Hyperlipidemias: Hacke W

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A digest of articles written 1999 and later, on the topic "Hyperlipidemias," originating from Planet Earth —» Hacke W.  Display:  All Citations ·  All Abstracts
1 Guideline Prevention. European Stroke Initiative. 2004

Leys D, Kwiecinski H, Bogousslavsky J, Bath P, Brainin M, Diener HC, Kaste M, Sivenius J, Hennerici MG, Hacke W, Anonymous00185, Anonymous00186. · No affiliation provided · Cerebrovasc Dis. · Pubmed #14707404 No free full text.

This publication has no abstract.

2 Review [Secondary prevention of stroke] 2006

Ringleb P, Hacke W. · Neurologische Klinik der Ruprecht-Karls-Universität, Im Neuenheimer Feld 400, 69120 Heidelberg. · Hamostaseologie. · Pubmed #17146547 No free full text.

Abstract: Patients suffering a transient ischaemic attack (TIA) or ischaemic stroke (IS) have a high recurrence risk. Secondary prevention aims to prevent not only further strokes but also cardiac events. Important parts of secondary prevention regimens are the modification of vascular risk factors and the inhibition of platelet function or anticoagulation if indicated. The inhibition of platelet function is effective in the reduction of secondary vascular events in patients with TIA or stroke. This is true for acetylsalicylic acid (ASA), clopidogrel, and the combination of ASA plus slow-release dipyridamole. A prediction model which allows to identify patients in whom clopidogrel or dipyridamol plus ASA is superior to ASA for the secondary prevention of stroke is presented.

3 Article Lack of association between polymorphisms of the toll-like receptor 4 gene and cerebral ischemia. 2004

Reismann P, Lichy C, Rudofsky G, Humpert PM, Genius J, Si TD, Dörfer C, Grau AJ, Hamann A, Hacke W, Nawroth PP, Bierhaus A. · Department Medicine I, University of Heidelberg, Germany. · J Neurol. · Pubmed #15258789 No free full text.

Abstract: Toll-like receptor-4 (TLR4), an important mediator of the innate immune response, is expressed in atherosclerotic lesions. The common single nucleotide exchange (Asp299Gly) of the TLR4 gene has been previously reported to impair TLR4 function and to be associated with a decreased risk of carotid atherosclerosis. Therefore, we aimed to detect the potential impact of TLR4 genotypes on the risk of cerebral ischemia. We studied the prevalence of two common polymorphisms of the TLR4 gene (Asp299Gly and Thr399Ile) in 3 independent study populations: (1.) in a cross-sectional study including 769 patients either with type 1 or type 2 diabetes mellitus, of whom 56 (7.2%) had a history of cerebral ischemia (study 1), (2.) a case-control study (study 2) including 128 consecutive patients with cerebral ischemia, mean age 60 +/- 10.9 years and 139 control subjects, and (3.) a case-control study (study 3) including 171 young adults aged < 50 years with cerebral ischemia and 204 control individuals. In all subjects, Asp299Gly and Thr399Ile were detected by restriction length analysis. The prevalence of the TLR4 genotypes was essentially the same between patients with cerebral ischemia and control subjects in all 3 study populations. Furthermore, there was also no association with the subgroup of atherosclerotic stroke in both case-control studies populations. Although TLR4 polymorphisms are associated with a decreased risk of carotid atherosclerotic lesions, our findings indicate that they do not influence the prevalence of cerebral ischemia. This implies that the Asp299Gly TLR4-allele might have a protective role in carotid atherosclerosis, but not in cerebral ischemia.