Download Inflammation and Cardiac Diseases by Giora Z. Feuerstein, Peter Libby, Douglas L. Mann PDF

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By Giora Z. Feuerstein, Peter Libby, Douglas L. Mann

Heart failure learn is a such a lot lively zone of analysis in educational, commercial and government-sponsored learn and gets extreme scientific consciousness. the hot reputation that irritation is a threat issue and prognostic issue for middle sickness has laid flooring for preventive drugs or even anti-infective suggestions in prevention and remedy of middle failure.

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JAMA 278: 1169-1175 Labarrere CA, Nelson DR, Miller SJ et al. (2000) Value of serum soluble intercellular adhesion molecule-l for the non-invasive risk assessment of transplant coronary artery disease, post-transplant coronary events and cardiac graft failure. Circulation 102: 1549-1555 Malik I, Danesh J, Whincup P, Bhatia V, Papacosta 0, Walker M, Lennon L, Thomson A (2001) Soluble adhesion molecule and prediction of coronary heart disease: a prospective study and meta-analysis. Lancet 358: 971-975 Ridker PM, Hennekens CH, Roitman-Johnson B, Stampfer MJ, Allen J (1998) Plasma concentration of soluble intercellular adhesion molecule 1 and risks of future myocardial infarction in apparently healthy men.

Taken together, these murine studies suggest a pivotal role for TGF-~ in the maintenance and balance between inflammation and fibrosis in atherosclerotic plaques. Clinical studies have shown decreased circulating plasma levels of TGF-~ in unstable angina patients. Interleukin-10 Interleukin-lO is considered a potent anti-inflammatory cytokine produced by Th2type T-cells, B-cells, monocytes, and macrophages [39]. Various mechanisms have 28 Inflammation and coronary artery disease been proposed for the manner in which IL-10 inhibits the synthesis of pro-inflammatory cytokines.

Potential mechanism(s) of fibrous cap rupture, as already discussed, focus around apoptotic cell death and the liberation of specific MMPs by inflammatory cells. Another suggested mechanism is high shear stress, which may also influence the composition and configuration of the fibrous cap [104]. It is well established that lumen 38 Inflammation and coronary artery disease area is conserved in the early phases of plaque progression, through mechanisms involving compensatory enlargement of the vessel [105].

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