The Kumowski Lab studies how the innate immune system shapes cardiac electrical stability in health and disease. Our research focuses on understanding how immune cells—particularly neutrophils, monocytes, and macrophages—interact with the heart to promote arrhythmias and sudden cardiac death.

While immune activation is a defining feature of many cardiovascular and systemic diseases, its role in disrupting cardiac electrophysiology remains poorly understood. We investigate how acute and chronic inflammatory states, including myocardial infarction, atherosclerosis, post-ischemic remodeling, heart failure and sepsis reprogram innate immune cells and alter their behavior within cardiac tissue. Our work explores how disease-conditioned immune cells influence cardiomyocyte membrane integrity, electrical coupling, and tissue organization to create arrhythmogenic substrates.

Using innovative mouse models, high-resolution inflammation imaging, and systems-level approaches, we examine immune–cardiac interactions across time—from acute injury to chronic disease. By integrating mechanistic discovery with clinical insight, the Kumowski Lab aims to define fundamental immune pathways that link systemic inflammation to electrical instability of the heart, providing a framework for improved translational understanding of arrhythmias in inflammatory disease.