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All effective approaches to Atherosclerotic Vascular Disease and Heart Failure involve Immune Modulation. 
Our Three DVD Presentation covers the fundamentals of this concept and discusses treatment options. 
 Case studies are presented with pre and post-treatment cardiac echo images.

Immune Mechanisms of Atherosclerosis and Heart Failure

Atherosclerosis is a maladaptive response of the immune system to what it perceives as infection of the artery wall with oxidized LDL.  Useful therapies must limit the amount of oxidized LDL within the vessel wall, quiet down this inappropriate immune response,  or carry out both actions.  Likewise, heart failure always involves maladaptive immune attack against altered and now "non-self" heart proteins.  Modulating this response will reduce symptoms and improve outcome in all patients with heart failure.

Development and Progression of Atherosclerosis - Early in life, LDL particles at high concentration focally infiltrate the artery wall at sites of intimal activation.  Inflammatory phospholipase enzymes modify the LDL phospholipids, causing the LDL particles to clump together.  This now trapped LDL can be oxidized by free radicals, reactive species generated via normal metabolism of the artery wall.  The now oxidized LDL no longer appears as "food".  It no longer fits the LDL receptor on our cell membranes; rather it now fits the "scavenger" microbe receptors on vascular wall macrophages (first line immune defense cells).  The macrophages internalize the oxidized LDL (oxLDL), attempt to degrade it, but die in the process.  We now have lipid laden dead macrophages, termed foam cells, within the artery wall.  This is the fatty streak, the initial and reversible stage of atherosclerosis, which is now appearing during childhood in our society.  In the process of dying, the macrophages release distress signals, calling in additional immune support.  Chemokines such as MCP-1 (Macrophage Chemotactic Factor) attract circulating immune defense cells (monocytes) towards this region of "early infection".  The endothelial cells lining the vessel wall elaborate adhesion molecules (ICAM, VCAM) which anchor the attracted monocytes to the vessel wall over this region of immune distress.  The "called in" monocytes infiltrate the artery wall, recognize the oxLDL as a microbe, and now, in full force internalize it and degrade it into tiny protein snippets 12-20 amino acids in length.  These snippets are presented to roving Th1 T Helper Cells.  - To be continued 4/15/11