How a person’s immune system responds to a protein called LL-37 may increase risk for developing acute coronary syndrome, but the response may also serve as a potential target for future treatments.
These findings come from a new research study led by investigators in the Smidt Heart Institute at Cedars-Sinai.
In this new study, published in JACC: Basic to Translational Science, the research team reports that LL-37 binds to antibodies, forming complexes that then bind to and activate platelets. These activated platelets form clots and can restrict blood flow.
To conduct the study, the investigators collaborated with the laboratory of Daniel Berman, MD, in the Smidt Heart Institute and the Department of Imaging. The laboratory is collecting blood plasma from study participants who undergo coronary artery CT imaging to evaluate their risk for a heart attack. They are following the patients over time to learn how the composition of their plasma changes.
The investigators studied the composition of the blood plasma of patients who went on to have a heart attack, as well as the blood plasma of patients who did not. Patients who suffered a heart attack had significantly higher levels of LL-37 antibodies before the heart attack than people who did not experience a heart attack. The investigators also found that people with acute coronary syndrome had increased levels of immune complexes that formed between these antibodies and LL-37.
Experiments demonstrated these complexes have the propensity to activate platelets, suggesting a novel immune-mediated pathway of platelet activation during a heart attack and potentially a target for therapy.
