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Evidence for a New Pathophysiological Mechanism for Coronary Artery Disease Regression: Hepatic Lipase–Mediated Changes in LDL Density
Open accessAbstract
BACKGROUND: Small, dense LDL particles are associated with coronary artery disease (CAD) and predict angiographic changes in response to lipid-lowering therapy. Intensive lipid-lowering therapy in the Familial Atherosclerosis Treatment Study (FATS) resulted in significant improvement in CAD. This study examines the relationship among LDL density, hepatic lipase (HL), and CAD progression, identifying a new biological mechanism for the favorable effects of lipid-altering therapy. METHODS AND RESULTS: Eighty-eight of the subjects in FATS with documented coronary disease, apolipoprotein B levels >/=125 mg/dL, and family history of CAD were selected for this study. They were randomly assigned to receive lovastatin (40 mg/d) and colestipol (30 g/d), niacin (4 g/d) and colestipol, or conventional therapy with placebo alone or with colestipol in those with elevated LDL cholesterol levels. Plasma hepatic lipase (HL), lipoprotein lipase, and LDL density were measured when subjects were and were not receiving lipid-lowering therapy. LDL buoyancy increased with lovastatin-colestipol therapy (7.7%; P<0.01) and niacin-colestipol therapy (10.3%; P<0.01), whereas HL decreased in both groups (-14% [P<0.01] and -17% [P<0.01] with lovastatin-colestipol and niacin-colestipol, respectively). Changes in LDL buoyancy and HL activity were associated with changes in disease severity (P<0.001). In a multivariate analysis, an increase in LDL buoyancy was most strongly associated with CAD regression, accounting for 37% of the variance of change in coronary stenosis (P<0.01), followed by reduction in apolipoprotein Bl (5% of variance; P<0.05). CONCLUSIONS: These studies support the hypothesis that therapy-associated changes in HL alter LDL density, which favorably influences CAD progression. This is a new and potentially clinically relevant mechanism linking lipid-altering therapy to CAD improvement.
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“Several prospective studies suggest that circulating levels of small, dense LDL particles are better predictors of coronary atherosclerosis, carotid atherosclerosis, and response to therapy than are levels of large, buoyant LDL particles (28,(31)(32)(33).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [28]
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“Hepatic lipase and cholesterol ester transfer protein contribute to the remodeling processes; whether hepatic lipase or cholesterol ester transfer protein has the predominant effect on the size and density of LDL and HDL particles depends on the triglyceride content of very low-density lipoproteins (VLDL) (27,28).”
From Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline (2012) · cites this paper as [28]
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Cites
OLSSON, A. G., McMurray, J. J. V., Thorgeirsson, G., Spaulding, C. M., Slattery, J., Pyörälà, K., Færgeman, O., Wright, R. S., Berg, K. M., Wilhelmsen, L., et al. (1994) · The Lancet · Cited by 8,467
Prevention of Coronary Heart Disease with Pravastatin in Men with Hypercholesterolemia
Shepherd, J., Cobbe, S. M., Ford, I., Isles, C. G., Lorimer, A. R., Macfarlane, P. W., McKillop, J. H., & Packard, C. J. (1995) · New England Journal of Medicine · doi:10.1056/nejm199511163332001 · Cited by 7,449
Sacks, F. M., Pfeffer, M. A., Moye, L. A., Rouleau, J. L., Rutherford, J. D., Cole, T. G., Brown, L., Warnica, J. W., Arnold, J. M. O., Wun, C.-C., et al. (1996) · New England Journal of Medicine · doi:10.1056/nejm199610033351401 · Cited by 7,439
PREVENTION OF CORONARY HEART DISEASE WITH PRAVASTATIN IN MEN WITH HYPERCHOLESTEROLEMIA
Hepherd, J. A. S., Obbe, S. T. M. C., Ord, I. A. F., Sles, C. H. G. I., Orimer, A. R. O. L., Acfarlane, P. E. W. M., Illop, J. A. H. M. C. K., Ackard, C. H. J. P., & Roup, S. T. G. (1995) · Cited by 3,453
Brown, G., Albers, J. J., Fisher, L. D., Schaefer, S. M., Lin, J.-T., Kaplan, C., Zhao, X.-Q., Bisson, B. D., Fitzpatrick, V. F., & Dodge, H. T. (1990) · New England Journal of Medicine · doi:10.1056/nejm199011083231901 · Cited by 2,159
Low-Density Lipoprotein Subclass Patterns and Risk of Myocardial Infarction
Austin, M. A. (1988) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.1988.03410130125037 · Cited by 1,780
Tuomilehto, J., Vidgrén, G., Toivanen, L., Tuomilehto‐Wolf, E., Kohtamäki, K., Stengård, J., Zimmet, P., Mackay, I. R., Rowley, M. J., & Koskela, P. U. (1994) · The Lancet · doi:10.1016/s0140-6736(94)92521-6 · Cited by 1,691
Atherogenic lipoprotein phenotype. A proposed genetic marker for coronary heart disease risk
Austin, M. A., King, M. C., Vranizan, K. M., & Krauss, R. M. (1990) · Circulation · doi:10.1161/01.cir.82.2.495 · Cited by 1,411
The Lipid Research Clinics Coronary Primary Prevention Trial Results
(1984) · JAMA · doi:10.1001/jama.1984.03340270043026 · Cited by 1,404
SERUM CHOLESTEROL, BLOOD PRESSURE, AND MORTALITY: IMPLICATIONS FROM A COHORT OF 361 662 MEN
Martin, M., Browner, W. S., Hulley, S. B., Kuller, L., & Wentworth, D. N. (1986) · The Lancet · doi:10.1016/s0140-6736(86)90597-0 · Cited by 1,117
Research works printed but not linked: 20
- 10.1161/circ.94.10.2351 · DOI
- 10.1161/atv91.12.2.1543692 · DOI
- 10.1161/circ.95.1.69 · DOI
- 10.1161/circ.82.2.2372896 · DOI
- 10.1161/atvb.16.5.697 · DOI
- 10.1161/atv91.13.2.8427851 · DOI
- 10.1161/atv91.14.6.8199180 · DOI
- 10.1161/atvb.15.11.1839 · DOI
- 10.1161/atvb.16.8.1040 · DOI
- Armitage P. Statistical Methods in Medical Research. Oxford UK: Blackwell Scientific Publications; 1971:314.
- 10.1161/circ.82.2.2372896 · DOI
- 10.1161/circ.95.1.1 · DOI
- 10.1161/atv91.11.2.1998647 · DOI
- 10.1161/circ.97.15.1440 · DOI
- 10.1161/circ.97.15.1446 · DOI
- Kinnunen PHJ, Virtanen JA, Vainio P. Lipoprotein lipase and hepatic endothelial lipase: their roles in plasma lipoprotein metabolism. Atheroscler Rev. 1983;11:65–105.
- 10.1161/atvb.17.11.2837 · DOI
- 10.1161/atvb.18.11.1723 · DOI
- Brunzell JD Deeb SS. Lipoprotein lipase apo CII and hepatic lipase deficiency. In: Scriver CR Beudet AL Sly WS Valle D Vogelstein B Childs B eds. The Metabolic and Molecular Basis of Inherited Disease. 8th ed. New York NY: McGraw-Hill. In press.
- 10.1161/circ.87.4.8484829 · DOI
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Superko, H. R. (1999) · Current Atherosclerosis Reports · doi:10.1007/s11883-999-0050-6 · Cited by 9
“Finally, the Familial Atherosclerosis Treatment Study has reported that change in LDL buoyancy was the best predictor of arteriographic change in that investigation [ 30 ].”
MethodRacial differences of lipoprotein subclass distributions in postmenopausal women.
Vora, A. N., Ouyang, P., Bittner, V., Tardif, J., Waters, D. D., & Vaidya, D. M. (2008) · PubMed · Cited by 8
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Bell, D. (2003) · The Endocrinologist · doi:10.1097/01.ten.0000098612.88907.4b · Cited by 8
Hogue, J., Lamarche, B., Gaudet, D., Tremblay, A. J., Després, J., Gagné, C., & Couture, P. (2005) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2005.03.027 · Cited by 6
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Karalis, D. G. (2007) · Preventive Cardiology · doi:10.1111/j.1520-037x.2007.07333.x · Cited by 6
“In a post hoc analysis from the Familial Atherosclerosis Treatment study, 12 the change in LDL size was the most important predictor of atherosclerotic regression, more important than the change in the level of LDL cholesterol itself.”
MethodFamily Coronary Heart Disease: A Call to Action
Superko, H. R., Roberts, R., Garrett, B. C., PENDYALA, L. K., & King, S. B. (2010) · Clinical Cardiology · doi:10.1002/clc.20684 · Cited by 5
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Miller, M. J. (1999) · Current Atherosclerosis Reports · doi:10.1007/s11883-999-0046-2 · Cited by 5
LDL oxidation and LDL particle size in the development of atherosclerosis
Liu, M. (2002) · Työväentutkimus Vuosikirja · Cited by 5
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Sprecher, D. L. (2001) · Current Cardiology Reports · doi:10.1007/s11886-001-0060-7 · Cited by 4
Lee, S., Kadambi, S., Yu, K. C.-W., David, C., Azhar, S., Cooper, A. D., & Choi, S. Y. (2004) · Journal of Lipid Research · doi:10.1194/jlr.m400184-jlr200 · Cited by 4
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Garvey, W. T., Arathuzik, G., Miller, G. D., & Ard, J. D. (2016) · Springer eBooks · doi:10.1007/978-3-319-24687-1_23 · Cited by 2
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Cho, H. K. (2004) · Korean Circulation Journal · doi:10.4070/kcj.2004.34.11.1015 · Cited by 2
Assessing Coronary Heart Disease Risk and Managing Lipids
Braun, L. T., & Rosenson, R. S. (2001) · The Nurse Practitioner · doi:10.1097/00006205-200112000-00005 · Cited by 2
Premature coronary artery disease and apolipoprotein B and apolipoprotein A-I
Ayyobi, A. F., Zambon, A., & Brunzell, J. D. (2007) · International Congress Series · doi:10.1016/j.ics.2007.03.019 · Cited by 2
Self-citationNiu, C., Zhang, F.-H., Li, Y., Liu, J., & Bao, C. (2018) · Annals of Hepatology · doi:10.5604/01.3001.0012.7199 · Cited by 1
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Tsimikas, S. (2006) · Wiley eBooks · doi:10.1002/9780470987575.ch11 · Cited by 2
Prevention of atherosclerosis progression in asymptomatic healthy elderly
Lees, R. S. (2007) · American Journal of Clinical Nutrition · doi:10.1093/ajcn/86.5.1569s · Cited by 2
“Other drugs that lower triacylglycerols almost all decrease the plasma concentration of small, dense LDLs, which are generally thought to be more atherogenic than LDL particles of normal size (11).”
BackgroundPreoperative Triglycerides Predict Post-Coronary Artery Bypass Graft Survival in Diabetic Patients
Sprecher, D. L., Pearce, G. L., Park, E. M., Pashkow, F. J., & Hoogwerf, B. J. (2000) · Cited by 2
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Bossé, Y. (2004) · Corpus Université Laval (Université Laval) · Cited by 2
Sorrentino, M. J. (2011) · Humana Press eBooks · doi:10.1007/978-1-60327-502-6_5 · Cited by 1
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Rizzo, M., TOMKIN, G. H., Angelo, M. P., Pepe, I., Maria, R. V., Rosa, S. D., Giovam, B. R., & Fede, G. D. (2011) · Clinical Lipidology · doi:10.2217/clp.11.46 · Cited by 1
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Rosenson, R. S., de Ferranti, S. D., Freeman, M. W., & Saperia, G. M. (2011) · Cited by 1
Brunzell, J. D. (2009) · Elsevier eBooks · doi:10.1016/b978-141605469-6.50010-x · Cited by 3
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Hurt‐Camejo, E., Sartipy, P., Peilot, H., Rosengren, B. E., Wiklund, O., & Camejo, G. (2003) · Advances in cell aging and gerontology · doi:10.1016/s1566-3124(03)12010-x · Cited by 1
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Winkelmann, B. R., Hoffmann, M. M., & März, W. (2004) · Handbook of experimental pharmacology · doi:10.1007/978-3-662-06214-2_5 · Cited by 1
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Ali, A., Hunt, J. A., & Sinclair, P. J. (2010) · Wiley eBooks · doi:10.1002/0471266949.bmc193 · Cited by 1
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Levine, T. B., & Levine, A. B. (2012) · Wiley eBooks · doi:10.1002/9781118480045.ch13 · Cited by 1
Saucan, L., & Brinton, E. A. (2001) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvb.21.11.1707 · Cited by 1
Transcriptional Regulation of the Human Hepatic Lipase Gene
Sijbrands, E. J. G., Verhoeven, A. J. M., & van Deursen, D. (2005) · Cited by 1
Bamji‐Mirza, M. (2011) · Library and Archives Canada (Government of Canada) · doi:10.20381/ruor-4710
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Pauletto, P., Ferri, C., Volpe, M., Agabiti‐Rosei, E., Muiesan, M. L., Puato, M., Faggin, E., Rattazzi, M., Plebani, M., Zambon, A., et al. (2003) · High Blood Pressure & Cardiovascular Prevention · doi:10.2165/00151642-200310010-00004
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Botma, G. J. (2006) · EUR Research Repository (Erasmus University Rotterdam)
The impact of dialysis therapy on metabolic syndrome traits at the Groote Schuur Hospital
Maree, M. J. (2015) · DUT Open Scholar (Durban University of Technology) · doi:10.51415/10321/1246
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Déniz, J. R. (2010) · Dipòsit Digital de la Universitat de Barcelona (Universitat de Barcelona)
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Berk-Planken, I. I. L. (2003) · RePub (Erasmus University Rotterdam)
Cyclic Relationships Between Diabetic Nephropathy and Cardiovascular Risk Factors
Charles, M., & Selam, J. (2005) · Metabolic Syndrome and Related Disorders · doi:10.1089/met.2005.3.203
Concentraciones de lípidos y lipoproteínas en menopáusicas tratadas con raloxifeno
Alfonzo, R., Reyna, E., Guerra, M., Mejia, J., Reyna, N., Torres, D., Santos, J., & Schloeter, J. (2009) · Clínica e Investigación en Ginecología y Obstetricia · doi:10.1016/j.gine.2009.03.003
Familial combined hyperlipidemia: an oligogenic disorder
Brunzell, J. D. (2010) · Clínica e Investigación en Arteriosclerosis · doi:10.1016/s0214-9168(10)70031-0
Self-citationInfluência do exercício físico nas lipoproteínas e no endotélio de pacientes com síndrome metabólica
Filho, A. C. (2007) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/t.5.2007.tde-10122007-215922
Miljkovic-Gacic, I. (2004) · D-Scholarship@Pitt (University of Pittsburgh)
Cardiovascular Complications of Obesity and the Metabolic Syndrome
Poirier, P., & Eckel, R. H. (2007) · Springer eBooks · doi:10.1007/978-1-84628-715-2_132
Bourg, A. L. (2006) · eCommons (Cornell University)
Hogue, J. (2008) · Corpus Université Laval (Université Laval)
Pang, J. (2012) · UWA Profiles and Research Repository (University of Western Australia)
Hyperlipidemia: Should Primary Care Providers Treat More Than LDL?
Masterman, C. B. (2012) · Research Exchange (Washington State University)
Oh, R. (2008) · New England Journal of Medicine · doi:10.1056/nejmc072844
Genetic variation in lipoprotein lipase and hepatic lipase in diabetes mellitus
Brownrigg, L. (2002) · UWA Profiles and Research Repository (University of Western Australia) · doi:10.26182/5d479e9df2422
Le, N., & Brown, W. V. (2007) · Humana Press eBooks · doi:10.1007/978-1-59259-878-6_28
Clinical Utility of Small, Dense LDL as an Atherogenic Risk Marker
(2022) · Biointerface Research in Applied Chemistry · doi:10.33263/briac132.199
“dense intermediate LDL and large LDL by hepatic lipase [25,26], LDL alteration by cholesterol ester transfer protein (CETP) [27,28], or liver secretion into plasma.”
BackgroundDyslipidemia Associated With Diabetes and Insulin Resistance Syndromes
Dushay, J. R., & Oettgen, J. P. (2006) · Humana Press eBooks · doi:10.1007/978-1-59259-985-1_11
“HL may also play a role in the clearance of HDL particles and in the conversion of IDL into LDL (19, 20 ).”
BackgroundTouati, S. (2010) · doi:10.70675/c9326786z6325z4f26zbae3ze520f1bdc32f
L’athérosclérose est une maladie inflammatoire
Mach, F. (2001) · Cardiovascular Medicine · doi:10.3390/cardiovascmed4030034
Vakkilainen, J. (2002) · Työväentutkimus Vuosikirja
Knopp, R. H., Paramsothy, P., Retzlaff, B. M., Dowdy, A. A., & Fish, B. E. (2005) · Current Atherosclerosis Reports · doi:10.1007/s11883-005-0056-7
Metadata
- Authors
- Zambon, A., Hokanson, J. E., Brown, B. G., & Brunzell, J. D.
- Affiliations
- University of Washington (US)
- Venue
- Circulation
- Published
- 1999-04-20
- Volume
- 99
- Issue
- 15
- Pages
- 1959-1964
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W1999551921
- Cited by
- 263
- References
- 54
- Citations by year
- 2022: 3 · 2021: 1 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 3 · 2015: 5 · 2014: 4 · 2013: 8 · 2012: 6
- FWCI
- 22.45
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Padua Research Archive (University of Padova) (submittedVersion, other-oa)
- Funders
- American Heart Association
- National Institutes of Health (5r01hl019451-14, DK35816, 1r01hl042419-01)
- National Heart, Lung, and Blood Institute (HL-42419, P01HL030086, HL3-0086, HL19451)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Keywords
- hepatic lipase, lipid-lowering therapy, lovastatin, nicotinic acid, colestipol, apolipoprotein B, coronary artery stenosis, lipoprotein lipase
- MeSH terms
- Aged, Anticholesteremic Agents, Hypolipidemic Agents, Apolipoproteins B, Centrifugation, Density Gradient, Chemistry, Physical, Colestipol, Combined Modality Therapy, Coronary Artery Disease, Drug Therapy, Combination, Humans, Lipase, Lipids, Lipolysis, Lipoproteins, Cholesterol, LDL, Liver, Lovastatin, Male, Middle Aged, Niacin, Chemical Phenomena
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