The DOI matches its Crossref record; 53 of the 54 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
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
“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]
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
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
Cited by
Sorted by citations
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
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
