Tissue plasminogen activator and plasminogen activator inhibitor in patients with acute ischemic stroke: Relation to stroke etiology

Citation
P. Zunker et al., Tissue plasminogen activator and plasminogen activator inhibitor in patients with acute ischemic stroke: Relation to stroke etiology, NEUROL RES, 21(8), 1999, pp. 727-732
Citations number
38
Categorie Soggetti
Neurosciences & Behavoir
Journal title
NEUROLOGICAL RESEARCH
ISSN journal
01616412 → ACNP
Volume
21
Issue
8
Year of publication
1999
Pages
727 - 732
Database
ISI
SICI code
0161-6412(199912)21:8<727:TPAAPA>2.0.ZU;2-H
Abstract
Recent studies suggest that high plasma levels of tissue-type plasminogen a ctivator (tPA) and its inhibitor (plasminogen activator inhibitor-1, PAI-1) are markers of an increased risk of atherothrombotic ischemic events such as stroke and myocardial infarction. In this prospective study, we measured tPA antigen, PAI-1 antigen and activity, as well as tPA/PAI-1 complex in p atients with acute stroke. Stroke subtypes were classified according to the TOAST criteria. From 132 consecutively screened patients, 89 (100%) were e nrolled in this study, including 42 patients (47%) with large artery athero sclerosis (LAA), 32 (36%) with small vessel occlusion (SVO), and 15 (17%) w ith cardioembolism (CE). Nineteen age-matched neurologic patients without m anifestations of cerebrovascular disease served as control subjects (CS). P atients with acute stroke had significantly higher plasma levels of tPA ant igen (p < 0.001), PAI-1 antigen (p < 0.05) and PAI activity (p < 0.05) than patients in the control group, t-PA antigen, PAI activity and tPA/PAI-1 co mplex levels were similar regardless of stroke etiology. Only PAI-1 antigen was lower in patients with cardioembolic stroke than in stroke patients wi th LAA (p < 0.05). Plasma tPA antigen, PAI-1 antigen, and PAI activity are significantly increased in patients with acute ischemic stroke. Except for PAI-1 antigen, this increase appears not to be related to the underlying st roke etiology.