Thrombosis, or the formation of blood clots in blood vessels or the cardiac chamber, can lead to many frequent and serious cardiovascular events, including heart attack, stroke and pulmonary embolism. Globally, one in four people die from the often-preventable conditions caused by thrombosis, making it a leading cause of death and disability.
Given the burden of these thrombotic conditions, researchers continue to investigate ways to advance patient care. One key consideration is the give and take of helping to prevent blood clots in situations where they should not occur, while allowing the blood to clot naturally in the instance of an injury or trauma. Achieving a better balance in this regard may help advance care for millions of individuals at risk of thrombotic events.
Clotting is a normal and important process that occurs in the body after an injury through a mechanism called coagulation. The coagulation cascade is a series of steps that trigger one another, with molecules called “coagulation factors” involved in a chain reaction that ultimately results in the formation of a clot.
However, the coagulation cascade is complex and can be activated in many ways, and clots can occur and amplify when they are not needed. These “bad clots” can block blood vessels, cutting off blood circulation to important parts of the body. This is called thrombosis and can lead to injury and even death.
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Anticoagulants, or medicines that help prevent blood clots, are an important part of treatment for thrombotic conditions, such as stroke, atrial fibrillation or heart attacks. Currently available direct oral anticoagulants, or DOACs, were a significant advancement for patients and brought renewed hope to the field. They work by stopping the coagulation cascade at a specific step, called a factor, and help to prevent blood clots.
There are many steps and pathways within the coagulation cascade, and depending on where a particular treatment works, the balance between stopping bad clots and allowing good clots can be influenced. Researchers are working to fine-tune that balance to help avoid an increased risk of bleeding while on an anticoagulant medicine. This would potentially make preventative treatments for stroke and heart attack, and combinations of treatments that were previously not an option, available for many more patients worldwide, particularly those who are predisposed to excess bleeding due to preexisting conditions.
Factor XIa (activated factor eleven), or FXIa, is a promising target within the cascade because it may help prevent the formation and growth of bad clots while allowing blood to clot normally when needed in response to an injury.
Unfortunately, large numbers of patients are not being sufficiently treated to reduce their risk of heart attack and stroke because they are predisposed to excess bleeding due to preexisting conditions. The space is ripe for innovation, and researchers at Bristol Myers Squibb and Johnson & Johnson are eager to continue research in thrombotic care on behalf of patients.
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