Abstract
Coronary Artery Disease (CAD), and the wider coronary heart disease family, account for hundreds of thousands of deaths annually in the United States alone. Further, despite the widespread connotation of CAD as a “man’s disease,” it has been well documented that CAD disproportionately affects women. Most evidently, women suffer from increased rates of mortality and reduced clinical interventions. To begin attempting to reduce this inequity, this work investigated several contributing aspects of this disparity’s etiology.
The first contributing factor to this disparity stemmed from biases in translational research and physiological interpretation. More specifically, this work investigated the early trend that men seemed to be more averse to CAD risk. By investigating how that connotation guided explanations for physiological trends, this work shined a light on our early explanations for cholesterol, iron levels, and plaque morphology. Together, these early translational and physiological studies were flawed on several levels, including both implicit and explicit biases.
Later, this work examined how clinical research and trials have harmed advancements in women’s heart health. By discussing how policy removed women from clinical studies, and then failed to adequately reverse this doctrine, this work exposed how culpability falls beyond that of just scientists. Further, this work employs a case study on how guidelines on estrogen replacement therapy have fluctuated significantly. Together, this analysis showed that even our corrections are far from perfect.
In addition, this analysis investigated the triumphs and missteps of the American Heart Association (AHA). For instance, this governing body had previously harmed women’s heart health by reinforcing female-biased symptoms as “atypical.” Further, this work discussed how the AHA may be unintentionally diluting the nuances of women’s heart health in favor of minor optimization.
Lastly, this piece analyzed how public and physician perception of this disease continues to contribute to this disparity. By investigating trends in public awareness, public health messaging, and physician competency, this work illustrated how fragile the public perception of the disease may be. Further, by projecting disapproval for presidential actions which attempted to reduce funding for sex-biased research, this work called for increased attention to this matter.
Together, this ethical thesis served to argue that many aspects worked in unison to perpetuate the incorrect, male-biased notion of CAD. As a severe consequence, CAD affects women more severely and claims millions of lives. The conclusions further warned that should society continue to ignore these biases, this devastating trend will continue indefinitely.
The technical project involved developing an R library to make multi-omic data analysis straightforward and efficient. Nearly twenty functions were created for bulk RNA-seq, ChIP-seq, and Single-Cell RNA-seq to remove the computational burden for analyzing these assays. For instance, many objects generated by functions for one assay may serve as inputs for a separate assay’s functions. Set in the context of evaluating a candidate gene in cardiac regeneration, this project was successful in identifying a state of cardiomyocytes enriched for regenerative processes that were associated with a candidate regeneration-mediating gene. Further, this package allowed for analysis of publicly available data across several common input formats. Lastly, this package is capable of plotting custom figures and graphs to visualize the computational results. Together, this package allows for rapid, integrated post-processing data analysis across all human and murine datasets and diseases.
