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Discover 9,675 clinical trials near Tennessee. Find research studies in your area.
Showing 2741-2760 of 9,675 trials
NCT03582163
Vanderbilt University Medical Center is one of the largest-volume DBS centers in the country. From 2007 through October 2017, 265 Parkinson's disease (PD) patients underwent deep brain stimulation (DBS), 168 of those implanted in subthalamic nucleus (STN) and 97 in globus pallidus interna (GPi). Pre-operatively, each patient is extensively evaluated with a battery of validated motor, cognitive, and mood instruments. This information is stored in RedCAP, a secure online database platform. In an attempt to capture longitudinal outcomes in this population of interest, we will recruit all PD patients two years or more status post DBS who are receiving regular care at Vanderbilt University Medical Center. Study participants will undergo a condensed evaluation of motor function (Unified Parkinson's Disease Rating Scale Part III), cognitive performance (Mini-Mental Status Examination), mood (Beck Depression Inventory), and quality of life (Parkinson's Disease Questionnaire-39). These results will be compared to baseline measures performed pre-operatively, allowing for assessment of interval change. STN and GPi DBS patients will be analyzed separately.
NCT06741436
Though cardiovascular disease (CVD) is the leading cause of mortality in women, traditional epidemiology in this area has focused on later life, when cardiometabolic risk has already exacted a cumulative toll on the vascular system. Recent data from the investigators and others has highlighted pregnancy as a unique, early moment of cardiovascular stress in young women that may "unmask" CVD propensity. It is unclear if PreE simply represents a "failed stress test" or directly contributes to the pathophysiology of future CVD. While mechanistic studies have largely been the purview of model-based studies, endothelial dysfunction has emerged as central to the pathogenesis of both PreE and peripartum cardiac dysfunction. Indeed, biomarkers of endothelial dysfunction and angiogenic imbalance during pregnancy have been shown to remain elevated at least 6 months post-partum. Moreover, peri-partum endothelial dysfunction can persist for years post-delivery and remains a significant risk factor for CVD (even after adjustment for other traditional risk factors). While these findings suggest that PreE-associated endothelial dysfunction and inflammation may contribute to early myocardial dysfunction that presages HF risk decades before its onset, the modifiable epidemiology of PreE-associated LVDD, including potential mechanisms of risk, remains unclear, limited by lack of precision molecular phenotypes accessible in a large number of American women across race. Ultimately, understanding the epidemiology and pathobiology of PreE-associated myocardial dysfunction affords a unique opportunity to identify women at risk with a longer lead-time for risk factor modification to interrupt CVD. The investigators hypothesize that persistent structural-functional myocardial alterations after PreE are linked to pre- and post-gravid cardiometabolic risk factors (SA1), functional and hemodynamic impairment (SA2) and select pathways of vascular and inflammatory stress relevant to HF risk (SA3). Despite extensive study on the role of inflammation/ischemia in PreE, there have been no large studies connecting these phenotypes with early PP functional response and biochemical alterations, a key barrier to designing studies for improving CVD/HF in women. SA1: To identify pregnancy-specific clinical factors related to postpartum HFpEF phenotypes Clinical Implication: Improve identification of women at highest risk for developing post-PreE LV diastolic dysfunction (a harbinger of HFpEF). SA2: To define functional and hemodynamic signatures of early HFpEF due to preeclampsia Clinical Implication: Identify women at highest risk for developing early HFpEF. SA3: To identify shared pathophysiologic mechanistic pathways for PreE-associated HFpEF Clinical Implication: Identify targetable pathways for post-PreE cardiac dysfunction that may prevent/ delay HFpEF development.