Myocardial Infarction in a Patient With Chronic Lymphocytic Leukemia: Acalabrutinib-Related Dehoming as a Potential Culprit

Patients with chronic lymphocytic leukemia (CLL) frequently suffer from atherosclerosis and its conventional risk factors.Bruton tyrosine kinase (BTK) inhibitor therapy is known to impact coronary and vascular risk.We report the case of a 71-year-old woman with CLL treated with a second-generation BTK inhibitor, well-controlled hypertension, and asymptomatic carotid stenosis who presented with an anterior ST-elevation myocardial infarction (STEMI) complicated by complete heart block shortly after beginning treatment with acalabrutinib.The patient was found to have significant treatment-related redistribution lymphocytosis following the initiation of BTK inhibitor therapy, with an absolute lymphocyte count (ALC) of 261 x 10 9 /L on admission.Despite a complicated clinical course including cardiac arrest, third-degree atrioventricular heart block requiring temporary transvenous pacing, cardiac ischemia treated with percutaneous coronary intervention (PCI) and intra-aortic balloon pump (IABP), and parietal and occipital strokes, she was ultimately discharged to a rehabilitation facility and subsequently returned home.We describe a patient with previously unrecognized severe multivessel coronary artery disease who developed a STEMI 28 days after acalabrutinib initiation in the setting of marked treatment-associated lymphocytosis.We hypothesize that redistribution lymphocytosis may have contributed to coronary plaque destabilization and subsequent myocardial infarction in the presence of pre-existing atherosclerotic disease, although causality cannot be established.This observation is hypothesis-generating and highlights the need for cardiovascular vigilance during the early weeks of BTK inhibitor therapy.