Thrombin as target for prevention of recurrent events after acute coronary syndromes.

The mechanism underlying thrombus formation in acute coronary syndrome (ACS) involves both platelets and thrombin. While both pathways are targeted in acute care, platelet inhibition has been predominantly administered in the chronic phase, yet thrombin plays a key role in platelet activation and fibrin formation. Among ACS patients, there is also a persistent chronic increase in thrombin generation, which is associated with a higher rate of adverse events. In the setting of post-ACS care with rivaroxaban or vorapaxar, targeting thrombin has been associated with decreased thrombin generation and reduced cardiovascular events, but has been associated with increased bleeding risk. We explored the evidence supporting thrombin generation in the pathophysiology of recurrent events post-ACS and the role of thrombin as a viable therapeutic target. One specific target is factor XI inhibition, which is involved in thrombin generation, but may also allow for the preservation of normal hemostasis.
Competing Interests: Declaration of competing interest Dr. Bahit receives modest honorarium from MSD, Pfizer, Bristol-Myers Squibb, CSL Behring, Janssen, Boehringer Ingelheim, Anthos; Dr. Gibson receives research support from Johnson & Johnson and Bristol-Myers Squibb, and consulting support from AstraZeneca, Johnson & Johnson, Janssen & Bayer.
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