Showing papers by "H. Bryan Brewer published in 2010"
TL;DR: In ACS patients, serial autologous infusions of selective HDL delipidated plasma are clinically feasible and well tolerated and this therapy may offer a novel adjunct treatment for patients presenting with ACS.
215 citations
TL;DR: This poster presents a poster presented at the 2016 American Academy of Clinical Lipidology conference on “Advances in Lipid Metabolism and Atherosclerosis: Foundations of Lipid Heart Disease Prevention and Response to Intervention.”
13 citations
01 Jan 2010
TL;DR: Patients with Tangier Disease, named after the Chesapeake Bay island home of the first two cases described, have marked HDL deficiency, moderate hypertriglyceridemia, and low density lipoprotein cholesterol levels that are about 50% of normal values.
Abstract: The ATP binding cassette A1 (ABCA1) transporter facilitates the efflux of free cholesterol and phospholipid onto high density lipoprotein (HDL) particles, mainly very small discoidal precursor HDL particles, known as prebeta 1 HDL. Once these particles pick up these lipids, they are converted to small discoidal alpha 4 migrating HDL and with cholesterol esterification mature into larger spherical alpha 3 and 2 HDL particles. Separate chapters in this book are devoted to HDL particle metabolism. Patients with Tangier Disease, named after the Chesapeake Bay island home of the first two cases described, have marked HDL deficiency, moderate hypertriglyceridemia, and low density lipoprotein (LDL) cholesterol levels that are about 50% of normal values. The only HDL particle detectable in the plasma of homozygotes is the very small precursor prebeta 1 HDL particle, which in these patients is rapidly catabolized by the kidneys. Homozygotes have lipid laden macrophages in their tonsils, spleen, liver, arterial wall, other tissues, and Schwann cells, which can result in enlarged orange tonsils, hepatosplenomegaly, premature coronary heart disease (CHD), and neuropathy. Their LDL is about 50% of normal, is smaller and more triglyceride enriched than normal LDL, and its protein component is cleared from plasma at twice the normal fractional rate. Heterozygotes with this disease have about 50% of normal HDL cholesterol, lack large alpha 1 HDL, and have an increased risk of premature CHD when compared to control subjects. Findings in this disease underscore the importance of ABCA1 in promoting free cholesterol efflux from a variety of cells and maintaining cellular cholesterol homeostasis.
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TL;DR: Focus has now turned to increasing HDL as a potential approach to reduce the residual cardiovascular risk in statin treated patients.
Abstract: Over the last three decades, clinical trials utilizing statins to reduce LDL in high risk patients have resulted in a 30-40% reduction in clinical events [1-6]. However, despite a significant reduction in LDL, many patients continue to have clinical events. The residual risk present in statin treated high risk patients has resulted in the search for additional therapeutic approaches to reduce clinical events. Epidemiological studies have identified HDL cholesterol (HDL-C) as an independent risk factor for cardiovascular disease [7, 8]. In addition, low HDL-C levels are often present in high risk patients [9], and analyses of clinical trials of statin therapy have indicated that the baseline level of HDL-C is an important determinant of the clinical benefit associated with statin treatment [1, 4, 5]. As a result, focus has now turned to increasing HDL as a potential approach to reduce the residual cardiovascular risk in statin treated patients.