In 1999, Dr. Valentin Fuster, M.D. published a Book called The Vulnerable Atherosclerotic Plaque. Dr. Fuster was at the time the President of The American Heart Association, and also was and still is the Chairman of the Department of Cardiology at Mount Sinai School of Medicine in New York City. This book shows that heart attacks do not occur in areas of maximal plaque buildup where calcium has hardened large deposits of cholesterol, but in fact occur in fresh, “vulnerable” plaques that get INFECTED with germs, such as Epstein Barr Virus, Herpes Virus, Cytomegalovirus, and other low level germs that infect humans.
Toxic heavy metals are ever ready to attack the endothelium. The endothelium, in an attempt to heal itself, launches an inflammatory response to get rid of the unwanted guests. Researchers are now in the process of studying and proving that these germs are more prevalent and “infectious” when N.O. is not present in sufficient amounts. By removing the circulatory heavy metal toxins, EDTA enhances cardiovascular blood flow and function. N.O. is a potent vasodilator and a strong anti-oxidant. When the endothelium is damaged, N.O. production is reduced. This leads to the reduction of vasodilatation, or conversely, an increase in vascular constriction. Reduced N.O. production, as a result of toxic metal insult, leads to a reduction in vascular lumen size, restriction of blood flow, and ultimately an increase in blood pressure. This means, in layman’s terms, an increased risk of stroke and heart attack.
The proper amount of NO secretion is therefore of paramount importance, as imbalance of this contractility function will lead to hypertension, the silent killer. If the local vascular homeostasis is disturbed, it will result in platelet deposition, aggregation and a release of factors that promote smooth muscle proliferation. When this happens, you may get fibrosis, atherosclerosis and thrombus formation. As imbalances are first initiated at the endothelial level, where insults excite an inflammatory response, the endothelium is therefore the first link between inflammation and coagulation.
Meanwhile, a small amount of LDL (“Bad”) cholesterol that has built up in the artery wall becomes oxidized. Oxidized LDL is one of the triggers that set off a chain reaction. It causes the endothelium to express a special kind of molecule “glue” called ELAMS (endothelial-leukocyte adhesion molecules). These molecules, which happen to be floating by in the bloodstream causes certain kinds of white blood cells (monocytes and T lymphocytes) to stick to the endothelium. At this point in time, the inflammatory response is still well under control and normal, whether it is in the artery or in the tissue.
Beyond this point, the healing process goes off track. The white blood cells will start to move between and below the endothelium and cause damage in two major ways. Firstly, they will cause some of the muscles cells in the artery walls to grow and secondly, they incorporate particles into the artery wall, consuming the oxidized LDL particles. What results from here is a fatty streak that becomes a fibrous plaque.
This intricate process begins in the tissue under the endothelium. Due to inflammatory reactions, the endothelium’s structure becomes permeable to lipoproteins, particularly low- density lipoproteins (LDL) and macrophages. These particles will enter into the site of injury, accumulate cholesterol as cholesterylester and develop into foam cells. A raised LDL-cholesterol and related cholesterol carrier called lipoprotein (a) concentration is recognized by many as a major risk factor for heart disease as it appears to be the donor of cholesterol deposited in the atherosclerotic plaque. Being adhesive, the cells will attract other substances, resulting in a continuous deposition of unwanted conglomerate which we call fatty streak. The latter consists of lipids (fats), complex carbohydrates, blood, blood products, fibrous tissue, oxidized ascorbates and calcium deposits. As the fatty streak becomes increasingly larger, this resulting fibrosis forms an “endothelial tumor” or a plaque. The process of plaque formation is called atherosclerosis. Atherosclerosis blocks the blood’s pathway and narrows the arteries over time. This affords a possible explanation for the beneficial effects of chelation. In addition, EDTA blocks the slow calcium currents in the arterial wall, resulting in arterial vasodilation.
Probably the major underlying condition leading to cardiovascular disease is atherosclerosis, also known as hardening of the arteries. In time, this degenerative disease can narrow or block arteries in the heart, brain, and other parts of the body. It may begin early in life. The linings of the arteries become thickened and roughened by deposits of fat, cholesterol, fibrin (a clotting material), cellular debris, and calcium. As this buildup on the inner walls becomes hard and thick, arteries lose their ability to expand and contract. The blood moves with difficultly through the narrowed channels. This makes it easier for a clot to form that will block the channel (lumen) and deprive the heart, brain, and other organs of the necessary blood supply. In such a situation, how can dilator drugs possibly be effective?