In both HFpEF and HFrEF, heart failure extends beyond the heart to the vasculature. Factors such as inflammation, oxidative stress, and structural changes impair normal vessel function which limits blood flow to organs and skeletal muscle, contributing to symptoms such as exercise intolerance.
In our lab, we study this by isolating small blood vessels from rodent models of heart failure and use a wire myograph to precisely measure how they contract and relax in response to pharmacological agents. This allows us to assess endothelial and smooth muscle function and uncover the mechanisms driving vascular impairment. By linking these mechanistic insights to the vascular abnormalities seen in patients, our work aims to assess novel therapeutic targets to improve vascular health and clinical outcomes in heart failure.
Vascular dysfunction in heart failure
