Related Experiment Videos
Tissue factor in human coronary atherosclerotic plaques
D Ardissino1, P A Merlini, R Arlens
1Division of Cardiology, I.R.C.C.S. Policlinico San Matteo and University of Pavia, Piazza Golgi 1, 27100, Pavia, Italy. ARDISOO1@planet.it
Insights
Coronary plaque rupture can lead to heart attack, but not all ruptures cause clots. Tissue factor in plaques influences thrombosis risk, varying significantly between stable and unstable coronary artery disease.
Area of Science:
- Cardiovascular Medicine
- Pathophysiology
- Thrombosis Research
Background:
- Coronary atherosclerotic plaque rupture and thrombosis are central to unstable angina and myocardial infarction.
- Plaque disruption is common in atherosclerosis, yet thrombosis occurs in only a fraction of cases.
Purpose of the Study:
- To investigate the role of tissue factor content and procoagulant activity in coronary atherosclerotic plaques.
- To understand variations in thrombotic response following plaque rupture.
Main Methods:
- Analysis of tissue factor content and procoagulant activity in human coronary atherosclerotic plaques.
- Comparison of plaques from patients with different clinical presentations (unstable angina, myocardial infarction, stable angina).
Main Results:
- Tissue factor content and procoagulant activity vary widely in coronary plaques.
- Higher levels of tissue factor were observed in plaques from patients with unstable angina, myocardial infarction, or coronary thrombosis compared to stable angina.
Conclusions:
- Variations in tissue factor content and activity are likely responsible for the differential thrombotic responses to coronary atherosclerotic plaque rupture.
- Tissue factor is a key determinant in the development of thrombosis after plaque disruption.
Abstract:
The rupture or fissuring of a coronary atherosclerotic plaque and subsequent thrombosis is considered the key event in the pathogenesis of unstable angina and myocardial infarction. Although plaque disruption frequently occurs during the evolution of atherosclerosis, only a minority of ruptured plaques develop thrombosis. The content and procoagulant activity of tissue factor in human coronary atherosclerotic plaques varies widely, and different studies confirm that it is higher in the plaques extracted from patients with unstable angina, myocardial infarction or histologic/angiographic evidence of coronary thrombosis than in those taken from patients with stable angina or uncomplicated coronary lesions. Variations in tissue factor content and activity may be responsible for the different thrombotic responses to human coronary atherosclerotic plaque rupture.