Thrombus formation on atherosclerotic plaques: pathogenesis and clinical consequences.
OBJECTIVE
To describe the characteristics of thrombus formation on atherosclerotic plaques, the clinical expression of atherothrombosis in vascular disease, and some of the most recent therapeutic approaches in cardiovascular disease.


METHODS
MEDLINE search for English-language articles on thrombosis and atherosclerosis published up to January 2000. Abstracts of recent international meetings on new aspects of thrombus formation and new therapeutic options were reviewed, and references from identified articles were selected and reviewed.


METHODS
Experimental, basic, clinical, and epidemiologic studies related to the pathophysiology of thrombosis on atherosclerotic lesions. Therapeutic approaches were obtained from experimental studies and large clinical investigations.


METHODS
Arterial vessel wall substrate, rheologic conditions, and blood thrombogenicity influence the process of thrombus formation in arteries. Thrombus formation on disrupted atherosclerotic plaques or arterial erosions 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 available as long-term treatment for patients with cardiovascular disease are often not effective enough to prevent acute thrombotic events and deterioration of atherosclerosis.


RESULTS
Improved understanding of the pathophysiology of thrombus formation on atherosclerotic plaques has led to the development of new therapeutic approaches. Glycoprotein IIb/IIIa, tissue factor, factor Xa, and thrombin inhibitors as well as combined antithrombotic therapy, such as aspirin 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 without causing bleeding complications could help reduce death from cardiovascular disease.
Rauch
U
U
Benjamin Franklin Clinic, Department of Cardiology, Free University of Berlin, Berlin, Germany.
Osende
J I
JI
Fuster
V
V
Badimon
J J
JJ
Fayad
Z
Z
Chesebro
J H
JH
D001161:Arteriosclerosis / Q000175:diagnosis / Q000209:etiology* / Q000503:physiopathology* / Q000628:therapy; D002986:Clinical Trials as Topic; D018450:Disease Progression; D004359:Drug Therapy, Combination; D065427:Factor Xa Inhibitors; D018056:Hemorheology; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors / Q000627:therapeutic use; D012307:Risk Factors; D013923:Thromboembolism / Q000503:physiopathology; D013925:Thromboplastin / Q000037:antagonists & inhibitors
D065427:Factor Xa Inhibitors; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D013925:Thromboplastin