Research Question and Objective
Cardiovascular diseases (CVDs), such as heart failure and atrial fibrillation, are leading causes of morbidity and mortality worldwide. Multiple factors, including frailty, genetic predisposition, metabolic dysregulation, and lifestyle behaviors, are known to influence CVD risk, but their combined impact on cardiac structure and function remains poorly understood. To address this gap, we aim to leverage the UK Biobank’s rich multi-omics (genomics, proteomics, metabolomics), cardiac imaging (e.g., MRI), and clinical data to:
Identify cardiac structural and functional alterations associated with key risk factors, including frailty, genetics, metabolism, and lifestyle.
Explore the molecular mechanisms (e.g., inflammation, oxidative stress) linking these factors to cardiovascular dysfunction.
Develop predictive models to stratify individuals at high risk of CVDs based on their combined risk profiles, enabling targeted interventions.
Scientific Rationale
Frailty, genetics, metabolism, and lifestyle are interconnected factors that contribute to CVD risk through shared pathways such as chronic inflammation, metabolic dysregulation, and oxidative stress. Previous studies have examined these factors in isolation, but their combined effects on cardiac health remain unclear. Additionally, prior research has primarily focused on the impact of these factors on cardiovascular event outcomes, often neglecting subclinical changes in cardiac structure and function.
By integrating cardiac MRI, multi-omics data (genomics, proteomics, metabolomics), and detailed clinical data from the UK Biobank, we can uncover novel biomarkers and mechanistic insights into how these factors jointly influence cardiovascular health. This integrated approach will provide a comprehensive understanding of CVD etiology, offering a robust foundation for personalized prevention and treatment strategies.