Thrombus formation on atherosclerotic plaques: Pathogenesis and clinical consequences

Citation
U. Rauch et al., Thrombus formation on atherosclerotic plaques: Pathogenesis and clinical consequences, ANN INT MED, 134(3), 2001, pp. 224-238
Citations number
173
Categorie Soggetti
General & Internal Medicine","Medical Research General Topics
Journal title
ANNALS OF INTERNAL MEDICINE
ISSN journal
00034819 → ACNP
Volume
134
Issue
3
Year of publication
2001
Pages
224 - 238
Database
ISI
SICI code
0003-4819(20010206)134:3<224:TFOAPP>2.0.ZU;2-W
Abstract
Purpose: To describe the characteristics of thrombus formation on atheroscl erotic plaques, the clinical expression of atherothrombosis in Vascular dis ease, and some of the most recent therapeutic approaches in cardiovascular disease. Data Sources: MEDLINE search for English-language articles on thrombosis an d atherosclerosis published up to January 2000. Abstracts of recent interna tional meetings on new aspects of thrombus formation and new therapeutic op tions were reviewed, and references from identified articles were selected and reviewed. Study Selection: Experimental, basic, clinical, and epidemiologic studies r elated to the pathophysiology of thrombosis on atherosclerotic lesions. The rapeutic approaches were obtained from experimental studies and large clini cal investigations. Data Extraction: Arterial vessel wall substrate, theologic conditions, and blood thrombogenicity influence the process of thrombus formation in arteri es. Thrombus formation on disrupted atherosclerotic plaques or arterial ero sions frequently causes acute coronary syndromes. Severe atherosclerosis of the aorta has been identified as an important morphologic indicator of an increased risk for thromboembolism. Current antithrombotic therapies availa ble as long-term treatment for patients with cardiovascular disease are oft en not effective enough to prevent acute thrombotic events and deterioratio n of atherosclerosis. Data Synthesis: Improved understanding of the pathophysiology of thrombus f ormation on atherosclerotic plaques has led to the development of new thera peutic approaches. Glycoprotein llb/llla, tissue factor, factor Xa, and thr ombin inhibitors as well as combined antithrombotic therapy, such as aspiri n plus a thienopyridine plus warfarin, are being evaluated as new possible options for the treatment of arterial thrombosis. Conclusions: Long-term treatment with potent antithrombotic drugs, such as tissue factor or factor Xa inhibitors, that effectively block thrombosis wi thout causing bleeding complications could help reduce death from cardiovas cular disease.