Abstract 4549: Hemodynamic Mecahnisms Of Endocardial Fibroelastosis (EFE) In The Developing Rat Heart
Background. The mechanisms for development and progression of EFE as well as its causal relationship to hypoplastic heart syndrome are unknown, although subendocardial ischemia in-utero has been invoked. We hypothesized that abnormal mechanical forces (fluid shear vs. mechanical strain) during development promote EFE.
Methods. To test this hypothesis we have unloaded one day, 1 week and 2 weeks old Lewis rat hearts (n=3– 4 per group) by heterotopic transplantation into the abdomens of 5– 6 weeks old syngeneic recipients. To render the heart unloaded donor ascending aorta was anastomosed to the recipient abdominal aorta and pulmonary artery to inferior vena cava. Control hearts of the same age were loaded by transplanting the donor lung en bloc with the heart. The donor superior vena cava was anastomosed to recipient inferior vena cava after the completion of the aortic anastomosis. Two weeks after transplantation unloaded and control hearts were excised and examined by H&E, trichrome and elastin stainings for the presence of EFE.
Results. All unloaded 1 day old hearts developed massive EFE, lining the whole LV chamber. Unloaded 1 week old hearts developed patchy EFE and no EFE was detected in unloaded 2 weeks old hearts. No EFE was detected in control loaded hearts of any age. EFE appeared as avascular, highly cellular, collagen and elastin rich tissue. These morphological features characterise EFE observed in clinical setting.
Conclusions. First, the preponderance of the heart to development of EFE appears age dependent with immature hearts being more susceptible. Second, a leading role of mechanical forces on EFE development can be inferred from our findings. However, it is impossible to discriminate between the roles of intracavitary fluid shear forces vs. wall strain with this model. Third, our findings argue against an “anoxic” hypothesis for EFE development since the coronary perfusion was equivalent in both groups.