Atrial fibrillation (AF), the most prevalent sustained arrhythmia globally, is a major driver of stroke, heart failure, sudden deaths, and cardiovascular disease. Although an arrhythmia more commonly affects the elderly, AF can manifest in young and middle-aged adults as well. Thromboembolic disease, particularly stroke in the young, can lead to increased long-term morbidity, which can affect relationships, education, and employment. These outcomes not only lead to substantial healthcare costs but also pose a significant burden on public health.
Despite its widespread occurrence, our understanding of its mechanisms remains incomplete, and the available therapeutic options exhibit limited efficacy while often carrying inherent risks. Existing animal models cannot truly reflect a human cardiovascular biology as discussed above.
This project aims to develop a bioengineering model of AF to understand the fundamental biological processes that control the sensitivity of endothelial cells and blood cells to arrhythmic flows.