Related Experiment Videos
Plasma predictors of ischemic complications of atherosclerosis: open issues
M Margaglione1, E Grandone, G Di Minno
1IRCCS-CSS, Viale Cappuccini, San Giovanni Rotondo, Italy.
Insights
Acute myocardial infarction, a leading cause of death, often involves atherosclerotic plaque rupture and thrombosis. Identifying specific hemostatic markers may improve prediction of ischemic events.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Epidemiology
Background:
- Acute myocardial infarction (MI) is a primary cause of death in Western countries, frequently linked to occlusive coronary thrombus on atherosclerotic plaques.
- While atherosclerosis is necessary for MI, thrombosis is often the critical event, though antiplatelet drugs only prevent 25-30% of these thrombotic events.
Purpose of the Study:
- To explore the role of various hemostatic parameters in predicting ischemic events.
- To identify key factors contributing to myocardial infarction beyond atherosclerosis.
Main Methods:
- Review of epidemiological studies identifying hemostatic parameters associated with ischemic risk.
- Analysis of factors such as fibrinogen, PAI-1, lipoprotein(a), anticardiolipin antibodies, lupus anticoagulant, leukocyte count, and blood viscosity.
Main Results:
- Abnormalities in fibrinogen, PAI-1, lipoprotein(a), ACA, LA, leukocyte count, and blood viscosity have been identified as potential predictors of ischemic events.
- Fibrinogen and PAI-1 are noted as acute-phase proteins, suggesting their role in the inflammatory aspect of thrombosis.
Conclusions:
- Atherosclerosis alone is insufficient to cause MI; thrombosis is usually required.
- Further research into hemostatic parameters is crucial for better prediction and prevention of myocardial infarction and related ischemic events.
Abstract:
In western countries, acute myocardial infarction is the commonest cause of morbidity and mortality [19]. An occlusive coronary thrombus on an ulcerated atherosclerotic plaque in the coronary arteries is the etiological event in more than 90% of patients with Q-wave myocardial infarction [38]. The underlying abnormality in non-Q-wave myocardial infarction is often a ruptured atherosclerotic plaque, which acts as a nidus for the deposition and activation of platelets. In this case, thrombosis occurs, but may not be totally occlusive, or an early spontaneous recanalization may occur. On the other hand, some clinical trials showed that a prolonged treatment with antiplatelet drugs significantly reduces the recurrence of coronary ischemia. Thus, atherosclerosis is a necessary condition for myocardial infarction, but it is not sufficient in that it usually needs the occurrence of thrombosis. However, only 25-30% of these thrombotic events are prevented by the administration of antiplatelets drugs. In recent years, epidemiological studies identified some hemostatic parameters whose abnormalities may help predict the risk of ischemic events: fibrinogen [14], plasminogen activator inhibitor-1 (PAI-1) [3], lipoprotein(a) [46], anticardiolipin antibodies (ACA) and lupus anticoagulant (LA) [10], leukocyte count [34], blood viscosity [34]. Some of these, such as fibronogen and PAI-1 are acute-phase proteins.(ABSTRACT TRUNCATED AT 250 WORDS)