Fat Embolism Does Not Alter Cardiac Structure or Induce Pathological Changes in a Rat Model

Fat embolism (FE) encompasses conditions in which fatty substance becomes embedded in a tissue/organ. Fat emboli most commonly affect the lungs in a trauma setting. This can lead to both significant pathology locally and systemically including changes in structure, inflammatory response, activation of the renin-angiotensin system, and subsequent hypoxia. In fact, changes in skin, brain, lungs, and kidneys have been noted in FE syndrome. Because there is an extensive record of pathology reports on this condition without evidence of direct cardiac involvement, as well as our studies showing apparent complete recovery after the acute embolism, we hypothesized that structural changes similar to the lung and at the same time course would not be observed in the heart.

We used a rat model of FE previously described by our group where we have documented significant lung pathology. In this study, we analyzed both pulmonary and cardiac structure, histology, and gene expression at 48 h and 10 wks post fat injection to mimic FE.

Despite severe inflammatory evidence and structural changes to the lung and vasculature up to 10 wks after FE, we found no significant alterations to cardiovascular morphometry including lumen patency ratio, adventitia/media ratio, fibrosis content, and heart chamber/wall dimensions in stained histological sections. Additionally, genetic markers of cardiac pathological hypertrophy were not significantly elevated 48 h or 10 wks after fat treatment. Oil Red O staining showed increased fat droplet content within lung and aorta tissue, but not in the myocardium.

Our study suggests that, in contrast to the lungs, the heart is more resistant to the inflammatory and remodeling responses that result from FE, possibly due to the organ-specific differences in fat retention.