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Evidence for a New Pathophysiological Mechanism for Coronary Artery Disease Regression: Hepatic Lipase–Mediated Changes in LDL Density
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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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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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Eckel, R. H., Alberti, K., Grundy, S. M., & Zimmet, P. (2010) · The Lancet · doi:10.1016/s0140-6736(09)61794-3 · Cited by 6,317
Eckel, R. H., Grundy, S. M., & Zimmet, P. (2005) · The Lancet · doi:10.1016/s0140-6736(05)66378-7 · Cited by 5,755
Brown, B. G., Zhao, X.-Q., Chait, A., Fisher, L. D., Cheung, M. C., Morse, J. S., Dowdy, A. A., Marino, E. K., Bolson, E. L., Alaupovic, P., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejmoa011090 · Cited by 1,979
Self-citationGarvey, W. T., Mechanick, J. I., Brett, E. M., Garber, A. J., Hurley, D. L., Jastreboff, A. M., Nadolsky, K., Pessah-Pollack, R., & Plodkowski, R. (2016) · Endocrine Practice · doi:10.4158/ep161365.gl · Cited by 1,914
Grundy, S. M. (2010) · Springer eBooks · doi:10.1007/978-1-4419-5839-6_1 · Cited by 1,227
Metabolic origins and clinical significance of LDL heterogeneity
Berneis, K. K., & Krauss, R. M. (2002) · Journal of Lipid Research · doi:10.1194/jlr.r200004-jlr200 · Cited by 896
Evaluation and Treatment of Hypertriglyceridemia: An Endocrine Society Clinical Practice Guideline
Berglund, L., Brunzell, J. D., Goldberg, A. C., Goldberg, I. J., Sacks, F., Murad, M. H., & Stalenhoef, A. F. H. (2012) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-3213 · Cited by 887
“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).”
Self-citationLipids and Lipoproteins in Patients With Type 2 Diabetes
Krauss, R. M. (2004) · Diabetes Care · doi:10.2337/diacare.27.6.1496 · Cited by 764
Lipoprotein Management in Patients With Cardiometabolic Risk
Brunzell, J. D., Davidson, M. H., Furberg, C. D., Goldberg, R. B., Howard, B. V., Stein, J. H., & Witztum, J. L. (2008) · Diabetes Care · doi:10.2337/dc08-9018 · Cited by 716
“Bile-acid resins in combination with a statin or nicotinic acid with a statin selectively decrease small dense LDL particles (59).”
BackgroundSelf-citationLipoprotein Management in Patients With Cardiometabolic Risk
Brunzell, J. D., Davidson, M. H., Furberg, C. D., Goldberg, R. B., Howard, B. V., Stein, J. H., & Witztum, J. L. (2008) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2008.02.034 · Cited by 526
Self-citationCarr, M. C., & Brunzell, J. D. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-0432 · Cited by 493
Self-citationBarter, P. J., Ballantyne, C. M., Carmena, R., Cabezas, M. C., Chapman, M. J., Couture, P., Graaf, J. D., Durrington, P. N., Færgeman, O., Frohlich, J., et al. (2006) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2006.01616.x · Cited by 465
Kamanna, V. S., & Kashyap, M. L. (2008) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2008.02.029 · Cited by 453
Effect of ritonavir on lipids and post-heparin lipase activities in normal subjects
Purnell, J. Q., Zambon, A., Knopp, R. H., Pizzuti, D. J., Achari, R., Leonard, J. M., Locke, C. S., & Brunzell, J. D. (2000) · AIDS · doi:10.1097/00002030-200001070-00006 · Cited by 384
“An increase in LDL particle buoyancy is associated with the regression of coronary artery disease after aggressive lipid-lowering therapy [24].”
BackgroundSelf-citationPathogenesis of atherosclerosis: A multifactorial process.
Singh, R. B., Mengi, S. A., Xu, Y., Arneja, A. S., & Dhalla, N. S. (2002) · PubMed Central · Cited by 382
Beyond Low-Density Lipoprotein Cholesterol
Arsenault, B. J., Rana, J. S., Stroes, E. S. G., Després, J.-P., Shah, P. K., Kastelein, J. J. P., Wareham, N. J., Boekholdt, S. M., & Khaw, K.-T. (2009) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2009.07.057 · Cited by 342
Sniderman, A. D., Scantlebury, T., & Cianflone, K. (2001) · Annals of Internal Medicine · doi:10.7326/0003-4819-135-6-200109180-00014 · Cited by 331
Tsimikas, S., Willerson, J. T., & Ridker, P. M. (2006) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2005.10.066 · Cited by 332
Contois, J. H., McConnell, J. P., Sethi, A. A., Csako, G., Devaraj, S., Hoefner, D. M., & Warnick, G. R. (2009) · Clinical Chemistry · doi:10.1373/clinchem.2008.118356 · Cited by 326
Clinical Utility of Bile Acid Sequestrants in the Treatment of Dyslipidemia: A Scientific Review
Insull, W. (2006) · Southern Medical Journal · doi:10.1097/01.smj.0000208120.73327.db · Cited by 308
“Small, dense LDL particles are emerging as a risk factor for CAD,(63) and colestipol has been shown to reduce LDL particle size, creating more atherogenic particles.(64) Therefore, the effect of colesevelam HCl on LDL particle size was examined.”
BackgroundRisk factors for coronary heart disease: implications of gender
van Lennep, J. R. (2002) · Cardiovascular Research · doi:10.1016/s0008-6363(01)00388-1 · Cited by 302
Rosenson, R. S., Otvos, J. D., & Freedman, D. S. (2002) · The American Journal of Cardiology · doi:10.1016/s0002-9149(02)02427-x · Cited by 293
Nieves, D. J., Cnop, M., Retzlaff, B., Walden, C. E., Brunzell, J. D., Knopp, R. H., & Kahn, S. E. (2003) · Diabetes · doi:10.2337/diabetes.52.1.172 · Cited by 281
“Both increased IAF and insulin resistance have been associated with increased hepatic lipase activity (33,59,60), leading to small dense LDL and decreased HDL2 cholesterol levels (61–64); maneuvers to decrease hepatic lipase correct this dyslipidemia (53,65).”
BackgroundSelf-citationKwiterovich, P. O. (2000) · The American Journal of Cardiology · doi:10.1016/s0002-9149(00)01461-2 · Cited by 270
Vakkilainen, J., Steiner, G. A., Ansquer, J.-C., Aubin, F., Rattier, S., Foucher, C., Hamsten, A., & Taskinen, M. (2003) · Circulation · doi:10.1161/01.cir.0000057982.50167.6e · Cited by 270
Low-density lipoprotein size and cardiovascular risk assessment
Rizzo, M., & Berneis, K. K. (2005) · QJM · doi:10.1093/qjmed/hci154 · Cited by 259
“These studies included the Stanford Coronary Risk Intervention Project, the Familial Atherosclerosis Treatment Study (FATS), the St Thomas’ Atherosclerosis Regression Study (STARS) and the Pravastatin Limitation of Atherosclerosis in the Coronary Arteries (PLAC-I) trial.(34,48,55,185) In all of these studies, therapeu…”
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Rosenson, R. S. (2003) · Atherosclerosis · doi:10.1016/s0021-9150(03)00239-9 · Cited by 264
Chapman, M. J., Assmann, G., Fruchart, J., Shepherd, J., & Sirtori, C. R. (2004) · Current Medical Research and Opinion · doi:10.1185/030079904125004402 · Cited by 257
Low-Density Lipoprotein Size and Cardiovascular Disease: A Reappraisal
Sacks, F. M., & Campos, H. (2003) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2003-030636 · Cited by 241
Freed, M. I., Ratner, R. E., Marcovina, S. M., Kreider, M. S., Biswas, N., Cohen, B. R., & Brunzell, J. D. (2002) · The American Journal of Cardiology · doi:10.1016/s0002-9149(02)02659-0 · Cited by 238
Self-citationHigh-Density Lipoprotein and Coronary Heart Disease
Natarajan, P., Ray, K. K., & Cannon, C. P. (2010) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2010.01.008 · Cited by 231
Nonalcoholic fatty liver disease and serum lipoproteins: The Multi-Ethnic Study of Atherosclerosis
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New Perspectives on the Use of Niacin in the Treatment of Lipid Disorders
McKenney, J. M. (2004) · Archives of Internal Medicine · doi:10.1001/archinte.164.7.697 · Cited by 217
“In the Familial AtherosclerosisTreatmentStudy(FATS), change in the size and buoyancy of LDL particles was the single most important factor associated with regression of coronary stenosis.(23)”
BackgroundKwiterovich, P. O. (2002) · The American Journal of Cardiology · doi:10.1016/s0002-9149(02)02749-2 · Cited by 208
Apolipoproteins: metabolic role and clinical biochemistry applications
Dominiczak, M. H., & Caslake, M. J. (2011) · Annals of Clinical Biochemistry: International Journal of Laboratory Medicine · doi:10.1258/acb.2011.011111 · Cited by 238
Hepatic lipase and dyslipidemia: interactions among genetic variants, obesity, gender and diet.
Deeb, S. S., Zambon, A., Carr, M. C., Ayyobi, A. F., & Brunzell, J. D. (2003) · Journal of Lipid Research · doi:10.1194/jlr.r200017-jlr200 · Cited by 193
Self-citationMikhailidis, D. P., Elisaf, M., Rizzo, M., Berneis, K. K., Griffin, B. A., Zambon, A., Athyros, V. G., Graaf, J. D., März, W., Parhofer, K. G., et al. (2011) · Current Vascular Pharmacology · doi:10.2174/157016111796642661 · Cited by 199
Self-citationLow-density lipoprotein particle number and risk for cardiovascular disease
Cromwell, W. C., & Otvos, J. D. (2004) · Current Atherosclerosis Reports · doi:10.1007/s11883-004-0050-5 · Cited by 198
“In three of six clinical intervention trials reviewed [ 38 ,40,41], on-trial LDL size achieved by lifestyle, statin, or fibrate therapy was predictive of CHD risk.”
BackgroundRegulation of reverse cholesterol transport and clinical implications
Rader, D. J. (2003) · The American Journal of Cardiology · doi:10.1016/s0002-9149(03)00615-5 · Cited by 191
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Ganji, S. H., Kamanna, V. S., & Kashyap, M. L. (2003) · The Journal of Nutritional Biochemistry · doi:10.1016/s0955-2863(02)00284-x · Cited by 190
Fibrates in 2003: therapeutic action in atherogenic dyslipidaemia and future perspectives
Chapman, M. J. (2003) · Atherosclerosis · doi:10.1016/s0021-9150(03)00156-4 · Cited by 181
Visceral obesity and the heart
Mathieu, P., Pîbarot, P., Larose, É., Poirier, P., Marette, A., & Després, J. (2008) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2007.12.001 · Cited by 173
Dyslipidemia in the metabolic syndrome and type 2 diabetes mellitus.
Brunzell, J. D., & Ayyobi, A. F. (2003) · The American Journal of Medicine · doi:10.1016/j.amjmed.2003.08.011 · Cited by 155
Self-citationApolipoprotein Concentrations During Treatment and Recurrent Coronary Artery Disease Events
van Lennep, J. E. R., Westerveld, H. T., van Lennep, H. W. O. R., Zwinderman, A. H., Erkelens, D. W., & van der Wall, E. E. (2000) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.20.11.2408 · Cited by 152
Mechanism of action of niacin on lipoprotein metabolism
Kamanna, V. S., & Kashyap, M. L. (2000) · Current Atherosclerosis Reports · doi:10.1007/s11883-000-0093-1 · Cited by 151
Knopp, R. H., Paramsothy, P., Retzlaff, B. M., Fish, B., Walden, C., Dowdy, A., Tsunehara, C., Aikawa, K., & Cheung, M. C. (2005) · Current Atherosclerosis Reports · doi:10.1007/s11883-005-0065-6 · Cited by 148
“Hepatic lipase activity is a key determinant of coronary artery disease progression during drug treatment and highly inversely correlated with HDL as well as LDL buoyancy [ 14 ].”
BackgroundBeyond Low-Density Lipoprotein Cholesterol
Mudd, J. O., Borlaug, B. A., Johnston, P. V., Kral, B. G., Rouf, R., Blumenthal, R. S., & Kwiterovich, P. O. (2007) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2007.07.045 · Cited by 136
Jansen, H., Verhoeven, A. J. M., & Sijbrands, E. J. G. (2002) · Journal of Lipid Research · doi:10.1194/jlr.r200008-jlr200 · Cited by 133
“Zambon and coworkers (19) showed in hypertriglyceridemic males with”
BackgroundAndersen, R. V., Wittrup, H. H., Tybjærg‐Hansen, A., Steffensen, R., Schnohr, P., & Nordestgaard, B. G. (2003) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(03)00407-8 · Cited by 127
“(21) demonstrated that a decrease in hepatic lipase activity is associated with regression of coronary artery disease.”
BackgroundSakai, T., Kamanna, V. S., & Kashyap, M. L. (2001) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/hq1001.096624 · Cited by 122
Smallest LDL Particles Are Most Strongly Related to Coronary Disease Progression in Men
Holl, L. G., Krauss, R. M., Williams, P. T., Superko, H. R., Haskell, W. L., Alderman, E. L., Patricia, J., & Blanche, P. J. (2015) · Cited by 122
Koba, S., Hirano, T., Ito, Y., Tsunoda, F., Yokota, Y., Ban, Y., Iso, Y., Suzuki, H., & Katagiri, T. (2006) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2005.12.002 · Cited by 121
Carr, M. C., Hokanson, J. E., Zambon, A., Deeb, S. S., Barrett, P. H. R., Purnell, J. Q., & Brunzell, J. D. (2001) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem.86.6.7586 · Cited by 120
“lowering (53), whereas those with large, buoyant LDL at”
BackgroundSelf-citationHigh-density lipoproteins and atherosclerosis
Rader, D. J. (2002) · The American Journal of Cardiology · doi:10.1016/s0002-9149(02)02635-8 · Cited by 116
Gender and racial differences in lipoprotein subclass distributions: the STRRIDE study
Johnson, J. L., Slentz, C. A., Duscha, B. D., Samsa, G. P., McCartney, J. S., Houmard, J. A., & Kraus, W. E. (2004) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2004.05.018 · Cited by 114
Zambon, A., Deeb, S. S., Brown, B. G., Hokanson, J. E., & Brunzell, J. D. (2001) · Circulation · doi:10.1161/01.cir.103.6.792 · Cited by 114
Self-citationExercise as a Polypill for Chronic Diseases
Pareja-Galeano, H., Garatachea, N., & Lucía, A. (2015) · Progress in molecular biology and translational science · doi:10.1016/bs.pmbts.2015.07.019 · Cited by 117
Effects of extended-release niacin on lipoprotein subclass distribution
Morgan, J. M., Capuzzi, D. M., Baksh, R. I., INTENZO, C. M., Carey, C. M., Reese, D., & Walker, K. (2003) · The American Journal of Cardiology · doi:10.1016/s0002-9149(03)00394-1 · Cited by 111
Metabolic abnormalities: triglyceride and low-density lipoprotein
Krauss, R. M., & Siri, P. W. (2004) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2004.03.016 · Cited by 102
“More recently, in the Familial Atherosclerosis Treatment Study of cholestyramine with or without statin or niacin therapy, increased LDL flotation rate (an index of increased size and reduced density) was the best predictor of reduced coronary artery stenosis [51] independent of other lipid and nonlipid risk factors.”
BackgroundHepatic lipase: a marker for cardiovascular disease risk and response to therapy
Zambon, A., Deeb, S. S., Pauletto, P., Crepaldi, G., & Brunzell, J. D. (2003) · Current Opinion in Lipidology · doi:10.1097/00041433-200304000-00010 · Cited by 103
Self-citationChanges in LDL Density across the Menopausal Transition
Carr, M. C., Kim, K. H., Zambon, A., Mitchell, E. S., Woods, N. F., Casazza, C. P., Purnell, J. Q., Hokanson, J. E., Brunzell, J. D., & Schwartz, R. S. (2000) · Journal of Investigative Medicine · doi:10.1177/108155890004800405 · Cited by 100
Self-citationD IETARY AND G ENETIC E FFECTS ON L OW -D ENSITY L IPOPROTEIN H ETEROGENEITY
Krauss, R. M. (2001) · Annual Review of Nutrition · doi:10.1146/annurev.nutr.21.1.283 · Cited by 99
Stein, J. H., Merwood, M. A., Bellehumeur, J. L., Aeschlimann, S. E., Korcarz, C. E., Underbakke, G. L., Mays, M. E., & Sosman, J. M. (2004) · American Heart Journal · doi:10.1016/j.ahj.2003.10.018 · Cited by 98
Recent advances in niacin and lipid metabolism
Kamanna, V. S., Ganji, S. H., & Kashyap, M. L. (2013) · Current Opinion in Lipidology · doi:10.1097/mol.0b013e3283613a68 · Cited by 97
Ayyobi, A. F., & Brunzell, J. D. (2003) · The American Journal of Cardiology · doi:10.1016/s0002-9149(03)00613-1 · Cited by 96
Self-citationThe C-514T polymorphism in the human hepatic lipase gene promoter diminishes its activity
Deeb, S. S., & Peng, R. (2000) · Journal of Lipid Research · doi:10.1016/s0022-2275(20)32086-1 · Cited by 95
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Superko, H. R., & Gadesam, R. (2008) · Current Atherosclerosis Reports · doi:10.1007/s11883-008-0059-2 · Cited by 91
“Zambon et al. [ 9 ] / 1999 Patients from FAT S trial”
BackgroundPhospholipase A2 and small, dense low-density lipoprotein
Hurt‐Camejo, E., Camejo, G., & Sartipy, P. (2000) · Current Opinion in Lipidology · doi:10.1097/00041433-200010000-00004 · Cited by 90
Metabolic syndrome: nature, therapeutic solutions and options
Onat, A. (2011) · Expert Opinion on Pharmacotherapy · doi:10.1517/14656566.2011.585462 · Cited by 86
“Nicotinic acid combined with a statin selectively decreases small, dense LDL particles [86].”
BackgroundReverse cholesterol transport: High-density lipoprotein’s magnificent mile
Toth, P. P. (2003) · Current Atherosclerosis Reports · doi:10.1007/s11883-003-0010-5 · Cited by 87
“As demonstrated in the Familial Atherosclerosis Treatment Study, the inhibition of HL with antilipidemic medications in patients with CAD and hypertriglyceridemia can stimulate coronary artery plaque regression [ 46 ].”
Bozovich, M., Rubino, C. M., & Edmunds, J. (2000) · Pharmacotherapy The Journal of Human Pharmacology and Drug Therapy · doi:10.1592/phco.20.17.1375.34895 · Cited by 86
Should we measure routinely the LDL peak particle size?
Rizzo, M., & Berneis, K. K. (2005) · International Journal of Cardiology · doi:10.1016/j.ijcard.2005.02.035 · Cited by 86
Norata, G. D., Raselli, S., Grigore, L., Garlaschelli, K., Vianello, D., Bertocco, S., Zambon, A., & Catapano, A. L. (2009) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2009.03.017 · Cited by 84
Self-citationFunctional variants in the lipoprotein lipase gene and risk of cardiovascular disease
Hokanson, J. E. (1999) · Current Opinion in Lipidology · doi:10.1097/00041433-199910000-00003 · Cited by 82
Self-citationAntiatherothrombotic effects of nicotinic acid
Rosenson, R. S. (2003) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2003.07.003 · Cited by 80
Battisti, W. P., Palmisano, J. J., & Keane, W. F. (2003) · Clinical Chemistry and Laboratory Medicine (CCLM) · doi:10.1515/cclm.2003.181 · Cited by 78
Statins moderate coronary stenoses but not coronary calcification: Results from meta-analyses
Henein, M. Y., & Owen, A. (2010) · International Journal of Cardiology · doi:10.1016/j.ijcard.2010.08.031 · Cited by 78
Who needs to care about small, dense low-density lipoproteins?
Rizzo, M., & Berneis, K. K. (2007) · International Journal of Clinical Practice · doi:10.1111/j.1742-1241.2007.01596.x · Cited by 77
Oxidative Stress: Dual Pathway Induction in Cardiorenal Syndrome Type 1 Pathogenesis
Virzì, G. M., Clementi, A., de Cal, M., Brocca, A., Day, S., Pastori, S., Bolin, C., Vescovo, G., & Ronco, C. (2015) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2015/391790 · Cited by 78
“Both in vitro and animal studies have demonstrated that several pathways are dysregulated in heart failure, leading to increased oxidative stress markers production and cardiac damage.”
BackgroundRole of extracellular retention of low density lipoproteins in atherosclerosis
Borén, J., Gustafsson, M. V., Skålén, K., Flood, C., & Innerarity, T. L. (2000) · Current Opinion in Lipidology · doi:10.1097/00041433-200010000-00002 · Cited by 75
Antioxidant Vitamins and Lipid Therapy
Brown, B. G., Cheung, M. C., Lee, A. C., Zhao, X.-Q., & Chait, A. (2002) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.0000034706.24149.95 · Cited by 75
Self-citationKoba, S., Hirano, T., Kondo, T., Shibata, M., Suzuki, H., Murakami, M., Geshi, E., & Katagiri, T. (2002) · American Heart Journal · doi:10.1067/mhj.2002.126119 · Cited by 73
Pihlajamäki, J., Karjalainen, L., Karhapää, P., Vauhkonen, I., Taskinen, M., Deeb, S. S., & Laakso, M. (2000) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.20.7.1789 · Cited by 71
Effect of Weight Loss with Reduction of Intra-Abdominal Fat on Lipid Metabolism in Older Men
Purnell, J. Q. (2000) · Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.85.3.977 · Cited by 161
“... of an increase in LDL particle size and a decrease in HL activity with weight loss is illustrated by prospective studies demonstrating that a smaller LDL size predicts future risk of cardiac events (47‐ 49) and that reduction of LDL density (or change to larger, more buoyant particles) and HL activity with lipid-l…”
MethodSelf-citationThe Clinical Relevance of Low-Density-Lipoproteins Size Modulation by Statins
Rizzo, M., & Berneis, K. K. (2006) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-006-8283-x · Cited by 71
“In addition, at multivariate analyses with adjustments for confounding factors, changes in LDL size by drug therapy were the best correlates of changes in coronary stenosis in FATS [91].”
MethodBerneis, K. K., Rizzo, M., Berthold, H. K., Spinas, G. A., Krone, W., & Gouni‐Berthold, I. (2010) · European Heart Journal · doi:10.1093/eurheartj/ehq181 · Cited by 69
Nicotinic Acid (Niacin) Receptor Agonists: Will They Be Useful Therapeutic Agents?
Kamanna, V. S., & Kashyap, M. L. (2007) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2007.09.080 · Cited by 69
Koba, S., Hirano, T., Yoshino, G., Sakai, K., Sakaue, T., Adachi, M., & Katagiri, T. (2002) · Atherosclerosis · doi:10.1016/s0021-9150(01)00580-9 · Cited by 69
Metabolic Syndrome and Cardiometabolic Risk Factors
Papakonstantinou, E., Lambadiari, V., Dimitriadis, G., & Zampelas, A. (2014) · Current Vascular Pharmacology · doi:10.2174/15701611113116660176 · Cited by 67
Eckel, R. H. (2007) · Proceedings of The Nutrition Society · doi:10.1017/s0029665107005320 · Cited by 69
“However, the direct relationship between small dense LDL and the natural history of atherosclerotic CVD is not entirely accepted (Lada & Rudel, 2004; Jungner et al. 2006).”
BackgroundInfluentialThe Therapeutic Role of Niacin in Dyslipidemia Management
Boden, W. E., Sidhu, M. S., & Toth, P. P. (2013) · Journal of Cardiovascular Pharmacology and Therapeutics · doi:10.1177/1074248413514481 · Cited by 69
Knopp, R. H., Paramsothy, P., Retzlaff, B. M., Fish, B. E., Walden, C. E., Dowdy, A. A., Tsunehara, C. H., Aikawa, K., & Cheung, M. C. (2006) · Current Cardiology Reports · doi:10.1007/s11886-006-0104-0 · Cited by 67
Tokuno, A., Hirano, T., Hayashi, T., Mori, Y., Yamamoto, T., Nagashima, M., Shiraishi, Y., Ito, Y., & Adachi, M. (2007) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.14.128 · Cited by 65
Bays, H. E., McGovern, M. E., & Kopin, L. (2003) · Preventive Cardiology · doi:10.1111/j.1520-037x.2003.03142.x · Cited by 64
Superko, H., & Garrett, B. (2022) · Biomedicines · doi:10.3390/biomedicines10040829 · Cited by 60
“These studies included the Stanford Coronary Risk Intervention Project (SCRIP), the Familial Atherosclerosis Treatment Study (FATS), the St. Thomas’ Atherosclerosis Regression Study (STARS), and the PLAC-I trial [31,55–57].”
MethodKang, H.-S., Gutin, B., Barbeau, P., Litaker, M., Allison, J., & Le, N. (2002) · International Journal of Obesity · doi:10.1038/sj.ijo.0802045 · Cited by 61
Xu, R., Li, S., Li, X., Zhang, Y., Guo, Y., Zhu, C., Wu, N., Qing, P., Sun, J., Dong, Q., et al. (2014) · Journal of clinical lipidology · doi:10.1016/j.jacl.2014.11.003 · Cited by 60
Brunzell, J. D., Zambon, A., & Deeb, S. S. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids · doi:10.1016/j.bbalip.2011.09.008 · Cited by 61
“In subjects with dense LDL particles [FCHL & Lp(a)] high HL activity was associated with coronary stenosis, and the decrease in HL activity caused an increase in the buoyancy of the dense LDL particles to those of bigger size, and predicted the regression or lack of progression of coronary stenosis [14] (Figures 5 and…”
BackgroundMethodInfluentialSelf-citationOlsson, B., Bohlooly‐Y, M., Brusehed, O., Isaksson, O. G. P., Åhrén, B., Olofsson, S., Oscarsson, J., & Törnell, J. (2003) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00444.2002 · Cited by 57
“Other factors associated with atherosclerosis and cardiovascular disease that connect chronic elevation of GH with the development of the diseases are the reduced gene expression of hepatic lipase (37, 71) and serum paraoxonase (25, 53) and the increased gene expression of serum amyloid A-3 protein (61).”
BackgroundVan, J. T., Pan, J., Wasty, T., Chan, E., Wu, X., & Charles, M. A. (2002) · The American Journal of Cardiology · doi:10.1016/s0002-9149(02)02333-0 · Cited by 55
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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