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Published on: July 21, 2023
Endogenous fibrinolysis inhibitors in acute coronary syndrome
1Chest Diseases Hospital, Kuwait.
Insights
Patients with acute coronary syndrome face high risks despite treatments. Impaired fibrinolysis, a key factor in cardiovascular events, and its inhibitors are crucial areas for new therapeutic strategies.
Area of Science:
- Cardiology
- Hematology
- Thrombosis Research
Background:
- Acute coronary syndrome (ACS) patients have significant residual ischemic risk despite current invasive and antithrombotic therapies.
- Early revascularization and stenting of non-hemodynamically significant lesions have not consistently reduced major adverse cardiovascular events.
- Impaired fibrinolysis is increasingly recognized as a critical independent risk factor for mortality and adverse outcomes in ACS.
Purpose of the Study:
- To review the association between impaired fibrinolysis and adverse cardiovascular outcomes in ACS.
- To explore the role of endogenous fibrinolysis inhibitors in ACS.
- To summarize experimental evidence on modulating fibrinolysis using profibrinolytic agents targeting these inhibitors.
Main Methods:
- Literature review of studies investigating fibrinolysis, endogenous inhibitors, and cardiovascular outcomes in ACS.
- Analysis of data linking impaired fibrinolysis to major adverse cardiovascular events.
- Summary of experimental research on therapeutic interventions targeting fibrinolytic pathways.
Main Results:
- Impaired fibrinolysis is strongly associated with increased cardiovascular mortality and adverse events in ACS patients.
- Endogenous fibrinolysis inhibitors are implicated in the pathophysiology of impaired fibrinolysis in ACS.
- Experimental data suggests potential for profibrinolytic agents to improve the fibrinolytic state.
Conclusions:
- Impaired fibrinolysis represents a significant therapeutic target in managing ACS.
- Targeting endogenous fibrinolysis inhibitors with profibrinolytic agents may offer novel strategies to reduce residual cardiovascular risk in ACS patients.
Abstract:
Patients with acute coronary syndrome have a high residual risk of ischemic events despite current treatment methods, both invasive and antithrombotic strategies. The strategy of very early revascularization although has been suggested to improve patient outcome, remains associated with a high residual risk of adverse events. Stenting of nonflow-limiting vulnerable plaques in addition to stenting of hemodynamically significant lesions in patients with acute coronary syndrome, has not shown a beneficial effect on major adverse cardiovascular events in early studies. Current antithrombotic therapy in acute coronary syndrome is focused mainly on antiplatelet agents, and to a lesser extent on oral anticoagulants. Besides thrombotic atherosclerotic plaque rupture and activated platelets, impaired fibrinolysis has gained attention as a strong independent risk factor for cardiovascular mortality and adverse outcome in patients with acute coronary syndrome. Various endogenous fibrinolysis inhibitors that act at different levels of the hemostatic process have been associated with the impaired fibrinolysis. This review presents available data for association of impaired fibrinolysis with major adverse cardiovascular outcome in acute coronary syndrome, and the potential role of endogenous fibrinolysis inhibitors in acute coronary syndrome. In addition, experimental evidence for modulation of impaired fibrinolytic state with profibrinolytic agents that target endogenous fibrinolysis inhibitors is summarized.
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