The DOI matches its Crossref record; 24 of the 24 references it cites were found in a registry or an index.
Plaque Neovascularization Is Increased in Ruptured Atherosclerotic Lesions of Human Aorta: Implications for Plaque Vulnerability
Open accessAbstract
Background— Growth of atherosclerotic plaques is accompanied by neovascularization from vasa vasorum microvessels extending through the tunica media into the base of the plaque and by lumen-derived microvessels through the fibrous cap. Microvessels are associated with plaque hemorrhage and may play a role in plaque rupture. Accordingly, we tested this hypothesis by investigating whether microvessels in the tunica media, the base of the plaque, and the fibrous cap are increased in ruptured atherosclerotic plaques in human aorta. Methods and Results— Microvessels, defined as CD34-positive tubuloluminal capillaries recognized in cross-sectional and longitudinal profiles, were quantified in 269 advanced human plaques by bicolor immunohistochemistry. Macrophages/T lymphocytes and smooth muscle cells were defined as CD68/CD3-positive and α-actin–positive cells. Total microvessel density was increased in ruptured plaques when compared with nonruptured plaques ( P =0.0001). Furthermore, microvessel density was increased in lesions with severe macrophage infiltration at the fibrous cap ( P =0.0001) and at the shoulders of the plaque ( P =0.0001). In addition, microvessel density was also increased in lesions with intraplaque hemorrhage ( P =0.04) and in thin-cap fibroatheromas ( P =0.038). Logistic regression analysis identified plaque base microvessel density ( P =0.003) as an independent correlate to plaque rupture. Conclusions— Thus, neovascularization as manifested by the localized appearance of microvessels is increased in ruptured plaques in the human aorta. Furthermore, microvessel density is increased in lesions with inflammation, with intraplaque hemorrhage, and in thin-cap fibroatheromas. Microvessels at the base of the plaque are independently correlated with plaque rupture, suggesting a contributory role for neovascularization in the process of plaque rupture.
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Chatzizisis, Y. S., Coskun, A. U., Jonas, M., Edelman, E. R., Feldman, C. L., & Stone, P. H. (2007) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2007.02.059 · Cited by 1,483
Nanotheranostics for personalized medicine
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L-selectin: A Major Regulator of Leukocyte Adhesion, Migration and Signaling
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Role of Angiogenesis in Cardiovascular Disease: A Critical Appraisal
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Metadata
- Authors
- Moreno, P. R., Purushothaman, K. R., Fuster, V., Echeverri, D., Truszczynska, H., Sharma, S. K., Badimon, J. J., & O’Connor, W. N.
- Venue
- Circulation
- Published
- 2004-10-05
- Volume
- 110
- Issue
- 14
- Pages
- 2032-2038
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2002131026
- Cited by
- 630
- References
- 24
- FWCI
- 9.23
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: Plaque Neovascularization Is Increased in Ruptured Atherosclerotic Lesions of Human Aorta: Implications for Plaque Vulnerability. https://app.cochat.ai/papers/10.1161/01.cir.0000143233.87854.23
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- Moreno, P. R., Purushothaman, K. R., Fuster, V., Echeverri, D., Truszczynska, H., Sharma, S. K., Badimon, J. J., & O’Connor, W. N. (2004). Plaque Neovascularization Is Increased in Ruptured Atherosclerotic Lesions of Human Aorta: Implications for Plaque Vulnerability. Circulation. https://doi.org/10.1161/01.cir.0000143233.87854.23
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
