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From the Neurovascular Unit (Drs. Arenillas, Molina, Montaner, and Álvarez-Sabín, M. Quintana), Lipid Research Unit (Dr. Chacón), and Magnetic Resonance (Drs. Rovira and Sánchez) and Computed Tomography (Dr. Coscojuela) Units, Department of Neuroradiology, Vall d’Hebron Hospital, Barcelona, Spain.
Address correspondence and reprint requests to Dr. Juan F. Arenillas Lara, Neurovascular Unit, Department of Neurology, Hospital Vall d’Hebron, Universitat Autònoma de Barcelona, Passeig Vall d’Hebron 119-129, 08035 Barcelona, Spain; e-mail: juanfarenillas{at}terra.es
Background: Lipoprotein (a) (Lp[a]) has important atherothrombogenic properties, but its role in intracranial atherosclerosis remains unclear.
Objective: To investigate the relationship between Lp(a) level and the extent of intracranial large-artery occlusive disease.
Methods: Between June 2001 and August 2003, 166 consecutive first-ever TIA or stroke patients had intracranial stenoses on transcranial Doppler, of which 100 fulfilled all inclusion criteria. The extent of intracranial large-artery occlusive disease was assessed by the number of angiographically confirmed intracranial stenoses. Serum Lp(a) was determined a minimum of 3 months after stroke onset.
Results: Two hundred eighty-one intracranial stenoses were documented. Fifty-one (51%) patients had three or more stenoses (greater-extent group). Patients in the highest Lp(a) quartile had a higher adjusted odds ratio (OR) for a greater extent than those in the lowest quartile (OR 3.43, 95% CI 1.04 to 11.33, p = 0.04). A positive correlation was found between Lp(a) concentration and the number of stenoses (r = 0.310, p = 0.002). Moreover, Lp(a) level increased gradually with the number of stenoses (p = 0.02). A multiple logistic regression model identified diabetes (OR 2.4, 95% CI 1.04 to 5.57, p = 0.04) and high Lp(a) (OR 2.52, 95% CI 1.03 to 6.18, p = 0.043) as independent markers of a greater extent of intracranial large-artery occlusive disease.
Conclusions: High Lp(a) level and diabetes mellitus are independent markers of a greater extent of intracranial large-artery occlusive disease. These findings support a role for Lp(a) in intracranial stenotic atherogenesis and might be useful for the selection of high-risk patients.
Received January 21, 2004. Accepted in final form March 3, 2004.
This article has been cited by other articles:
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L. B. Goldstein, R. Adams, M. J. Alberts, L. J. Appel, L. M. Brass, C. D. Bushnell, A. Culebras, T. J. DeGraba, P. B. Gorelick, J. R. Guyton, et al. Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Stroke Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline. Stroke, June 1, 2006; 37(6): 1583 - 1633. [Abstract] [Full Text] [PDF]
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J. F. Arenillas, J. Alvarez-Sabin, J. Montaner, A. Rosell, C. A. Molina, A. Rovira, M. Ribo, E. Sanchez, and M. Quintana Angiogenesis in Symptomatic Intracranial Atherosclerosis: Predominance of the Inhibitor Endostatin Is Related to a Greater Extent and Risk of Recurrence Stroke, January 1, 2005; 36(1): 92 - 97. [Abstract] [Full Text] [PDF]
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