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Abstract
<jats:title>ABSTRACT</jats:title> <jats:sec> <jats:title>Background</jats:title> <jats:p> The <jats:italic>JAK2V617F</jats:italic> mutation is a driver mutation in Philadelphia‐negative chronic myeloproliferative neoplasms (MPNs), including polycythemia vera, essential thrombocythemia, and myelofibrosis. Recent studies have revealed a significant prevalence of <jats:italic>JAK2V617F</jats:italic> as clonal hematopoiesis of indeterminate potential (CHIP) in the general population, particularly in individuals over 50 years. CHIP‐ <jats:italic>JAK2V617F</jats:italic> carriers exhibit increased mortality, driven by cardiovascular diseases and cancer. Given the prothrombotic and inflammatory nature of <jats:italic>JAK2V617F</jats:italic> , we investigated its prevalence in patients with acute coronary syndrome (ACS). </jats:p> </jats:sec> <jats:sec> <jats:title>Methods</jats:title> <jats:p> We screened 526 consecutive ACS patients for the <jats:italic>JAK2V617F</jats:italic> mutation using sensitive droplet digital PCR (ddPCR) and allele‐specific real‐time quantitative PCR (RQPCR). Clinical and laboratory data were analyzed to assess associations. </jats:p> </jats:sec> <jats:sec> <jats:title>Results</jats:title> <jats:p> The <jats:italic>JAK2V617F</jats:italic> mutation was detected in 6.1% (32/526) of ACS patients, significantly higher than the general population prevalence (3.1%). </jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion</jats:title> <jats:p> Our findings suggest that <jats:italic>JAK2V617F</jats:italic> may contribute to ACS pathogenesis through prothrombotic and inflammatory mechanisms. Screening for <jats:italic>JAK2V617F</jats:italic> in high‐risk cardiovascular patients could identify individuals who may benefit from targeted therapies. </jats:p> </jats:sec>