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High-density lipoprotein

About: High-density lipoprotein is a research topic. Over the lifetime, 9022 publications have been published within this topic receiving 400119 citations. The topic is also known as: HDL & Lipoproteins, HDL.


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Journal ArticleDOI
TL;DR: The major potent lipid risk factor was HDL cholesterol, which had an inverse association with the incidence of coronary heart disease in either men or women and these associations were equally significant even when other lipids and other standard risk factors for coronaryHeart disease were taken into consideration.

5,054 citations

Journal ArticleDOI
TL;DR: Gemfibrozil therapy resulted in a significant reduction in the risk of major cardiovascular events in patients with coronary disease whose primary lipid abnormality was a low HDL cholesterol level, suggesting that the rate of coronary events is reduced by raising HDL cholesterol levels and lowering levels of triglycerides without lowering LDL cholesterol levels.
Abstract: Background Although it is generally accepted that lowering elevated serum levels of low-density lipoprotein (LDL) cholesterol in patients with coronary heart disease is beneficial, there are few data to guide decisions about therapy for patients whose primary lipid abnormality is a low level of high-density lipoprotein (HDL) cholesterol. Methods We conducted a double-blind trial comparing gemfibrozil (1200 mg per day) with placebo in 2531 men with coronary heart disease, an HDL cholesterol level of 40 mg per deciliter (1.0 mmol per liter) or less, and an LDL cholesterol level of 140 mg per deciliter (3.6 mmol per liter) or less. The primary study outcome was nonfatal myocardial infarction or death from coronary causes. Results The median follow-up was 5.1 years. At one year, the mean HDL cholesterol level was 6 percent higher, the mean triglyceride level was 31 percent lower, and the mean total cholesterol level was 4 percent lower in the gemfibrozil group than in the placebo group. LDL cholesterol levels...

3,327 citations

Journal ArticleDOI
TL;DR: The body cholesterol pool increases with decreasing plasma-high-density-lipoprotein (H.D.L.) but is unrelated to the plasma concentrations of total cholesterol and other lipoproteins, and it is proposed that a reduction of plasma-H.H.L.D., is reduced in several conditions associated with an increased risk of future ischaemic heart-disease, by impairing the clearance of cholesterol from the arterial wall.

2,626 citations

Journal ArticleDOI
Benjamin F. Voight1, Benjamin F. Voight2, Benjamin F. Voight3, Gina M. Peloso4, Gina M. Peloso5, Marju Orho-Melander6, Ruth Frikke-Schmidt7, Maja Barbalić8, Majken K. Jensen3, George Hindy6, Hilma Holm9, Eric L. Ding3, Toby Johnson10, Heribert Schunkert11, Nilesh J. Samani12, Nilesh J. Samani13, Robert Clarke14, Jemma C. Hopewell14, John F. Thompson12, Mingyao Li2, Gudmar Thorleifsson9, Christopher Newton-Cheh, Kiran Musunuru3, Kiran Musunuru1, James P. Pirruccello1, James P. Pirruccello3, Danish Saleheen15, Li Chen16, Alexandre F.R. Stewart16, Arne Schillert11, Unnur Thorsteinsdottir9, Unnur Thorsteinsdottir17, Gudmundur Thorgeirsson17, Sonia S. Anand18, James C. Engert19, Thomas M. Morgan20, John A. Spertus21, Monika Stoll22, Klaus Berger22, Nicola Martinelli23, Domenico Girelli23, Pascal P. McKeown24, Christopher Patterson24, Stephen E. Epstein25, Joseph M. Devaney25, Mary Susan Burnett25, Vincent Mooser26, Samuli Ripatti27, Ida Surakka27, Markku S. Nieminen27, Juha Sinisalo27, Marja-Liisa Lokki27, Markus Perola4, Aki S. Havulinna4, Ulf de Faire28, Bruna Gigante28, Erik Ingelsson28, Tanja Zeller29, Philipp S. Wild29, Paul I.W. de Bakker, Olaf H. Klungel30, Anke-Hilse Maitland-van der Zee30, Bas J M Peters30, Anthonius de Boer30, Diederick E. Grobbee30, Pieter Willem Kamphuisen31, Vera H.M. Deneer, Clara C. Elbers30, N. Charlotte Onland-Moret30, Marten H. Hofker31, Cisca Wijmenga31, W. M. Monique Verschuren, Jolanda M. A. Boer, Yvonne T. van der Schouw30, Asif Rasheed, Philippe M. Frossard, Serkalem Demissie5, Serkalem Demissie4, Cristen J. Willer32, Ron Do3, Jose M. Ordovas33, Jose M. Ordovas34, Gonçalo R. Abecasis32, Michael Boehnke32, Karen L. Mohlke35, Mark J. Daly3, Mark J. Daly1, Candace Guiducci1, Noël P. Burtt1, Aarti Surti1, Elena Gonzalez1, Shaun Purcell1, Shaun Purcell3, Stacey Gabriel1, Jaume Marrugat, John F. Peden14, Jeanette Erdmann11, Patrick Diemert11, Christina Willenborg11, Inke R. König11, Marcus Fischer36, Christian Hengstenberg36, Andreas Ziegler11, Ian Buysschaert37, Diether Lambrechts37, Frans Van de Werf37, Keith A.A. Fox38, Nour Eddine El Mokhtari39, Diana Rubin, Jürgen Schrezenmeir, Stefan Schreiber39, Arne Schäfer39, John Danesh15, Stefan Blankenberg29, Robert Roberts16, Ruth McPherson16, Hugh Watkins14, Alistair S. Hall40, Kim Overvad41, Eric B. Rimm3, Eric Boerwinkle8, Anne Tybjærg-Hansen7, L. Adrienne Cupples5, L. Adrienne Cupples4, Muredach P. Reilly2, Olle Melander6, Pier Mannuccio Mannucci42, Diego Ardissino, David S. Siscovick43, Roberto Elosua, Kari Stefansson17, Kari Stefansson9, Christopher J. O'Donnell3, Christopher J. O'Donnell4, Veikko Salomaa4, Daniel J. Rader2, Leena Peltonen27, Leena Peltonen44, Stephen M. Schwartz43, David Altshuler, Sekar Kathiresan 
11 Aug 2012
TL;DR: In this paper, a Mendelian randomisation analysis was performed to compare the effect of HDL cholesterol, LDL cholesterol, and genetic score on risk of myocardial infarction.
Abstract: Methods We performed two mendelian randomisation analyses. First, we used as an instrument a single nucleotide polymorphism (SNP) in the endothelial lipase gene (LIPG Asn396Ser) and tested this SNP in 20 studies (20 913 myocardial infarction cases, 95 407 controls). Second, we used as an instrument a genetic score consisting of 14 common SNPs that exclusively associate with HDL cholesterol and tested this score in up to 12 482 cases of myocardial infarction and 41 331 controls. As a positive control, we also tested a genetic score of 13 common SNPs exclusively associated with LDL cholesterol. – ¹³) but similar levels of other lipid and non-lipid risk factors for myocardial infarction compared with noncarriers. This diff erence in HDL cholesterol is expected to decrease risk of myocardial infarction by 13% (odds ratio [OR] 0·87, 95% CI 0·84–0·91). However, we noted that the 396Ser allele was not associated with risk of myocardial infarction (OR 0·99, 95% CI 0·88–1·11, p=0·85). From observational epidemiology, an increase of 1 SD in HDL cholesterol was associated with reduced risk of myocardial infarction (OR 0·62, 95% CI 0·58–0·66). However, a 1 SD increase in HDL cholesterol due to genetic score was not associated with risk of myocardial infarction (OR 0·93, 95% CI 0·68–1·26, p=0·63). For LDL cholesterol, the estimate from observational epidemiology (a 1 SD increase in LDL cholesterol associated with OR 1·54, 95% CI 1·45–1·63) was concordant with that from genetic score (OR 2·13, 95% CI 1·69–2·69, p=2×10

1,878 citations

Journal ArticleDOI
TL;DR: Cholesterol efflux capacity from macrophages, a metric of HDL function, has a strong inverse association with both carotid intima-media thickness and the likelihood of angiographic coronary artery disease, independently of the HDL cholesterol level.
Abstract: We measured cholesterol efflux capacity in 203 healthy volunteers who underwent assessment of carotid artery intima–media thickness, 442 patients with angiograph ically confirmed coronary artery disease, and 351 patients without such angiographically confirmed disease. We quantified efflux capacity by using a validated ex vivo system that involved incubation of macrophages with apolipoprotein B–depleted serum from the study participants. Results The levels of HDL cholesterol and apolipoprotein A-I were significant determinants of cholesterol efflux capacity but accounted for less than 40% of the observed variation. An inverse relationship was noted between efflux capacity and carotid intima–media thickness both before and after adjustment for the HDL cholesterol level. Furthermore, efflux capacity was a strong inverse predictor of coronary disease status (adjusted odds ratio for coronary disease per 1-SD increase in efflux capacity, 0.70; 95% confidence interval [CI], 0.59 to 0.83; P<0.001). This relationship was attenuated, but remained significant, after additional adjustment for the HDL cholesterol level (odds ratio per 1-SD increase, 0.75; 95% CI, 0.63 to 0.90; P = 0.002) or apolipoprotein A-I level (odds ratio per 1-SD increase, 0.74; 95% CI, 0.61 to 0.89; P = 0.002). Additional studies showed enhanced efflux capacity in patients with the metabolic syndrome and low HDL cholesterol levels who were treated with pioglitazone, but not in patients with hypercholesterolemia who were treated with statins. Conclusions Cholesterol efflux capacity from macrophages, a metric of HDL function, has a strong inverse association with both carotid intima–media thickness and the likeli hood of angiographic coronary artery disease, independently of the HDL cholesterol level. (Funded by the National Heart, Lung, and Blood Institute and others.)

1,728 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202379
2022214
2021152
2020169
2019176
2018213