into macrophages which will ingest the oxidized lipoprotein particles. The macrophages sometimes become so overloaded with oxidized lipoprotein particles, the cholesterol contained therein and membrane-laden that they are called foam cells. Some of these cells die in place, releasing their fat and cholesterol-laden membranes into the intercellular space. This attracts more macrophages and smooth muscle cell migration and proliferation. Smooth muscle cells migrate from the media to the intima, proliferate, and develop an extracellular matrix made up of collagen and proteoglycans. In some regions of increased macrophage activity, macrophage-induced-enzymes erode away the fibrous membrane beneath the endothelium so that the cover separating the plaque from blood flow in the lumen becomes thin and fragile. Mechanical stretching and contraction of the artery, with each heart beat, i.e. the pulse, results in rupture of the thin covering membrane, spewing clot-promoting plaque contents into the blood stream. The clotting system reacts and forms clots both on the particles shed into the blood stream and locally over the rupture. The clot, if large enough, can block all blood flow. Since all the blood, within seconds, passes through 5-micrometre capillaries, any particles much larger than 5 micrometres block blood flow. (most of the occlusions are too small to see by angiography). Most ruptures and clotting events are too small to produce symptoms, though they still produce heart muscle damage, a slow progressive process resulting in ischemic heart disease, the most common basis for congestive heart failure. The clot organizes and contracts over time, leaving behind narrowing(s) called stenoses. These narrowing(s) are responsible for the symptoms of the disease and are identified, after the fact, by the changes seen on stress tests and angiography, and treated with bypass surgery and/or angioplasty, with or without stents. When this inflammation is combined with other stresses, such as high blood pressure (increased mechanical stretching and contraction of the arteries with each heart beat), it can cause the thin covering over the plaque to split, spilling the contents of the vulnerable plaque into the bloodstream. Recent studies have shown cholesterol crystals within the plaque play a key role in splitting the plaque and also inducing inflammation. The sticky cytokines on the artery wall capture blood cells (mainly platelets) that accumulate at the site of injury. When these cells clump together, they form a thrombus, sometimes large enough to block the artery. The most frequent cause of a cardiac event following