Welcome to my blog which is dedicated to sharing and analyzing cardiology trends and information ranging from the basics, all the way to new, cutting edge discoveries. In this site you will find lectures, journal reviews, guidelines, researches, news ,CMEs and articles. Students and professionals alike are invited. I hope you will enjoy reading and sharing your valuable perspectives too. "Dr.Nabil Paktin , MD.,F.A.C.C."
Saturday, January 16, 2016
Classification of cardiogenic shock according to Inotropic/vasopressor and mechanical circulatory support .(What are Pre-Shock, Mild-shock, profound and severe refractory cardiogenic shock ?)
Tuesday, January 12, 2016
Diabetes mediated vessels toxicity (How high blood sugar can damage the heart's vessels)
High levels of glucose can also damage extracellularly and increase the production of advanced glycosylation end-products (AGEs) in the circulation and on matrix proteins.
The AGEs directly affect cell function, arterial wall stiffness or gene expression of interacting cells. They are ligands for a number of scavenger receptors and the receptor for AGEs (RAGE). As reviewed by Goldberg and Dansky (2006), two lines
of evidence strongly support the theory that AGEs mediate diabetic complications:
-infusions of soluble RAGE, which is presumed to complex AGEs, reduce and stabilise atherosclerotic lesions, and inhibition of AGE formation reduces lesions; and diets enriched in AGEs promote lesions. Beyond AGEs, other mechanisms also link hyperglycaemia to oxidative stress and vascular dysfunction, as well as adverse effects on vascular smooth-muscle cells (Sundell, 2005) (Figure above).
-Finally, hyperglycaemia, at least at the experimental level, has also been shown to induce MMP expression in both endothelial cells and macrophages (Sundell, 2005).
As discussed above, such changes are likely to render the plaque less stable and more susceptible to rupture and hence luminal thrombosis.
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