From the publishers of the New England Journal of Medicine Atherosclerosis is often called "hardening of the arteries." In this disease -- the leading cause of heart attacks and strokes -- solid or semi-solid deposits (plaques) stiffen artery walls and block blood flow. But based on what scientists have learned recently, this condition could also be termed "inflammation of the arteries." In addition to LDL (bad) cholesterol, plaque contains inflammatory white blood cells, connective tissue, smooth muscle cells, and platelets (blood components that promote clotting). The diverse makeup and inflammatory nature of plaque may help explain why half the people with clogged arteries have normal blood-cholesterol levels.
The first step in atherosclerosis is subtle damage to the smooth, flat cells (endothelium) lining the insides of arteries. This sets the stage for inflammation, tissue's attempt to heal itself after being irritated, injured or infected. Scientists suspect the initial damage to arteries comes from LDL cholesterol that's been modified by free radicals: highly reactive renegade molecules that harm healthy cells. Free radicals are abundant in people who smoke tobacco and who have high blood pressure or diabetes. Scientists have also suspected high levels of homocysteine (a byproduct of the breakdown of protein) and bacteria such as Chlamydia pneumoniae in early assaults on artery linings. Most likely, the incipient damage arises from a combination of factors.
After initial injury, cells lining the artery release chemicals that signal white blood cells to rush in. These cells gobble up harmful substances and stimulate the formation of antibodies, but they also release inflammatory chemicals. The endothelium also secretes chemicals that make the artery's slippery lining stickier. This increase in stickiness creates a magnet for circulating LDL cholesterol. Clot-producing platelets also stick to the site, and they secrete more inflammatory chemicals. Early-stage plaque formations, known as fatty streaks, consist of foam cells (white blood cells coated with LDL particles), smooth muscle cells that move in from deeper layers of the artery wall, and platelets. Healthy Living
The key to preventing atherosclerosis is avoiding damage to the artery lining so inflammation doesn't start. Treating early-stage atherosclerosis focuses on minimizing the factors that feed inflammation. In both cases, eating foods that are low in saturated fat and cholesterol, exercising (to control cholesterol and blood pressure), and not smoking will help. Although homocysteine's role in atherosclerosis remains unclear, it couldn't hurt to eat plenty of foods rich in the B vitamin folic acid, such as orange juice, green leafy vegetables, wheat germ, and bananas. Folic acid stimulates an enzyme that breaks down homocysteine.
It's uncertain whether antioxidants (substances that neutralize free radicals) can prevent or stall atherosclerosis. But since free radicals are probably the first link in the disease chain, you should consume the recommended daily amount of antioxidant vitamins for adults (60 milligrams of vitamin C and 30 international units of vitamin E). And limiting the amount of sodium you eat is a good hedge against high blood pressure. A Time for Medication
For some people, healthy lifestyles aren't enough to prevent or stall atherosclerosis, partly because of genetic predispositions toward clogged arteries. If doctors determine that blockages exist but are not too severe, they often prescribe one or several drugs that can hinder atherosclerosis: statins, which lower LDL; gemfibrozil and nicotinic acid, which boost HDL (good) cholesterol; several blood-pressure-lowering drugs, including angiotensin-converting-enzyme (ACE) inhibitors; and aspirin or warfarin, which prevent blood clots. Aspirin, statins, and ACE inhibitors also have anti-inflammatory action.
While bacteria have been found in plaque, no one knows if the germs cause atherosclerosis. A study in the December 1999 Journal of the American College of Cardiology found that people with very high levels of bacteria-produced toxins in their blood were much more likely to develop plaque in their carotid arteries than people with low toxin levels. But until research reveals more about infection's role in atherosclerosis, doctors are unlikely to prescribe antibiotics for prevention or first-line treatment. Mechanical Interventions
If drugs are not effective in people with atherosclerosis, doctors often recommend more invasive measures such as angioplasty (flattening the plaque with a balloon-tipped catheter to open the artery), stents (tubes inserted after angioplasty that prop open a once-clogged artery), endarterectomy (surgical removal of plaque, often from carotid arteries), or bypass surgery (grafting veins taken from the leg to bypass blocked arteries).
Controlling the factors that injure arteries and fuel inflammation, either by changes in lifestyle or with medications, is the key to sidestepping the adverse health consequences of atherosclerosis. While we've learned much about this complex but common condition in recent years, further discoveries about the roles of antioxidants, antibiotics and anti-inflammatory agents should benefit patients in years to come. -- The Editors
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