Atrial fibrillation (AF) is the most common arrhythmia and poses a significant burden to patients and healthcare systems globally. AF generates unpleasant symptoms, and a high arrhythmia burden is associated with higher risks of stroke, mortality, and hospitalization for heart failure worldwide. The current literature argues that epicardial adipose tissue, fibrosis, inflammation, altered coagulation and blood flow, all contribute to the atrial changes in AF (atrial myophaty), but the succession of the steps, the interaction of the different components and the magnitude of each one's contribution, constitute the knowledge gap in this research area.
The overall goal of my research is to create a deeper understanding of the presence of intramural fibrosis and epicardial adipose tissue in and around the atrial wall, and how these parameters correlate to inflammation during the progression of AF. Further on, the aim is to analyze the blood flow pattern in the AF patients and its relation to hypercoagulability, inflammation, fat, and fibrosis. My tools are blood samples (for inflammation and coagulation), cardiac CT (for atrial volume, epicardial adipose tissue and flow), and cardiac MRI (for atrial volume, epicardial adipose tissue, fibrosis and flow).
The overall goal of my research is to create a deeper understanding of the presence of intramural fibrosis and epicardial adipose tissue in and around the atrial wall, and how these parameters correlate to inflammation during the progression of AF. Further on, the aim is to analyze the blood flow pattern in the AF patients and its relation to hypercoagulability, inflammation, fat, and fibrosis. My tools are blood samples (for inflammation and coagulation), cardiac CT (for atrial volume, epicardial adipose tissue and flow), and cardiac MRI (for atrial volume, epicardial adipose tissue, fibrosis and flow).
