Infections might also act from a distance, in what I call an echo effect. When the body fights infections, inflammatory mediators can escape into the blood and travel to distant sites. These substances can, in theory, stimulate the white cells in atherosclerotic plaques, thereby prompting plaque growth or rupture. Clinical trials to see whether limited courses of antibiotics will prevent recurrent heart attacks are under way. A recently completed trial suggests, however, that antibiotics do not forestall recurrences in heart attack survivors.
Reducing Danger
INFLAMMATION’S essential role in atherosclerosis implies that anti-inflammatory medicines might slow this disease, and some (including aspirin) are already in use or under study. But logic and the investigations conducted so far suggest a need to look elsewhere as well.
Aspirin belongs to the class of drugs called NSAIDs (nonsteroidal anti-inflammatory drugs), a group that also claims such popular painkillers as ibuprofen and naproxen. Like other NSAIDs, aspirin can block the formation of certain lipid mediators of inflammation, including the prostaglandins, which generate pain and fever. Strong data from well-performed clinical trials indicate that aspirin shields against heart attacks and, in some patients, against mini strokes (technically, transient ischemic attacks, or TIAs). But the low doses that afford this protection probably reduce the clotting propensity of blood instead of quieting inflammation.
Scientists have little clinical data relating to the effects of other NSAIDs on atherosclerosis, and some evidence suggests that selective inhibitors of the prostaglandin- producing enzyme COX-2 might actually enhance thrombus development in some patients. Cortisone and related steroids could prove too toxic for longterm use, and no data support their utility in reducing atherosclerotic complications.
Even if anti-inflammatory drugs proved effective, they might have to be given for years on end to keep atherosclerosis at bay. That prospect worries me, because ongoing interference with inflammation could come at too high a price: increased risk of infection. One day someone could devise a way to halt the chronic, destructive inflammation of atherosclerosis without undermining overall immunity. But I suspect that a more practical strategy would concentrate on defusing the triggers at the root of arterial inflammation.
Fortunately, some means are at hand already. A heart-healthy diet, regular exercise and, for obese individuals, weight loss can reduce the risk of a heart attack and combat diabetes. In addition, since 1994 several impeccably designed and executed clinical trials have established beyond a doubt that lipid-lowering drugs can reduce the likelihood of atherosclerotic complications and can prolong life seemingly across the board—that is, in individuals with a broad range of risk levels. Researchers have not yet nailed down the mechanism behind the success of the lipid-lowering drugs, which do not seem to reduce arterial stenosis substantially. But studies of cells, whole animals and humans suggest that lipid lowering (as might be expected from the foregoing discussion) might help by limiting inflammation, thereby minimizing plaque buildup and make existing plaques less likely to rupture.
Recent analyses of the statins (widely prescribed lipid-controlling drugs) support this notion. They confirm that the drugs can decrease inflammation in patients. Experiments on isolated cells and laboratory animals indicate as well that the drugs’ anti-inflammatory effects may not depend entirely on changing the concentrations of lipids in the blood. Statins— which decrease the levels of LDL and related bad lipids by increasing their disposal in the body—also limit the availability of chemicals that enable cells to respond to inflammatory mediators.
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Add CommentLinus Pauling wrote in 1986 that vitamin C decreases LDL and increases HDL in the blood. C binds to cholesterol and transports it to the liver, where it is converted to bile and excreted. Vitamin C is a component of collagen, an essential structural component of arteries. Dr. Pauling wrote that atherosclerotic plaque is an evolutionary adaptation to the chronically low levels of vitamin C in humans, one of the few species who do not synthesize vitamin C internally. The medical-pharmaceutical establishment does not advocate vitamin C to prevent heart disease because there is far greater profit in treating heart disease, by means of medical procedures and drugs.
Reply | Report Abuse | Link to thisAlthough most people don’t realize it, atherosclerosis is a disease which, in addition to being a lipid storage disorder, also has components of inflammatory and immunologic disease. Thanks to television commercials, the cartoon image of cholesterol plaques that most people have in their head is if a yellow cholesterol plaque stuck to a red arterial wall. The truth is that most of that yellow plaque is not make up of cholesterol; it is made up of the body’s own cells responding to an endothelial disturbance, in addition to cellular markers of inflammation such as TNF-a, IL-6, hsCRP, foam cells, among many others. One of the main differences in the effectiveness of HMG CoA reductase inhibitors or “statins” in addition to their ability to increase the metabolism of cholesterol, is their ability to decrease inflammation. The two drugs that are best at decreasing inflammation cholesterol metabolism are Lipitor (atorvastatin) and Crestor (rosuvasatin). No currently marked drug exists which can affect the immunologic or cell migration effect in atherosclerotic plaques.
Reply | Report Abuse | Link to thisI suggest a new round of actualization now in 2010. Influenza would sure receive more consideration today regarding myocardial infarction triggering. But I continue to insist that triggering not its sole contribution.
Reply | Report Abuse | Link to thisMaria Ines Azambuja, MD
see Connections Braz J Med Biol Res January 2008, Volume 41(1) 1-4
I came to this article to see what a respected institution had to say about the causes of Atherosclerosis. The lipid theory has been significantly discredited by most research untouched by big pharma. This piece while not directly advocating it is pointing to statin therapy, and relating Atherosclerosis to LDL levels. When research said that there is no difference amongst patients who have had a heart attack in terms of their cholesterol levels - the proponents say we need to lower the LDL threshold, despite the almost total lack of evidence that LDL serum levels have anything to do with MI. What is disappointing is that there is NO discussion about what causes the inflammation in the first place. The levels of MI in our society have increased steadily in the past 100 years or so. These breakthroughs (in statin therapy) have not provided any solution to this health issue. The key is understanding lies in what causes the inflammation that leads to Atherosclerosis and modifying our lifestyle and diet to suit. The information must be there somewhere - there is somehting that has changed in the past 100 yrs that have made this MI epidemic, but maybe its not in the interest of some stakeholders for us to find out. Unfortunately SA have added more fuel to the old song about cholesterol myth and I await patiently when this Stalin billion dollar scam blows open.
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