By Ron Waksman, Patrick W. Serruys, Johannes Schaar
Due to the fact that book of the 1st variation, advances within the analysis and prevention and remedy suggestions of the susceptible plaque have necessitated this significantly elevated moment variation. With a number of new chapters protecting ordinarily diagnostic and healing procedures, The guide of the susceptible Plaque will stay the benchmark textual content for all interventional cardiologists treating susceptible sufferers by way of delivering the health care professional with accomplished perception into the area of the susceptible plaque.
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Extra info for Handbook of the vulnerable plaque
Schonbeck U, Sukhova GK, Shimizu K, Mach F, Libby P. Inhibition of CD40 signaling limits evolution of established atherosclerosis in mice. Proc Natl Acad Sci USA 2000; 97:7458–63. 58. Andre P, Prasad KS, Denis CV et al. CD40L stabilizes arterial thrombi by a beta3 integrin-dependent mechanism. Nat Med 2002; 8:247–52. 59. Henn V, Slupsky JR, Grafe M et al. CD40 ligand on activated platelets triggers an inflammatory reaction of endothelial cells. Nature 1998; 391:591–4. 60. Lindmark E,Tenno T, Siegbahn A.
The underlying plaque in 50% of cases shows layering of the fibrin with interspersed smooth muscle cells and proteoglycans. 31 Calcified nodule The third type of lesion is an infrequent cause of thrombosis in patients dying a sudden coronary death and its incidence in stable or unstable angina and acute myocardial infarction is unknown. The term refers to a lesion with fibrous cap disruption, absence of endothelium and thrombus associated with eruptive, dense calcified nodule with bone formation.
In contrast, unstable angina, non-ST-elevation and ST-elevation myocardial infarction represent a continuum and are usually characterized by an abrupt cessation in coronary blood flow. In unstable angina, plaque disruption may lead to acute changes in plaque morphology and reduction in coronary blood flow. In addition to plaque disruption other mechanisms also contribute to reduce coronary blood flow. Platelets attach to the damaged endothelium and exposed media and release vasoactive substances including TXA2 and serotonin leading to further platelet aggregation and vasoconstriction.