Cited by 263Lipoproteins and Cardiovascular HealthLipid metabolism and disordersCholesterol and Lipid Metabolism

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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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Zambon, Alberto, Hokanson, John E., Brown, B. Greg, Brunzell, John D.·1999·Circulation

DOI 10.1161/01.cir.99.15.1959

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Abstract

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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Effects of Atorvastatin and Simvastatin on Low-Density Lipoprotein Subtraction Profile, Low-Density Lipoprotein Oxidizability, and Antibodies to Oxidized Low-Density Lipoprotein in Relation to Carotid Intima Media Thickness in Familial Hypercholesterolemia
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Authors: Zambon, A., Hokanson, J. E., Brown, B. G., & Brunzell, J. D.
Affiliations: University of Washington (US)
ORCID: Zambon, Alberto
Hokanson, John E.
Brunzell, John D.
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 1999-04-20
Volume: 99
Issue: 15
Pages: 1959-1964
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/01.cir.99.15.1959
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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Evidence for a New Pathophysiological Mechanism for Coronary Artery Disease Regression: Hepatic Lipase–Mediated Changes in LDL Density

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