Pulmonary arterial hypertension (PAH) is a life-threatening progressive disease that is  characterized by pulmonary vascular remodeling and is represented by narrowing of blood  vessels in the lungs. PAH effects females four times more likely than males, specifically females  between the ages of 30-60 years old, leading to an interesting paradox known as the estrogen  puzzle. Past research has resulted in contradicting conclusions; some of which show a  protective effect of estrogen on PAH versus others showing a disease promoting effect. It is  known that right ventricular (RV) function and morphology are important indicators of the  severity of PAH. I am interested in determining the role that estrogen plays on the right  ventricle during the progression of PAH. I hypothesize that estrogen plays a major role in the  remodeling of the RV leading to an overall protective effect against right heart failure. I aim to  quantify the hemodynamics of the right ventricle throughout the progression of PAH using a rat  model and to identify the sex dependent effects of estrogen in the remodeling and mechanics  of the RV. After the induction of PAH using a Sugen-Hypoxia protocol, terminal procedures are  conducted, in which in vivo blood pressure-volume relationships are measured, with the goal of  investigating changes due to pressure overload. I am currently focusing on these pressure volume loops for each subset of animals with the goal of finding patterns to describe the  differences in the hearts function for males, non-ovariectomized females, and ovariectomized  females. I am looking at the PV loop as a whole, the slope of the isovolumic contraction and  relaxation phases, and am attempting to determine if we can expect to see a specific range of  values for the PV curves for a given group. My future plans are to dive more into the estrogen  component of RV remodeling in PAH and relate estrogen levels to PV loops and overall heart  function.

The video of this presentation is available here.