The DOI matches its Crossref record; 45 of the 45 references it cites were found in a registry or an index.
Hyperlipidemia and Coronary Disease: Correction of the Increased Thrombogenic Potential With Cholesterol Reduction
Abstract
Background Hypercholesterolemia is a risk factor for coronary disease, and platelet reactivity is increased with hypercholesterolemia, suggesting a prethrombotic risk. The aim of this study was to measure mural platelet thrombus formation on an injured arterial wall in a model simulating vessel stenosis and plaque rupture in hypercholesterolemic coronary disease patients before and after cholesterol reduction. Methods and Results Thirty-two patients with stable coronary disease were studied. Platelet thrombus formation and serum lipids were measured in 16 hypercholesterolemic patients (cholesterol >5.2 mmol/L) before and after a mean of 2.5 months of pravastatin therapy (40 mg/d) and in 16 normocholesterolemic control patients. Thrombus formation was assessed by exposing porcine aortic media to the patient’s flowing venous blood for 3 minutes at a shear rate of 754 or 2546 s −1 at 37°C in an ex vivo superfusion chamber. Quantitative morphometric platelet thrombus formation at baseline was higher in the hypercholesterolemic patients at both the high and low shear rates: 4.8±1.0 and 3.3±0.7 μm 2 /mm, respectively, compared with normocholesterolemic patients: 2.1±0.5 and 1.6±0.4 μm 2 /mm (both P <.05). In the hypercholesterolemic patients, pravastatin decreased total cholesterol from 6.5±0.2 to 4.5±0.2 mmol/L and LDL cholesterol from 4.5±0.2 to 2.8±0.1 mmol/L (both P <.05). Platelet thrombus formation at high and low shear rates decreased to 2.0±0.3 and 1.3±0.3 μm 2 /mm, respectively (both P <.05). Conclusions Thus, hypercholesterolemia is associated with an enhanced platelet thrombus formation on an injured artery, increasing the propensity for acute thrombosis. Platelet thrombus formation at both high and low shear rates decreased as total and LDL cholesterol levels were reduced with pravastatin. Cholesterol lowering may therefore reduce the risk of acute coronary events in part by reducing the thrombogenic risk.
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Grundy, S. M., Bilheimer, D. W., Chait, A., Clark, L. T., Denke, M. A., Havel, R. J., Hazzard, W. R., Hulley, S. B., Hunninghake, D. B., Kreisberg, R. A., et al. (1993) · JAMA · doi:10.1001/jama.269.23.3015 · Cited by 27,947
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
The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes
Epstein, F. H., Fuster, V., Badimon, L., Badimon, J. J., & Chesebro, J. H. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201303260506 · Cited by 3,725
The Pathogenesis of Coronary Artery Disease and the Acute Coronary Syndromes
Epstein, F. H., Fuster, V., Badimon, L., Badimon, J. J., & Chesebro, J. H. (1992) · New England Journal of Medicine · doi:10.1056/nejm199201233260406 · Cited by 2,717
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
Can lifestyle changes reverse coronary heart disease?
Ornish, D., Brown, S. E., Billings, J. H., Scherwitz, L. W., Armstrong, W. T., Ports, T. A., McLanahan, S. M., Kirkeeide, R. L., Gould, K. L., & Brand, R. J. (1990) · The Lancet · doi:10.1016/0140-6736(90)91656-u · Cited by 2,110
The pathogenesis of coronary artery disease and the acute coronary syndromes (First of two parts)
Fuster, V. (1992) · New England Journal of Medicine · Cited by 1,954
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
Blankenhorn, D. H. (1987) · JAMA: The Journal of the American Medical Association · doi:10.1001/jama.1987.03390230069027 · Cited by 1,655
Cited by
Schwartz, G. G. (2001) · JAMA · doi:10.1001/jama.285.13.1711 · Cited by 2,499
PLEIOTROPIC EFFECTS OF STATINS
Liao, J. K., & Laufs, U. (2005) · Annual Review of Pharmacology and Toxicology · doi:10.1146/annurev.pharmtox.45.120403.095748 · Cited by 1,994
Ridker, P. M., Rifai, N., Pfeffer, M. A., Sacks, F. M., Moye, L. A., Goldman, S., Flaker, G. C., & Braunwald, E. (1998) · Circulation · doi:10.1161/01.cir.98.9.839 · Cited by 1,389
Platelet CD36 links hyperlipidemia, oxidant stress and a prothrombotic phenotype
Podrez, E. A., Byzova, T. V., Febbraio, M., Salomon, R. G., Ma, Y., Valiyaveettil, M., Poliakov, E., Sun, M., Finton, P. J., Curtis, B. R., et al. (2007) · Nature Medicine · doi:10.1038/nm1626 · Cited by 513
Liao, J. K. (2005) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2005.06.009 · Cited by 304
Metadata
- Authors
- Lacoste, L., Lam, J. Y. T., Hung, J., Letchacovski, G., Solymoss, C. B., & Waters, D.
- Venue
- Circulation
- Published
- 1995-12
- Volume
- 92
- Issue
- 11
- Pages
- 3172-3177
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W1968144530
- Cited by
- 441
- References
- 45
- FWCI
- 22.49
- Type
- journal article
- Language
- en
- Open access
- closed
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- Lacoste, L., Lam, J. Y. T., Hung, J., Letchacovski, G., Solymoss, C. B., & Waters, D. (1995). Hyperlipidemia and Coronary Disease: Correction of the Increased Thrombogenic Potential With Cholesterol Reduction. Circulation. https://doi.org/10.1161/01.cir.92.11.3172
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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