Androgen deprivation therapy ideally suppresses serum androgens to castrate levels and is a mainstay-treatment for prostate cancer, the most common subcutaneous cancer in older men. Surgical castration and GnRH agonist therapy are both effective methods of decreasing circulating testosterone, with the latter gaining popularity because of its inherent non-invasiveness and perceived reversibility. Androgen deprivation therapy is associated with numerous health risks. However, implementing this therapy through GnRH agonist treatment appears to carry additional cardiac risks not seen in castrate groups. It has been known for some time that the myocardium expresses GnRH receptor messenger RNA and it has recently been shown that cardiac myocytes are capable of positive chronotropic and ionotropic responses to GnRH in vitro. It is my hypothesis that chronic GnRH agonist exposure does not result in the downregulation of the GnRH receptor protein or messenger RNA levels, causing undue stress on the myocardium for the duration of treatment.