct lacunar arteriopathy, but existing studies have limitations. We overcame these by pooling individual data on 2875 patients with first-ever ischemic stroke from 5 collaborating prospective stroke registers that used similar, unbiased methods to define risk factors and classify stroke subtypes.
Methods-We compared risk factors between lacunar and nonlacunar ischemic strokes, altering the comparison groups in sensitivity analyses, and incorporated these data into a meta-analysis of published studies.
Results-Unadjusted and adjusted analyses gave similar results. We found a lower prevalence of cardioembolic source (adjusted odds ratio, 0.33; 95% CI, 0.24 to 0.46), ipsilateral carotid stenosis (odds ratio, 0.21; 95% CI, 0.14 to 0.30), and ischemic heart disease (odds ratio, 0.75; 95% CI, 0.58 to 0.97) in lacunar compared with nonlacunar patients but no difference for hypertension, diabetes, or any other risk factor studied. Results were robust to sensitivity analyses and largely confirmed in our meta-analysis.
Conclusions-Hypertension and diabetes appear equally common in lacunar and nonlacunar ischemic stroke, but lacunar stroke is less likely to be caused by embolism from the heart or proximal arteries, and the lower prevalence of ischemic heart disease in lacunar stroke provides additional support for a nonatherosclerotic arteriopathy causing many lacunar ischemic strokes. Our findings have implications for how clinicians classify ischemic stroke subtypes and highlight the need for additional research into the specific causes of and treatments for lacunar stroke. (Stroke. 2010;41:624-629.)