It is generally established that the unstable plaque is the major cause of acute clinical sequelae of atherosclerosis. Unfortunately, terms indicating lesions prone to plaque instability, such as "vulnerable plaque," and the different phenotypes of unstable plaques, such as plaque rupture, plaque fissuring, intraplaque hemorrhage, and erosion, are often used interchangeably. Moreover, the different phenotypes of the unstable plaque are mostly referred to as plaque rupture. In the first part of this review, we will focus on the definition of true plaque rupture and the definitions of other phenotypes of plaque instability, especially on intraplaque hemorrhage, and discuss the phenotypes of available animal models of plaque instability. The second part of this review will address the pathogenesis of plaque rupture from a local and a systemic perspective. Plaque rupture is thought to occur because of changes in the plaque itself or systemic changes in the patient. Interestingly, contributing factors seem to overlap to a great extent and might even be interrelated. Finally, we will propose an integrative view on the pathogenesis of plaque rupture.
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http://dx.doi.org/10.1161/01.ATV.0000097783.01596.E2 | DOI Listing |
Int J Med Sci
January 2025
Department of Cardiology, Jiangbin Hospital of Guangxi Zhuang Autonomous Region, Nanning 530021, Guangxi, People's Republic of China.
Coronary microembolization (CME) is defined as atherosclerotic plaque erosion, spontaneous rupture, or rupture of the plaque while undergoing interventional therapy resulting in the formation of tiny emboli that obstruct the coronary microcirculatory system. For percutaneous coronary intervention, CME is a major complication, with a periprocedural incidence of up to 25%. Recent studies have demonstrated that regulatory cell death (RCD) exerts a profound influence on CME through its modulation of inflammatory responses, oxidative stress, cell death, and angiogenesis.
View Article and Find Full Text PDFFront Med (Lausanne)
December 2024
CENECON, Faculty of Medical Sciences, Universidad de Buenos Aires, and Pontificia Universidad Catolica Argentina, Buenos Aires, Argentina.
Atherosclerosis is the underlying factor in the premature death of millions of humans annually. The cause of death is often a result of the rupture of an atherosclerotic plaque followed by the discharge of the associated molecular debris into the vessel lumen which occludes the artery leading to ischemia of downstream tissue and to morbidity or mortality of the individual. This is most serious when it occurs in the heart (heart attack) or brain (stroke).
View Article and Find Full Text PDFObjective: Aim: To summarise what is known about the inflammatory nature of atherosclerosis to date.
Patients And Methods: Materials and Methods: We conducted the search using Google Scholar and Medline and selected state-of-the-art articles that were consistent with the aim of study.
Conclusion: Conclusions: To date, there is sufficient evidence that atherosclerosis is driven by the inflammatory process.
Curr Atheroscler Rep
December 2024
Department of Medicine, Division of Cardiology, New York University Langone Medical Center, NYU Langone Health System, 550 1st Ave, New York, NY, 10010, USA.
Inflammation has been demonstrated to negatively impact patients in the peri-ACS period. This narrative review outlines the inflammatory response in ACS, highlighting the role of the NLRP3 inflammasome pathway following acute plaque rupture and coronary intervention and its potential as a pharmacologic target. RECENT: nvestigators have leveraged medications targeting the NLRP3 inflammasome currently used for other inflammatory pathologies, including colchicine, tocilizumab and anakinra.
View Article and Find Full Text PDFCureus
November 2024
Biochemistry, Nizam's Institute of Medical Sciences, Hyderabad, IND.
Background Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a key enzyme selectively expressed in unstable, rupture-prone atherosclerotic plaques. Previous research has established a strong link between the gene and the development of coronary artery disease (CAD). While traditional risk factors like cholesterol levels and blood pressure are valuable, there remains a need for more specific biomarkers to identify individuals at heightened risk of atherosclerosis before the onset of clinical symptoms.
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