By David Brown
Illustrating the advance and determinants of attainable plaque rupture, Cardiovascular Plaque Rupture offers an in-depth overview of the pathology, etiology, mobile and molecular biology, prognosis, and remedy of plaque within the cardiovascular system-exploring the jobs of actual rigidity, irritation, and infectious brokers at the development of heart problems. symbolize and determine susceptible plaque utilizing novel imaging modalities and transformations of present invasive and noninvasive applied sciences! Containing fresh info on preventive gene remedy and antibiotic stabilization of plaque, >Cardiovascular Plaque Rupture considers ·serine proteinase and metalloproteinase inhibitors within the prevention of plaque rupture ·lipid reducing to stabilize plaque ·clinical trial designs to illustrate healing prevention of plaque rupture ·and extra! Discussing present tools of plaque review, together with intravascular ultrasound and elastography, in vivo spectroscopic research, optical coherence tomography, thermography, and magnetic resonance imaging, Cardiovascular Plaque Rupture is an crucial advisor for cardiologists, vascular and cardiac surgeons, radiologists, vascular biologists, endocrinologists, and fellows, citizens, and scientific institution scholars in those disciplines.
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Extra resources for Cardiovascular Plaque Rupture (Fundamental and Clinical Cardiology, 45)
Both PDGF and FGF can act as chemotactic agents for SMC, and there also appears to be a SMC-derived factor that acts as an autoregulatory agent that mediates SMC migration (218). During migration, SMC do not appear to proliferate, but on arrival in the intima, many of the SMC begin another phase of cell division (202). Thus, there are two stages of proliferation involved in neointimal formation, the initial dedifferentiation of SMC followed by proliferation within the media, and a second proliferative stage after migration into the intima has occurred.
SMC from injured arteries secrete only the PDGF-AA despite expressing the genes for both chains (184). Yet the receptor type that is expressed in these SMC is the βreceptor (185). It is uncertain why these cells would express one ligand and another type of receptor. The answer may be that different isoforms are generated for different functions with different target cells. Injury to the artery also exposes the underlying SMC to circulating platelets, which have been shown to adhere to the injured vessel, as well as being a source of PDGF-BB (186).
VI. DETERMINANTS OF PLAQUE STABILITY Atherosclerosis results in the development of various symptoms, depending on the vascular bed that is affected (9). The most signiﬁcant and potentially lethal manifestations of atherosclerosis are the development of unstable angina, myocardial infarction, or cerebral vascular ischemia, which can result from plaque rupture with thrombus formation (98). Understanding the determinants of plaque stability and factors that can lead to instability and rupture of a plaque is crucial in preventing these complications of atherosclerosis.