The Effects of Endocrine Dysfunction on the Cerebrovasculature and Stroke

Abstract

Stroke is the third leading cause of death in the United States and the leading cause of disability among adults.1 According to the American Heart Association Heart Disease and Stroke 2008 Update,1 there is, on average, 1 stroke every 40 seconds in the United States, and every 3-4 minutes someone dies of a stroke. Furthermore, stroke is a major financial burden on the healthcare system, and its prevalence will only continue to increase as the prevalence of its risk factors continues to increase. These risk factors include but are not limited to hypertension, atherosclerosis, diabetes, smoking, and obesity. Currently, therapy for ischemic stroke is very limited. The only approach for acute treatment of ischemic stroke approved by the Food and Drug Administration is clot lysis with tissue plasminogen activator (tPA), based on findings from the National Institute of Neurological Disorders and Stroke recombinant tPA Stroke Study Group demonstrating improvement in clinical outcome with tPA therapy compared to placebo-control patients.2 Patients receiving tPA therapy showed improvements in neurological outcome 3 months after stroke compared to patients receiving placebo. However, the window of treatment for tPA is very small and only a small percentage (<10%) of eligible 2 patients receive therapy. Although efforts to develop safe and effective treatment options for stroke patients continue, a gap remains between promising findings from the bench and positive results in clinical trials. In light of this, it is especially important that research is also focused on gaining better understanding of mechanisms that lead to increased stroke occurrence and increased stroke damage in order to make progress in diminishing the occurrence of stroke.