Filter results

Clinical Studies

Open

  • A Cross-sectional Study Examining Adipose Tissue in Obstructive Sleep Apnea Rochester, Minn.

    Studies show that sleep apnea increases the risk of cardiovascular disease and is associated with obesity. However, it is unclear how sleep apnea affects fat tissue. Studies have shown that fat tissue is likely involved in developing cardiovascular disease. The purpose of this study is to see how sleep apnea changes fat tissue.

  • A Prevalence and Incidence Study Investigating the Burden of Atrial and Ventricular Arrhythmias in Patients with Sleep Apnea and Hypertrophic Cardiomyopathy Rochester, Minn.

    The purpose of this study is to determine prevalence of sleep apnea in patients with hypertrophic cardiomyopathy and the risk of atrial and ventricular arrhythmias.

  • Cardiovascular Effects of Energy Drinks in Healthy Adults Rochester, Minn.

    This study is being done to look at the cardiovascular response, if any, to intake of commercially available energy drink. We hypothesize that energy drink consumption compared to a control drink in healthy adults alters the cardiovascular hemodynamic system.

  • Evaluating the Prevalence and Implications of Obstructive Sleep Apnea Among Somali-Americans: A Translational Research Study (Somali OSA) Rochester, Minn.

    The purpose of this study is to advance the understanding of obstructive sleep apnea as it relates to different ethnic origins as well as sex differences. The investigators will compare Somali patients with known obstructive sleep apnea (OSA) to individuals without OSA, and to individuals of other ethnic/racial origins to determine the risk factors (genetic and/or physiologic) associated with developing cardiovascular diseases. This will help the investigators to understand the unique sleep pathology of individuals of African descent.

  • Genetic Markers of Cardiovascular Diseases and the Potential Role in Sudden Unexpected Death in Epilepsy. Rochester, Minn.

    Epilepsy is a common condition which affects over 3 million people in the US. Patients with uncontrolled epilepsy have a lifetime risk of sudden unexpected death (SUDEP) of 35%, which is greatest in those under 40 years of age. The exact mechanisms and causes are not understood but can be due to underlying conditions which affect the heart and brain, which may lead to dangerous heart rhythms and death. Some of these conditions which affect heart and brain have an identifiable genetic cause. This study aims to identify known genetic causes of heart rhythm and sudden death related disorders in patients with epilepsy.

  • HELP-HY: Health Education and sLeep Program in HYpertension Rochester, Minn.

    Hypertension is the major risk factor for cardiovascular and cerebrovascular diseases worldwide. The escalating prevalence of inadequate sleep now parallels that of hypertension. Observational and experimental evidence favoring a causal relation between insufficient sleep and hypertension are particularly compelling - sleeping 6 hours or less per night is associated with a 20-32% higher probability of incident hypertension. Since sleep curtailment is largely voluntary, sleep deficiency may be corrected and the detrimental health consequences potentially reversed. In this study the investigators aim to investigate the effects of 8 weeks of sleep enhancement/extension vs health education in prehypertensive and stage 1 hypertensive subjects who report habitual short sleep (=6.5 hours/night).

  • Implications of the Human Microbiota for Health and Disease Rochester, Minn.

    The primary purpose of this study is to examine the human microbiota in healthy subjects.

     

  • Neural Circulatory and Respiratory Control in Patients With Epilepsy and the Risk of Sudden Unexpected Death. (NC-SUDEP) Rochester, Minn.

    The investigators believe epilepsy alters the way the body controls blood pressure, heart rate and breathing, and these changes increase the risk of sudden unexpected death in patients with epilepsy (SUDEP). SUDEP-7 is a risk scoring tool which may correlate with these changes to the heart and blood vessels. This research study measures those differences which may help identify new markers to help predict those patients at greatest risk in the future.

  • Physiologic Effects of Sleep Restriction Rochester, Minn.

    Evidence suggests a relationship between sleep deprivation and cardiovascular disease. The investigators wish to determine whether 9 nights of modest sleep restriction results in activation of cardiovascular disease mechanisms, thus potentially increasing the risk of cardiovascular disease. The investigators hypothesize that sleep restriction will result in elevated blood pressure, inflammation, and neurocognitive deficits.

  • Sleep Restriction and Obesity Rochester, Minn.

    Insufficient sleep may be one of the most common, and most preventable, obesity risk factors. The investigators wish to determine whether 14 nights of modest sleep restriction results in increased energy balance, thus potentially increasing the risk of obesity. The investigators hypothesize that sleep restriction will result in increased energy balance.

  • Statins and CPAP in Adipose Tissue: A Randomized Clinical Trial in Obstructive Sleep Apnea (SCAT-OSA) Rochester, Minn.

    This study is aimed at examining the alterations in adipose tissue in obstructive sleep apnea (OSA) patients in response to treatment with atorvastatin in continuation with standard treatment with continuous positive airway pressure (CPAP).

Closed for Enrollment

  • Effect of Sleep Deprivation on Reflex Activation of the Sympathetic Nervous System Rochester, Minn.

    The purpose of this study is to see if the lack of sleep changes how the body controls blood pressure

  • Fat Biology, Sleep Disorders, and Cardiovascular Disease Rochester, Minn.

    Endothelial dysfunction, or abnormal functioning of the lining of blood vessels, appears to be a key process in the development of cardiovascular disease. Endothelial dysfunction appears to be caused by both sleep disordered breathing and obesity. As endothelial dysfunction is among the first clinical marker that predicts future cardiovascular events, understanding molecular mechanisms leading to impairment of endothelial function is very important. Endothelial function requires the proper functioning of endothelial nitric oxide synthase (eNOS). eNOS activity is tightly regulated by caveolin-1, a protein important in the formation of cellular structures called caveolae. Low levels of caveolin-1 facilitate optimal nitric oxide synthesis in endothelial cells as caveolin-1 helps to spatially organize eNOS in close proximity to signaling proteins that are important for eNOS activation. In certain diseases however, the balance of caveolin-1 and eNOS can be disrupted resulting in impaired nitric oxide synthesis and leading to endothelial dysfunction.

    The investigators therefore seek to characterize levels of caveolin-1, and correlate this with the presence or absence of sleep disordered breathing, obesity, and cardiovascular disease. The current IRB protocol covers the performance of fat biopsies on subjects who have recently completed a sleep study either in the Center for Sleep Medicine or in our sleep laboratory and were found to have sleep disordered breathing or no sleep disordered breathing, subject with sleep disordered breathing who have been treated successfully with continuous positive airway pressure for 3-6 months, and subjects undergoing other studies in our lab who are obese or non-obese and subjects who have known cardiovascular disease and subjects without known cardiovascular disease.

  • Interactions Between Leptin and Neural Circulatory Control Rochester, Minn.

    The purpose of this study is to test the hypothesis that obesity is associated with impairment of cardiovascular reflex control, and that this impairment is linked to deficient leptin activity.

  • Leptin Biology in Adipose Tissue Rochester, Minn.

    Leptin is a fat hormone which acts in maintaining energy balance. However, leptin levels are high in obese subjects indicating resistance to the actions of leptin. High leptin levels have been associated with increased cardiovascular and metabolic risks, but it is not clear if increased leptin or leptin resistance contributes to the increased cardiovascular risk. Further, even though leptin receptors are present in fat tissue, leptin's role in fat tissue functions are not completely investigated in humans. Based on preliminary data the investigators hypothesize that resistance to leptin action in obese adipose tissue is responsible for altering the expression of adipose tissue proteins which contribute to the development of cardiovascular and metabolic dysfunction. To test this hypothesis the investigators propose a novel study directed at investigating the leptin dependent changes in adipose tissue protein expression using adipose tissue obtained from lean and obese human subjects

  • Lowering Blood Pressure by Sleep Extension: a Randomized, Controlled Trial Rochester, Minn.

    Evidence suggests that roughly 30% of the US adult population sleeps less than 7 hours per night, and those who do show 20-52% increased risk to develop cardiovascular diseases, particularly hypertension. 

    The purpose of this study is to look at the cardiovascular and metabolic effects of prolonged sleep in prehypertensive and stage 1 hypertensive people who report habitual short sleep.

  • Pilot Study to Examine the Effects of Weight Gain on Adipose Tissue Rochester, Minn.

    This study aims to examine the role of weight gain in adipose tissue immune cell influx and development of obesity related cardiometabolic disorders. Adipose tissue-mediated chronic systemic inflammation is implicated in the development of cardiometabolic disorders in obesity. Therefore, resolution of adipose tissue inflammation may be key to ameliorating obesity-associated dyslipidemia, insulin-resistance, and cardiovascular disease. Proinflammatory cytokines contribute to the initial influx of immune cells into adipose tissue during weight gain. However, mechanisms regulating these cytokines in the adipose tissue milieu and the effects of weight gain on adipose tissue are not completely understood.

    The study proposes to investigate the molecular events contributing to increased infiltration of macrophages and T-cells into adipose tissue during weight gain. The central hypothesis is that in lean subjects (with low body fat mass), healthy fat gain which is associated with decreased expression of proinflammatory cytokines. However, in obesity (high body fat mass), adipose tissue is altered, which permits increased expression of inflammatory cytokines and further fat gain results in influx of immune cells. To test the hypothesis, adipose tissue from well characterized lean (control, with low body fat) and obese individuals (with high body fat) at baseline and after a modest 5% weight gain will be used. Adipose tissue samples after subsequent weight loss will also be examined.

    For this study, obesity will be defined by body composition rather than body mass index (BMI), as several studies have shown that BMI does not adequately define obesity and several individuals with normal BMI may indeed have high body fat mass. Individuals with body fat content ≤25% for men, & <35% for women) will be considered lean and individuals with body fat content >25% for men, ≥35% for women will be considered obese.

  • Sleep Apnea and Vascular Function Rochester, Minn.

    Obstructive sleep apnea (OSA) is associated with endothelial dysfunction and the development of cardiovascular disease. It is unclear how OSA results in endothelial dysfunction, but given the association between OSA and obesity, adipose-derived hormones (adipokines) are likely to be involved. Leptin, an adipokine upregulated in patients with OSA, has been shown to be associated with deleterious effects on vascular function resulting in impaired endothelial function. This proposal is directed at investigating the molecular mechanisms of endothelial dysfunction in OSA patients. We hypothesize that endothelial dysfunction associated with OSA is a result of molecular alterations within endothelial cells. As a part of these studies we will look at NO signaling pathways in adipose tissue and microvessels from normal and OSA subjects.

  • The Effects of Sleep on Human Microbiota: Implications for Health and Disease Rochester, Minn.

    The microorganisms inhabiting the human body can be regarded as a dynamic reflector of both healthy and disease states, altering in response to changes in the environment. This may precede clinically detectable disease, and could be used to predict disease onset, monitor response to treatment and predict prognosis. The purpose of this study is to show that human microbial communities are influenced by sleep and altered in humans with abnormal sleep patterns. They may ultimately be related to disease risk.

.