This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Approximately 15% of strokes are caused by spontaneous intracerebral hemorrhage (ICH) (1). ICH is the most disabling, and the least treatable form of stroke. Nearly 50% of the estimated 37,000 Americans who suffered an ICH in 1997 were dead at one-month follow-up and only 20% were living independently at 6 months (2,3). Hematoma size is strongly correlated with outcome, and early hematoma expansion occurs in a sizable proportion of patients presenting with acute ICH (up to 40%) (4,5). Understanding the pathophysiology of hematoma expansion is therefore an important first step toward developing potential avenues for medical intervention. It is well established that certain coagulopaties are associated with acute spontaneous ICH. In addition, several convenience samples and our clinical series have suggested that patients with ICH may have underlying dysfunction of platelets and hemostatic pathways (6-8,22). However, no prospective study of primary hemostasis has been performed in ICH despite the high mortality and morbidity of this disease. Our central hypothesis is that ICH size and progression are associated with defects of primary hemostasis occurring at the platelet and vessel wall. Thus we propose to investigate the presence and causation of bleeding abnormalities in patients with spontaneous ICH, their association with initial ICH size and their impact on ICH expansion. Findings from this study will provide greater understanding of bleeding mechanisms of spontaneous ICH and ICH expansion, which will impact therapeutic decisions directed towards these critically ill patients.
Showing the most recent 10 out of 1014 publications
