Cardiac Biopsy Mechanics
Human heart disease is multifactorial and develops over decades, essentially meaning that no two hearts behave the same. This can be seen in family members carrying heart-disease causing mutations where one family member develops heart failure early in life and another never does. Little is known about the molecular mechanisms that give rise to this divergence, but they are a key to preventing patients with known cardiac mutations from developing heart failure. Our lab is extremely interested in developing tools that can be taken from bedside to benchtop and back. To this end, we employ computational tools to correlate mechanical and functional differences in patient tissue with clinical data to determine how changes at the molecular level manifest in patient quality of life. The dream is that as we refine our ability to mimic cardiac function in biopsy preparations, we will have a predictive tool that can be used to test patient tissue and directly personalize therapeutic strategies.
Altering myocardial viscoelastic properties changes diastolic performance.
Cardiac tissue from HFpEF patients is relatively more viscoelastic than HFrEF myocardium. A, Histological analysis of nonfailing versus HFrEF and HFpEF myocardium. B, Comparison of viscoelastic properties between HFrEF and HFpEF tissue. C, The relative proportion of viscoelastic to elastic stress (Stress Relaxation/Steady State Stress) as a function of strain. D, Relative energy loss (energy dissipated/energy stored) E, Effect of colchicine on stress relaxation during ascending staircase of HFrEF and HFpEF trabecula. Statistical significance determined via 2-way, repeated-measures ANOVA, *P<0.05, **P<0.01, ***P<0.001.
Picosirius Red Staining of Collagen in Human Left Ventricular Myocardium taken on Zeiss 980 with Airyscan 2 at 20x