PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 11520480

Going from immutable to mutable atherosclerotic plaques.

M J Davies
View original source ↗Export metadata ↓

Abstract

Atherosclerotic coronary disease develops over several decades and was once thought to be an inevitable, irreversible consequence of aging. Atherogenesis is an inflammatory response that occurs after injury to the endothelium. Thrombosis, because of either endothelial erosion or plaque disruption, precipitates acute coronary events. Effective lipid lowering with statins has consistently and significantly decreased the risk that acute ischemic events will occur. The beneficial effects of statins likely result not only from their lipid-lowering effects but also from mechanisms that influence plaque behavior. Atherosclerotic plaques are not immutable; rather, their structure and composition can be altered by therapeutic modification. Ample evidence from clinical trials supports statin treatment in patients with stable coronary disease. Results of recent clinical trials support early treatment of high-risk patients with unstable coronary disease; early and aggressive statin treatment resulted in fewer recurrent ischemic events in patients with an acute coronary syndrome. Additional studies are needed to confirm the benefit of early statin treatment in patients with unstable coronary disease and to elucidate the reasons for the occurrence of events in treated patients. Research is also necessary to clarify the role of other lipids, as well as nonlipid risk factors, in the occurrence of acute ischemic events.

Explore related subjects

Coronary Artery DiseaseCoronary ThrombosisCoronary VesselsHumansHypolipidemic AgentsMyocardial IschemiaRisk FactorsJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M J Davies. 2001-08-16. Going from immutable to mutable atherosclerotic plaques.. https://doi.org/10.1016/s0002-9149(01)01870-7

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Investigating the mechanisms linking vitamin D to coronary artery disease: A mediating proteomics Mendelian randomisation study.

Coronary artery disease (CAD) is a leading cause of mortality and morbidity globally, with its elevated rates of disability and death posing a significant public health concern. Vitamin D is a crucial bioactive compound involved in numerous physiological processes and has garnered considerable interest due to its potential health benefits. The association between vitamin D and CAD has been a prominent focus of scholarly investigation. However, there remains considerable debate regarding whether vitamin D confers protective effects against CAD, and the underlying mechanisms by which vitamin D influences CAD remain inadequately understood. Mendelian randomization analysis was performed using large-scale genome-wide association study data to examine the causal relationship between serum 25-hydroxyvitamin D (25(OH)D) levels and CAD. Plasma proteomics data were subsequently employed for mediation analysis, followed by enrichment analysis to identify intermediary metabolic or signaling pathways through which serum 25(OH)D may mediate the onset and progression of CAD. The Mendelian randomization analysis indicated that higher serum 25(OH)D levels were associated with a reduced risk of CAD (odds ratio [95% confidence interval]: 0.799 [0.643-0.993], P = .043). No evidence of pleiotropy (P = .949) or heterogeneity (P = .630) was observed in the results. The protein-mediated analysis identified 19 plasma proteins, including Serine/threonine-protein kinase TBK1, membrane associating domain domain-containing protein 2, and interleukin-17D, as key mediators through which reduced vitamin D levels contribute to the development of CAD. The mediation effects ranged from 4.85 to 34.49%. Following the identification of these 19 mediating proteins, 59 intermediary pathways were further pinpointed through which serum vitamin D influences CAD risk. Increased levels of 25(OH)D may reduce the risk of CAD. Further, plasma proteomics-mediated analyses have uncovered potential mechanisms through which 25(OH)D influences the development of CAD, offering a detailed framework for understanding the relationship between vitamin D deficiency and CAD progression. This provides novel evidence to support the recommendation of appropriate vitamin D supplementation as part of lifestyle guidance for CAD patients.

Coronary Artery Disease↗
PubMed2007

From here to eternity: a unified kinetic model for the pathophysiology of atherosclerotic events.

Two operative pathophysiological models underlie the clinical management of ischemic heart disease: a physical model founded on the magnitude of vascular stenosis and a biochemical model founded on the inflammatory processes within the atherosclerotic plaque. Despite their complementary natures, these 2 models are implicitly competitive--the stenotic model supporting the primacy of aggressive interventional procedures and the inflammatory model supporting the primacy of conservative medical management. We unified these alternative perspectives through a kinetic model that characterizes the pathophysiology of cardiovascular events as a network of exponential transitions between the inflammatory and stenotic states. According to this model, the prevalence of the normative (nonstenotic and noninflammatory) state falls exponentially, while the prevalences of the inflammatory and stenotic states rise to a peak and then fall off exponentially. According to this model, event rate increases as a complex function of both myocardial ischemia and vascular inflammation. Although the model has yet to be prospectively validated, it provides a theoretical foundation for predicting the degree to which atherosclerotic events are due to inflammation versus stenosis and the degree to which they can thereby be prevented by treatment strategies directed at plaque stabilization or relief of ischemia.

Coronary Artery Disease↗