Abstract
We previously reported that plasma lipoprotein(a) [Lp(a)]1 is an independent risk factor for coronary artery disease, abdominal aortic aneurysm, peripheral arterial disease, and ischemic stroke (1). Although the exact pathophysiological role of Lp(a) has not been definitively established, both atherogenic and thrombogenic mechanisms have been proposed. In this study, we measured plasma Lp(a) in ischemic stroke patients who had been subdivided into etiologic subtypes with the TOAST (Trial of ORG 10172 in Acute Stroke Treatment) classification to determine if stroke subtype is a confounder of the Lp(a) association. Ischemic stroke patients (n = 245) and arterial disease–free and stroke-free controls (n = 435) were recruited from the Otago region of New Zealand as previously reported (1). Stroke patients were placed into TOAST classification subtypes by means of a computer algorithm developed by Goldstein and colleagues(2). The TOAST subgroups were large-artery atherosclerosis (LAA), cardioembolism, small-artery occlusion (SAO), undetermined due to 2 or more causes (multiple etiologies) (ME), or undetermined etiology due to negative or incomplete evaluation. Inclusion criteria for controls were an age >52 years and no history of ischemic heart disease or stroke, including transient ischemic attack [Questionnaire for Verifying Stroke-Free Status (QVSFS) score = 0]. Plasma lipoprotein and demographic risk factors were assessed as previously described(1). The study …
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