University of Hertfordshire

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Original languageEnglish
JournalJournal of Thrombosis and Thrombolysis
Journal publication date31 Jan 2019
Publication statusAccepted/In press - 31 Jan 2019

Abstract

The likelihood of coronary thrombosis culminating in arterial occlusion is dependent on the effectiveness of endogenous fibrinolysis in breaking up the forming thrombus(1). Reduced fibrinolytic potential increases the risk of lasting occlusion.
Laboratory studies have shown abnormally dense fibrin thrombi in populations at risk of arterial thrombosis, such as acute coronary syndrome (ACS), stent thrombosis, diabetes, renal failure and those with family history of premature MI(2). Impaired endogenous fibrinolysis is a recently-described risk factor for adverse cardiovascular events in ACS patients(3-5). How structural thrombus characteristics relate to endogenous fibrinolytic potential, is unknown. We aimed to identify structural alterations in thrombus composition that underlie resistance to endogenous fibrinolysis.

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