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PATHOLOGY PERSPECTIVES taking up LDL: low density lipoproteins that carry cholesterol. Eventually this becomes visible to the naked eye in deposits of cholesterol called fatty streaks. At this point no obstruction is present, no symptoms occur, and the whole process may be reversible. Chronic high blood pressure, chemicals derived from cigarette smoke, and blood that is high in glucose (i.e., uncontrolled diabetes) are particularly damaging to artery linings. Fatty streaks are most likely to develop in places where arteries divide: the turbulence of blood appears to be an important factor in the erosion process. INVESTMENT OF PLAQUE Chemicals released by fat-filled macrophages trigger the production of connective tissue in the area: collagen and elastin fibers are spun, and smooth muscle cells may proliferate around the new material. At this point, the lesion is big enough to intrude into the lumen of the artery, and it infiltrates both the tunica intima and the muscular layer of the vessel wall. PLAQUES COMPLICATE The development of a fatty plaque in an arterial wall triggers a sequence of reactions that can make the situation much worse. The plaque may accumulate calcium deposits, which causes the artery to lose its ability to appropriately dilate and constrict. Any roughness in a blood vessel attracts platelets (thrombocytes), which then secrete pro-inflammatory chemicals and clotting factors. When clots accumulate around the site of the lesion, this obviously increases the size of the obstruction. An obstruction composed primarily of clotted blood that is stationary and grows on-site is called a thrombus. If a portion of a thrombus or other debris breaks loose and travels, this is The wonderful thing about human physiology is that we have a remarkable ability to grow new blood vessels wherever existing vessels are not keeping up with our needs. an embolism. Plaques can grow large enough to limit blood flow, but they can also rupture, and fragments of blood clot, fat, and other substances can travel or embolize further along the artery. Any tissue that was meant to receive oxygen and nutrients from that blood vessel will die. When this happens with the coronary artery, it is called a heart attack or myocardial infarction. Anywhere else, it is just called an infarction. Regardless of location, the result is dead tissue and loss of function. There is good news, however. The wonderful thing about human physiology is that we have a remarkable ability to grow new blood vessels wherever existing vessels are not keeping up with our needs. This process, called angiogenesis, allows us to create collateral vasculature that does the work of the obstructed arteries. Angiogenesis takes time, however, so a new situation may be more threatening than an older one. WHO HAS PAD? So far this discussion has focused on PAD as a variant of cardiovascular disease. It is important to point out that this condition can develop under other circumstances as well. Any circumstance that involves damage or injury to peripheral blood vessels can lead to PAD. This includes chronic inflammatory diseases like lupus, or trauma. Clotting disorders can also contribute to PAD, as can exposure to radiation or anatomical anomalies that make the arteries vulnerable to ongoing damage. These cases are in the minority, however. Most people with PAD have it in combination with other cardiovascular compromise and are consequently at a very increased risk for both heart attack and stroke. Because PAD is virtually silent until damage is extensive, it is difficult to project how many people may live with this condition. A simple test has been developed that compares blood pressure readings from the arm and the ankle: this is called ankle-brachial index (ABI). When the ratio is under .95, PAD may be present. Estimates suggest that about 3 percent of the adult population under age 60 have a positive ABI. Not surprisingly, this number goes up with age: about 20 percent of people over age 70 have a positive ABI.1 Risk factors for PAD are the same as those for other forms of cardiovascular disease. Age, activity levels, a body mass index of 30 or above, and personal or family history with other forms of heart disease are predictive of a risk for damage to both core and peripheral 98 massage & bodywork september/october 2010