{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T11:04:19Z","timestamp":1785409459937,"version":"3.56.0"},"reference-count":42,"publisher":"Wiley","license":[{"start":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T00:00:00Z","timestamp":1785369600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T00:00:00Z","timestamp":1785369600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Bruton tyrosine kinase inhibitors (BTKi) have transformed the management of chronic lymphocytic leukaemia and other B\u2010cell malignancies, yet their therapeutic benefit is tempered by clinically relevant cardiovascular toxicities (predominantly atrial fibrillation, hypertension, bleeding and ventricular arrhythmias). Pharmacological differences in cardiotoxicity arise from binding mode and kinase selectivity profiles. First\u2010 and second\u2010generation covalent BTKi (ibrutinib, acalabrutinib, zanubrutinib) irreversibly target Cys481, leading to off\u2010target engagement of other kinases that regulate cardiac electrophysiology and also express homologous cysteine residues. In contrast, non\u2010covalent BTKi, such as pirtobrutinib, achieve selective and persistent BTK occupancy through Cys481\u2010independent interactions, substantially attenuating off\u2010target kinase inhibition and associated cardiotoxicity. Mechanistic insights support proactive baseline cardiovascular risk assessment and structured longitudinal surveillance to enable early detection, risk\u2010adapted management and sustained BTKi therapy. This mini\u2010review describes how such concepts apply to the issue of BTKi\u2010associated cardiovascular adverse events.<\/jats:p>","DOI":"10.1111\/bph.70620","type":"journal-article","created":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T10:11:41Z","timestamp":1785406301000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Bruton tyrosine kinase inhibitors and cardiovascular adverse events"],"prefix":"10.1111","author":[{"given":"Massimiliano","family":"Camilli","sequence":"first","affiliation":[{"name":"Department of Cardiovascular Sciences A. 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