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Plasma HDL cholesterol and risk of myocardial infarction: a mendelian randomisation study
Open accessAbstract
Background High plasma HDL cholesterol is associated with reduced risk of myocardial infarction, but whether this association is causal is unclear. Exploiting the fact that genotypes are randomly assigned at meiosis, are independent of non-genetic confounding, and are unmodified by disease processes, mendelian randomisation can be used to test the hypothesis that the association of a plasma biomarker with disease is causal.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.Findings Carriers of the LIPG 396Ser allele (2·6% frequency) had higher HDL cholesterol (0·14 mmol/L higher, p=8×10(-13)) but similar levels of other lipid and non-lipid risk factors for myocardial infarction compared with non-carriers. This difference 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(-10)).Interpretation Some genetic mechanisms that raise plasma HDL cholesterol do not seem to lower risk of myocardial infarction. These data challenge the concept that raising of plasma HDL cholesterol will uniformly translate into reductions in risk of myocardial infarction.Funding US National Institutes of Health, The Wellcome Trust, European Union, British Heart Foundation, and the German Federal Ministry of Education and Research.
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In the citing paper
“In contrast, Mendelian randomization studies do not provide compelling evidence that HDL-C is causally associated with the risk of ASCVD [49,61,62].”
From 2019 ESC/EAS guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk (2019) · cites this paper as [61]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Mendelian randomization studies further support the notion that HDL-C may not be causally related to CHD risk”
From The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk (2019) · cites this paper as [111]
Experimental — accuracy not yet measuredIn the citing paper
“The causative role of HDL-C for protection against CVD has been questioned in several studies utilizing Mendelian randomization. 87,89,91,92”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [92]
In the citing paper
“As described below, findings from GWAS have increasing translational impact through identification of novel therapeutic targets67, prioritization (and deprioritization) of existing ones68 and development of polygenic scores that quantify individual genetic risk69.”
From A brief history of human disease genetics (2020) · cites this paper as [68]
In the citing paper
“The causative role of HDL-C for protection against CVD has been questioned in several studies utilizing Mendelian randomization.87,89,91,92”
From 2016 ESC/EAS Guidelines for the Management of Dyslipidaemias (2016) · cites this paper as [92]
In the citing paper
“Dietary interventions which raise HDL-C may not necessarily translate into CVD risk reduction, as serum HDL-c has recently been called into question regarding its role in the causal pathway of CVD (110).”
From Food Consumption and its Impact on Cardiovascular Disease: Importance of Solutions Focused on the Globalized Food System (2015) · cites this paper as [110]
In the citing paper
“With increasing availability of large-scale phenotyping (and genotyping), MR is being widely applied to quantitative traits (e.g. markers or adiposity, such as body mass index 13-16 ; blood lipids such as HDL-cholesterol 17-19 ; inflammation-related proteins such as interleukin-6 receptor 20,21 12 ) with the aim of discovering modifiable risk factors for disease that are causal and amenable to the”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [20]
In the citing paper
“For example, whilst inflammation in general has long been postulated to influence vascular disease 49,50 , MR has been able to test whether particular elements in the inflammatory response cause 20 or are caused by 51 disease.”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [20]
In the citing paper
“The interleukin 6 receptor (IL6R) is a drug target that alters CRP (see Figure 3 ), and for which genetic evidence supports a causal role of IL6R in CHD 20 54”
From Integrating genomics with biomarkers and therapeutic targets to invigorate cardiovascular drug development (2021) · cites this paper as [20]
In the citing paper
“In contrast, recent studies have failed to demonstrate that high HDL-C acquired naturally or pharmacologically, is associated with reduced CVD risk.5-11,18”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [11]
In the citing paper
“Similarly, a Mendelian randomization study failed to identify polymorphisms associated with high HDL-C that correlate with reduced CVD risk.11”
From Is Isolated Low High-Density Lipoprotein Cholesterol a Cardiovascular Disease Risk Factor?: New Insights From the Framingham Offspring Study (2016) · cites this paper as [11]
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“Deletions in the gene encoding endothelial lipase (LIPG) result in modest elevations in HDL-C levels due to reduced phospholipolysis (5) but have not been shown to be associated with expected decreased or paradoxically increased risk (6).”
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“However recently, a mendelian randomization analysis revealed that a single nucleotide polymorphism in the endothelial lipase gene (LIPG Asn396Ser) associated with increased HDL-C levels in the population did not decrease the risk of myocardial infarction, despite a 13% reduction expected from the increased HDL-C leve…”
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“Further evidence that HDL itself may simply be a biomarker rather than a causal factor for CVD came from recent genetic studies performed in tens of thousands of patients, which found (1) an inverse association of CHD risk in patients with genetically reduced CETP function(64) and (2) that certain genetic variants tha…”
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“At this time, the European Society of Cardiology [43] recommend an intake of at least 2-3 servings of fish per week for CVD prevention and suggest that supplementation of 2-3 g/day of EPA-DHA may be useful for reduction of triglycerides.”
BackgroundInfluentialCan we revive CETP-inhibitors for the prevention of cardiovascular disease?
Nicholls, S. J., Ray, K. K., Nelson, A. J., & Kastelein, J. J. P. (2022) · Current Opinion in Lipidology · doi:10.1097/mol.0000000000000854 · Cited by 19
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“MR has been previously used to investigate the causal role of high-density lipoprotein((18)) and C-reactive protein((19)) in predisposition to cardiovascular disease and has provided evidence that PCSK9 inhibition prevents cardiovascular disease.”
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“Notably, Mendelian randomization studies investigating the HDL-C hypothesis of CAD suggested that raising HDL-C was unlikely to be an effective therapeutic approach [40,41] prior to clinical trial results from A Study of Evacetrapib in HighRisk Vascular Disease [42] and the Randomized EValuation of Anacetrapib through…”
ResultIn-depth Mendelian randomization analysis of causal factors for coronary artery disease
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“Unlike traditional observational epidemiology, genotypes are independent of nongenetic confounding factors and are not susceptible to reverse causality in disease processes (35).”
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ResultGenetic Risk Factors and Mendelian Randomization in Cardiovascular Disease
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“After 14 days, mice were injected intraperitoneally with 500 μL [3H]cholesterol-loading macrophages (~5 × 106 cells) containing (5-10) × 106 counts per minute (cpm).”
MethodHDL-c and arterial calcification in midlife women: does an HDL paradox exist?
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“Medications raising HDL-c did not lower (and some even increased) risk of coronary heart disease,(8,9) and Mendelian randomization studies have shown that genetically determined HDL-c is not linked to risk of coronary heart disease.(10)”
BackgroundLevels of Blood Biomarkers among Patients with Myocardial Infarction in Comparison to Control Group
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“The inference based on the other IV group shows no causal link from HDL to CAD, consistent with previous studies 22,30 .”
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Tachometer for Reverse Cholesterol Transport?
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“plaque load that were expected from epidemiological studies.(2,3,5) Because of these controversial data, the pathogenic role of HDL and its suitability as a therapeutic target have been”
BackgroundHigh-density lipoprotein: quantity or quality?
Τζιόμαλος, Κ. (2016) · Journal of Thoracic Disease · doi:10.21037/jtd.2016.11.67 · Cited by 7
“In contrast, Mendelian randomization studies showed that single nucleotide polymorphisms that modulate HDL-C levels do not affect the incidence of coronary heart disease (8,9).”
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“64 However, low HDL profile is more frequently seen in SCI compared with the general population.”
BackgroundThe pathophysiology of excess plasma-free cholesterol
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BackgroundSports and HDL-Quality Reflected By Serum Amyloid A and Surfactant Protein B
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A Long Road Ahead for Discovering New HDL Metrics That Reflect Cardiovascular Disease Risk ∗
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“Indeed, genetic variations that associate with altered HDL-C do not strongly associate with altered CVD risk (4,5).”
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“MR studies employ genetic variations (single-nucleotide polymorphisms [SNPs]) associated with an exposure to investigate its effect on an outcome [24 – 27].”
Parámetros lipídicos y objetivos terapéuticos
Cordero, A., Sirera, D., & Bertoméu, V. (2012) · Revista Española de Cardiología Suplementos · doi:10.1016/s1131-3587(12)70040-7 · Cited by 5
Identifying Genetic Markers Associated with Susceptibility to Cardiovascular Diseases
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Milk and butter. From the Neolithic to the current nutritional aspects
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The time for lipoprotein(a) based intervention has arrived: where will the light shine?
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“Given the lack of association between genetic polymorphisms influencing HDL-C levels and cardiovascular risk, this is not necessarily surprising (7,8).”
BackgroundCai, Z., Deng, L., Chen, Y., & Ling, Y. (2022) · Endocrine · doi:10.1007/s12020-022-03024-9 · Cited by 3
Sphingolipids and HDL Metabolism
Jiang, X., Li, Z., & Yazdanyar, A. (2013) · Elsevier eBooks · doi:10.1016/b978-0-12-407867-3.00006-8 · Cited by 4
The High Density Lipoprotein Cholesterol Hypothesis Revisited
Meiliana, A., Dewi, N. M., & Wijaya, A. (2018) · The Indonesian Biomedical Journal · doi:10.18585/inabj.v10i2.465 · Cited by 2
“(2,5,156,157) Moreover, in several inborn errors of human HDL metabolism and genetic mouse models with altered HDL metabolism, the changes in HDL-C levels were not associated with accompanying changes in cardiovascular risk or atherosclerotic plaque load, respectively, as has been expected from epidemiological studies…”
BackgroundResultUpdate in Cardiology: Vascular Risk and Cardiac Rehabilitation
Galve, E., Castro, A., Cordero, A., Dalmau, R., Fácila, L., García-Romero, A., Mazón, P., Sanmartín, M., & Garcia, A. A. (2012) · Revista Española de Cardiología (English Edition) · doi:10.1016/j.rec.2012.10.007 · Cited by 3
“Furthermore, certain genetic mutations have been identified that lead to higher HDLc values but which are not associated with decreased CV disease risk.(42) However, in a study comparing patients with chest pain admitted to a single center, HDLc levels were 22% higher in patients discharged with a diagnosis of noncoro…”
BackgroundAsl, S. K., Rahimzadegan, M., & Asl, A. K. (2024) · Heliyon · doi:10.1016/j.heliyon.2024.e28983 · Cited by 2
High density lipoprotein cholesterol and risk of death
Al‐Aly, Z. (2016) · Journal of Thoracic Disease · doi:10.21037/jtd.2016.12.65 · Cited by 2
“Recent Mendelian randomization analyses show that genetic mechanisms that raise plasma HDL-C do not result in lowering the risk of myocardial infarction (6).”
BackgroundLiu, H., Wang, F., Li, Y., Xia, H., Pan, D., Yang, L., Wang, S., & Sun, G. (2020) · Preprints.org · doi:10.20944/preprints202010.0563.v1 · Cited by 1
“Voight et al reported that an increased in HDL levels alone does not decrease the incidence of cardiovascular events in CAD patients [45].”
BackgroundMeyer, A., Amiot, A., & Carbonnel, F. (2023) · Alimentary Pharmacology & Therapeutics · doi:10.1111/apt.17432 · Cited by 2
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Cholesterol HDL — friend or foe?
Banach, J., & Sinkiewicz, W. (2013) · Kardiologia Polska · doi:10.5603/kp.2013.0045 · Cited by 1
Role of Conventional Risk Factors in Genetic Susceptibility to Cardiovascular Diseases
Swerdlow, D. I., Michail, M., & Zacharias, K. A. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-803312-8.00008-2 · Cited by 2
Cholesteryl Ester Transfer Protein Inhibitors – Future Soon to be REVEALed
Huggins, C., Charolidi, N., & COCKERILL, G. W. (2015) · European Cardiology Review · doi:10.15420/ecr.2015.10.01.64 · Cited by 1
Compuestos fenólicos y su efecto en las dislipidemias en seres humanos: Una revisión sistemática
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Genetic Disorders of Lipoprotein Metabolism: Diagnosis and Management
Cupido, A. J., Stoekenbroek, R. M., & Kastelein, J. J. P. (2016) · Springer eBooks · doi:10.1007/978-3-319-44203-7_21 · Cited by 1
CETP inhibitors and cardiovascular disease: Time to think again
Miller, N. E. (2014) · F1000Research · doi:10.12688/f1000research.4705 · Cited by 1
Owens, D. A., & Tomkin, G. H. (2018) · Current Cardiology Reviews · doi:10.2174/1573403x1404181008143841 · Cited by 1
“[15] examined 14 common Single Nucleotide Polymorphisms (SNP) that exclusively associate with HDL”
BackgroundMendelian Randomization with Instrumental Variable Synthesis (IVY)Preprint
Kuang, Z., Córdova‐Palomera, A., Sala, F. G., Wu, S., Dunnmon, J., Ré, C., & Priest, J. R. (2019) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/657775 · Cited by 1
“However, such an association is spurious, as demonstrated by various clinical trials and Mendelian randomization studies (Schwartz et al., 2012; Voight et al., 2012).”
BackgroundProteomics: a tool to investigate of composition and function of HDL in hyperlipidemia
da Silva, A. R. M. (2022) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.46.2022.tde-26082022-123137 · Cited by 1
Lipoprotein(a) After HORIZON: Causal Culprit, Risk Marker, or Unfulfilled Therapeutic Promise?
Borovac, J. A., & Belančić, A. (2026) · Journal of Cardiovascular Pharmacology and Therapeutics · doi:10.1177/10742484261492865 · Cited by 1
Anacetrapib: potential for the prevention and treatment of coronary heart disease
Cannon, C. P., Steen, D. L., & Khera, A. V. (2013) · Research Reports in Clinical Cardiology · doi:10.2147/rrcc.s27769
Biomarker des Lipoproteinstoffwechsels
von Eckardstein, A. (2015) · Cardiovascular Medicine · doi:10.4414/cvm.2015.00297
Theodorou (2018) · Research Publications (Maastricht University) · doi:10.26481/dis.20180119kt
Al‐Aly, Z. (2017) · Journal of Thoracic Disease · doi:10.21037/jtd.2017.11.95
V. Lipid Managements from the Point of View of Human Genetics
Tada, H., Kawashiri, M., & Yamagishi, M. (2017) · Nihon Naika Gakkai Zasshi · doi:10.2169/naika.106.711
Cartolano, F. D. C. (2019) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.6.2019.tde-10102018-080400
Özdoğan, Ö., Başaran, Ö., Güngör, B., Si̇nan, Ü. Y., & Kayıkçıoğlu, M. (2021) · Minerva Cardiology and Angiology · doi:10.23736/s2724-5683.20.05222-6
Zhou, Y., Sun, S., & Hu, F. (2021) · Archives of Medical Science · doi:10.5114/aoms/132472
“2 Arch Med Sci changes in lifestyle and eating habits predispose a significant number of individuals to myocardial infarction across the globe in the coming years [2, 3].”
BackgroundTang, X., Mao, L., Jin, C., Zhang, T., Weng, S., Guo, X., Kuang, J., Yu, B., & Peng, D. (2020) · Research Square · doi:10.21203/rs.3.rs-66204/v1
“In addition, a genetically increased HDL-C does not necessarily translate to a decreased risk of myocardial infarction [4].”
BackgroundTani, S., Atsumi, W., Imatake, K., Suzuki, Y., Yagi, T., Matsumoto, N., & Okumura, Y. (2021) · Research Square · doi:10.21203/rs.3.rs-679869/v1
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Innovative Lipid Biomarkers and Long-Term Outcomes
Anderson, J. L. C. (2021) · University of Groningen research database (University of Groningen / Centre for Information Technology) · doi:10.33612/diss.192996734
Metadata
- Authors
- Voight, B. F., Peloso, G. M., Orho-Melander, M., Frikke-Schmidt, R., Barbalic, M., Jensen, M. K., Hindy, G., Hólm, H., Ding, E. L., Johnson, T., Schunkert, H., Samani, N. J., Clarke, R., Hopewell, J. C., Thompson, J. F., Li, M., Thorleifsson, G., Newton-Cheh, C., Musunuru, K., Pirruccello, J. P., Saleheen, D., Chen, L., Stewart, A. F., Schillert, A., Thorsteinsdottir, U., Thorgeirsson, G., Anand, S., Engert, J. C., Morgan, T., Spertus, J., Stoll, M., Berger, K., Martinelli, N., Girelli, D., McKeown, P. P., Patterson, C. C., Epstein, S. E., Devaney, J., Burnett, M.-S., Mooser, V., Ripatti, S., Surakka, I., Nieminen, M. S., Sinisalo, J., Lokki, M.-L., Perola, M., Havulinna, A., de Faire, U., Gigante, B., Ingelsson, E., Zeller, T., Wild, P., de Bakker, P. I. W., Klungel, O. H., Maitland-van der Zee, A.-H., Peters, B. J. M., de Boer, A., Grobbee, D. E., Kamphuisen, P. W., Deneer, V. H. M., Elbers, C. C., Onland-Moret, N. C., Hofker, M. H., Wijmenga, C., Verschuren, W. M., Boer, J. M., van der Schouw, Y. T., Rasheed, A., Frossard, P., Demissie, S., Willer, C., Do, R., Ordovas, J. M., Abecasis, G. R., Boehnke, M., Mohlke, K. L., Daly, M. J., Guiducci, C., Burtt, N. P., Surti, A., Gonzalez, E., Purcell, S., Gabriel, S., Marrugat, J., Peden, J., Erdmann, J., Diemert, P., Willenborg, C., König, I. R., Fischer, M., Hengstenberg, C., Ziegler, A., Buysschaert, I., Lambrechts, D., Van de Werf, F., Fox, K. A., El Mokhtari, N. E., Rubin, D., Schrezenmeir, J., Schreiber, S., Schäfer, A., Danesh, J., Blankenberg, S., Roberts, R., McPherson, R., Watkins, H., Hall, A. S., Overvad, K., Rimm, E., Boerwinkle, E., Tybjaerg-Hansen, A., Cupples, L. A., Reilly, M. P., Melander, O., Mannucci, P. M., Ardissino, D., Siscovick, D., Elosua, R., Stefansson, K., O'Donnell, C. J., Salomaa, V., Rader, D. J., Peltonen, L., Schwartz, S. M., Altshuler, D., & Kathiresan, S.
- Affiliations
- University of Pennsylvania (US)
- Boston University (US)
- Harvard University (US)
- Lund University (SE)
- deCODE Genetics (Iceland) (IS)
- Brigham and Women's Hospital (US)
- Queen Mary University of London (GB)
- University of Lübeck (DE)
- University of Leicester (GB)
- University of Oxford (GB)
- Broad Institute (US)
- University of Cambridge (GB)
- Ottawa Heart Institute (CA)
- Population Health Research Institute (CA)
- McGill University (CA)
- Vanderbilt University (US)
- University of Missouri–Kansas City (US)
- University of Münster (DE)
- University of Verona (IT)
- Queen's University Belfast (GB)
- MedStar Washington Hospital Center (US)
- GlaxoSmithKline (United States) (US)
- University of Helsinki (FI)
- Helsinki University Hospital (FI)
- Finnish Institute for Health and Welfare (FI)
- Karolinska Institutet (SE)
- Johannes Gutenberg University Mainz (DE)
- Utrecht University (NL)
- University Medical Center Utrecht (NL)
- University Medical Center Groningen (NL)
- St. Antonius Ziekenhuis (NL)
- National Institute for Public Health and the Environment (NL)
- Center for Non-Communicable Diseases (PK)
- University of Michigan (US)
- Massachusetts General Hospital (US)
- University of North Carolina at Chapel Hill (US)
- Hospital del Mar Research Institute (ES)
- University Hospital Regensburg (DE)
- Universitair Ziekenhuis Leuven (BE)
- University of Edinburgh (GB)
- University Hospital Schleswig-Holstein (DE)
- Max Rubner Institut (DE)
- Christian-Albrechts-Universität zu Kiel (DE)
- University of Leeds (GB)
- Aarhus University (DK)
- The University of Texas Health Science Center at Houston (US)
- Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico (IT)
- Ospedale di Parma (IT)
- University of Washington (US)
- Corresponding author
- Kathiresan, Sekar
- ORCID
- Voight, Benjamin F
- Peloso, Gina M
- Jensen, Majken K
- Hindy, George
- Hólm, Hilma
- Ding, Eric L
- Johnson, Toby
- Schunkert, Heribert
- Samani, Nilesh J
- Clarke, Robert
- Hopewell, Jemma C
- Thompson, John F
- Li, Mingyao
- Musunuru, Kiran
- Pirruccello, James P
- Saleheen, Danish
- Chen, Li
- Stewart, Alexandre FR
- Schillert, Arne
- Anand, Sonia
- Engert, James C
- Morgan, Thomas
- Spertus, John
- Stoll, Monika
- Martinelli, Nicola
- Girelli, Domenico
- McKeown, Pascal P
- Patterson, Christopher C
- Mooser, Vincent
- Ripatti, Samuli
- Surakka, Ida
- Nieminen, Markku S
- Sinisalo, Juha
- Lokki, Marja-Liisa
- Perola, Markus
- Havulinna, Aki
- Gigante, Bruna
- Ingelsson, Erik
- Zeller, Tanja
- Wild, Philipp
- Klungel, Olaf H
- Peters, Bas J M
- Grobbee, Diederick E
- Kamphuisen, Pieter W
- Deneer, Vera H M
- Elbers, Clara C
- Wijmenga, Cisca
- Verschuren, WM Monique
- Boer, Jolanda MA
- Demissie, Serkalem
- Willer, Cristen
- Do, Ron
- Abecasis, Gonçalo R
- Boehnke, Michael
- Mohlke, Karen L
- Daly, Mark J
- Burtt, Noël P
- Purcell, Shaun
- Gabriel, Stacey
- Marrugat, Jaume
- Erdmann, Jeanette
- König, Inke R
- Fischer, Marcus
- Hengstenberg, Christian
- Ziegler, Andreas
- Buysschaert, Ian
- Lambrechts, Diether
- Fox, Keith A
- Schreiber, Stefan
- Danesh, John
- Blankenberg, Stefan
- McPherson, Ruth
- Watkins, Hugh
- Hall, Alistair S
- Overvad, Kim
- Rimm, Eric
- Boerwinkle, Eric
- Cupples, L Adrienne
- Reilly, Muredach P
- Melander, Olle
- Mannucci, Pier M
- Ardissino, Diego
- Siscovick, David
- Salomaa, Veikko
- Rader, Daniel J
- Peltonen, Leena
- Altshuler, David
- Kathiresan, Sekar
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2012-08
- Volume
- 380
- Issue
- 9841
- Pages
- 572-580
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- PMC
- PMC3419820
- OpenAlex
- W1240353884
- Cited by
- 148
- References
- 36
- Citations by year
- 2026: 11 · 2025: 4 · 2024: 5 · 2023: 8 · 2022: 9 · 2021: 19 · 2020: 16 · 2019: 9 · 2018: 10 · 2017: 8 · 2016: 12 · 2015: 8 · 2014: 9 · 2013: 6 · 2012: 13
- FWCI
- 1.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- The Lancet (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (publishedVersion)
- Edinburgh Research Explorer (University of Edinburgh) (submittedVersion, other-oa)
- Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
- University of Regensburg Publication Server (University of Regensburg) (submittedVersion)
- Figshare (submittedVersion, cc-by)
- Leicester Research Archive (University of Leicester) (submittedVersion, other-oa)
- Lund University Publications (Lund University) (submittedVersion)
- mediaTUM (Technical University of Munich) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Research Portal (Queen's University Belfast) (submittedVersion)
- Rivm Repository (Netherlands National Institute for Public Health and the Environment) (submittedVersion)
- Hirsla (Landspítali University Hospital) (submittedVersion)
- STM:n Hallinnonalan avoin julkaisuarkisto (Julkari) (submittedVersion)
- OpenAgrar (submittedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- WOS
- Funders
- Wellcome Trust (090532)
- British Heart Foundation (RG/08/014/24067)
- National Institutes of Health (n01hc25195-41-0-1)
- National Heart, Lung, and Blood Institute (N01-HC-025195)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Paraoxonase enzyme and polymorphisms
- Keywords
- HDL cholesterol, myocardial infarction, causal inference, endothelial lipase, genetic score, LDL cholesterol, cardiovascular risk, genetic instruments, single nucleotide polymorphisms, lipid biomarkers, confounding by indication, reverse causality
- MeSH terms
- Gene Frequency, Humans, Lipase, Cholesterol, HDL, Cholesterol, LDL, Myocardial Infarction, Prospective Studies, Risk Factors, Biomarkers, Case-Control Studies, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Mendelian Randomization Analysis
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