NIH Research Festival
Effects of sepsis on the heart evaluated by Cardiac Magnetic Resonance (CMRs) in a canine model of Staphylococus aureus pneumonia that reproduces the reversible cardiac dysfunction of human septic shock.
For 96h a protocol using fluid boluses maintained normal cardiac filling pressures. No exogenous catecholamines were given.
Sepsis within 48h after bacterial challenge resulted in a significant increase in LV wall edema of >2-3% on T2 CMR, which could explain the cardiac dysfunction seen during sepsis. Edema was confirmed on histology to be interstitial, affecting both myocytes and endothelial cells. In the first 24h, as cardiac dysfunction increased in septic animals, ventricular chamber size initially decreased in the presence of normal cardiac filling pressures. This suggests that the observed edema might result in a ‚Äúrestrictive-like‚Äù cardiomyopathy. From 24-48h cardiac chamber size increased. During this time the ventricular wall thinned along with a significant loss of dry mass (approximately 1 gram/day of tissue). This loss of mass occurred as cardiac function recovered, suggesting that it may represent a reparative remodeling of the heart. Wall thinning might in part explain the increase in ventricular chamber size. Biochemical and histological data suggest that myocytes are relatively preserved. Endothelial cells are next most common cell type in the LV wall, which like myocytes developed edema as seen by electron microscopy. This pattern of cardiac injury as well as mechanisms underlying the reparative process associated with dry mass loss are being actively investigated.
Scientific Focus Area: Clinical Research
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