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Regression of Coronary Artery Disease as a Result of Intensive Lipid-Lowering Therapy in Men with High Levels of Apolipoprotein B
Open accessAbstract
BACKGROUND AND METHODS: The effect of intensive lipid-lowering therapy on coronary atherosclerosis among men at high risk for cardiovascular events was assessed by quantitative arteriography. Of 146 men no more than 62 years of age who had apolipoprotein B levels greater than or equal to 125 mg per deciliter, documented coronary artery disease, and a family history of vascular disease, 120 completed the 2 1/2-year double-blind study, which included arteriography at base line and after treatment. Patients were given dietary counseling and were randomly assigned to one of three treatments: lovastatin (20 mg twice a day) and colestipol (10 g three times a day); niacin (1 g four times a day) and colestipol (10 g three times a day); or conventional therapy with placebo (or colestipol if the low-density lipoprotein [LDL] cholesterol level was elevated). RESULTS: The levels of LDL and high-density lipoprotein (HDL) cholesterol changed only slightly in the conventional-therapy group (mean changes, -7 and +5 percent, respectively), but more substantially among patients treated with lovastatin and colestipol (-46 and +15 percent) or niacin and colestipol (-32 and +43 percent). In the conventional-therapy group, 46 percent of the patients had definite lesion progression (and no regression) in at least one of nine proximal coronary segments; regression was the only change in 11 percent. By comparison, progression (as the only change) was less frequent among patients who received lovastatin and colestipol (21 percent) and those who received niacin and colestipol (25 percent), and regression was more frequent (lovastatin and colestipol, 32 percent; niacin and colestipol, 39 percent; P less than 0.005). Multivariate analysis indicated that a reduction in the level of apolipoprotein B (or LDL cholesterol) and in systolic blood pressure, and an increase in HDL cholesterol correlated independently with regression of coronary lesions. Clinical events (death, myocardial infarction, or revascularization for worsening symptoms) occurred in 10 of 52 patients assigned to conventional therapy, as compared with 3 of 46 assigned to receive lovastatin and colestipol and 2 of 48 assigned to receive niacin and colestipol (relative risk of an event during intensive treatment, 0.27; 95 percent confidence interval, 0.10 to 0.77). CONCLUSIONS: In men with coronary artery disease who were at high risk for cardiovascular events, intensive lipid-lowering therapy reduced the frequency of progression of coronary lesions, increased the frequency of regression, and reduced the incidence of cardiovascular events.
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“Several studies have shown that the combination of nicotinic acid and colestipol causes a higher frequency of absolute regression of atherosclerotic lesions than colestipol alone.144”
From ESC/EAS Guidelines for the management of dyslipidaemias (2011) · cites this paper as [144]
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“Moreover, there have been reports on suspected teratogenicity in pregnant patients who incidentally took statins during early pregnancy662); therefore, at present, it appears that statins must not be used in women who are pregnant, possibly pregnant, trying to conceive, or lactating.”
From Japan Atherosclerosis Society (JAS) guidelines for prevention of atherosclerotic cardiovascular diseases 2017 (2018) · cites this paper as [662]
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Cites
The Pathogenesis of Atherosclerosis — An Update
Ross, R. (1986) · New England Journal of Medicine · doi:10.1056/nejm198602203140806 · Cited by 4,885
Helsinki Heart Study: Primary-Prevention Trial with Gemfibrozil in Middle-Aged Men with Dyslipidemia
Frick, M. H., Elo, O., Haapa, K., Heinonen, O. P., Heinsalmi, P., Helo, P., Huttunen, J. K., Kaitaniemi, P., Koskinen, P., Manninen, V., et al. (1987) · New England Journal of Medicine · doi:10.1056/nejm198711123172001 · Cited by 3,881
Compensatory Enlargement of Human Atherosclerotic Coronary Arteries
Glagov, S., Weisenberg, E. S., Zarins, C. K., Stankunavicius, R., & Kolettis, G. (1987) · New England Journal of Medicine · doi:10.1056/nejm198705283162204 · Cited by 3,614
Incidence of Coronary Heart Disease and Lipoprotein Cholesterol Levels
Castelli, W. P. (1986) · JAMA · doi:10.1001/jama.256.20.2835 · Cited by 2,512
Paradoxical Vasoconstriction Induced by Acetylcholine in Atherosclerotic Coronary Arteries
Ludmer, P. L., Selwyn, A. P., Shook, T., Wayne, R. R., Mudge, G. H., Alexander, R. W., & Ganz, P. (1986) · New England Journal of Medicine · doi:10.1056/nejm198610233151702 · Cited by 2,422
Warnick, G. R., Benderson, J., & Albers, J. J. (1982) · Clinical Chemistry · doi:10.1093/clinchem/28.6.1379 · Cited by 2,154
Self-citationBook ReviewAmbulatory Pediatric Care
Steinberg, J. B. (1989) · New England Journal of Medicine · doi:10.1056/nejm198901053200122 · Cited by 2,105
Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin
Canner, P. L., Berge, K. G., Wenger, N. K., Stamler, J., Friedman, L., Prineas, R. J., & Friedewald, W. (1986) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(86)80293-5 · Cited by 1,824
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
Research works printed but not linked: 6
- 10.1001/jama.251.3.351 · DOI · Paper page
- Brown, 1989, Arteriosclerosis, 9, 1–81
- Bruce, 1971, Ann Clin Res, 3, 323
- SAS Institute Inc. SAS user's guide: statistics; version 5 edition. Cary, N.C.: SAS Institute, 1985:607–14.
- Rosner B. Fundamentals of biostatistics. 2nd ed. Boston: Duxbury Press, 1986:326–32.
- Wagner, 1980, Am J Pathol, 100, 633
Cited by
Sorted by citations
The pathogenesis of atherosclerosis: a perspective for the 1990s
Ross, R. (1993) · Nature · doi:10.1038/362801a0 · Cited by 10,618
Grundy, S. M., Cleeman, J. I., Merz, C. N. B., Brewer, H. B., Clark, L. T., Hunninghake, D. B., Pasternak, R. C., Smith, S. C., & Stone, N. J. (2004) · Circulation · doi:10.1161/01.cir.0000133317.49796.0e · Cited by 6,902
Non-invasive detection of endothelial dysfunction in children and adults at risk of atherosclerosis
Celermajer, D. S., Sorensen, K. E., Gooch, V. M., Spiegelhalter, D. J., Miller, O. I., Sullivan, I. D., Lloyd, J. K., & Deanfield, J. E. (1992) · The Lancet · doi:10.1016/0140-6736(92)93147-f · Cited by 4,742
The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes
Epstein, F. H., Fuster, V., Badimón, L., Badimón, L., & Chesebro, J. H. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201303260506 · Cited by 3,792
ESC/EAS Guidelines for the management of dyslipidaemias
Reiner, Ž., Catapano, A. L., De Backer, G., Graham, I., Taskinen, M.-R., Wiklund, O., Agewall, S., Alegria, E., Chapman, M. J., Durrington, P., et al. (2011) · European Heart Journal · doi:10.1093/eurheartj/ehr158 · Cited by 3,549
Metadata
- Authors
- 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.
- Affiliations
- University of Washington (US)
- Venue
- New England Journal of Medicine
- Publisher
- Massachusetts Medical Society
- Published
- 1990-11-08
- Volume
- 323
- Issue
- 19
- Pages
- 1289-1298
- ISSN
- 0028-4793 (ISSN-L)
- 1533-4406
- OpenAlex
- W2324712847
- Cited by
- 2,159
- References
- 53
- Citations by year
- 2026: 2 · 2025: 8 · 2024: 10 · 2023: 9 · 2022: 8 · 2021: 3 · 2020: 10 · 2019: 14 · 2018: 13 · 2017: 17 · 2016: 28 · 2015: 29 · 2014: 29 · 2013: 38 · 2012: 48
- FWCI
- 202.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- New England Journal of Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01hl019451-14)
- National Heart, Lung, and Blood Institute (P01HL030086, R01 HL 19451)
- National Center for Research Resources (RR 37)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Keywords
- coronary artery disease, apolipoprotein B, intensive lipid-lowering therapy, lovastatin, nicotinic acid, colestipol, LDL cholesterol, HDL cholesterol, systolic blood pressure, cardiovascular events, revascularization, myocardial infarction, mortality, nutrition counseling
- MeSH terms
- Adult, Apolipoproteins B, Colestipol, Coronary Disease, Diet, Double-Blind Method, Drug Therapy, Combination, Humans, Cholesterol, HDL, Cholesterol, LDL, Lovastatin, Male, Middle Aged, Niacin, Multivariate Analysis, Coronary Angiography
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