Experimental drugs that aim at other risk factors for heart disease and stroke might exert useful anti-inflammatory effects as well. Agents that raise levels of HDL or limit the action of angiotensin II come to mind. But treatment with antioxidant vitamins has proved disappointing.
No matter how good a drug is, it will be of no value if it sits unused on pharmacy shelves. Doctors need better ways of detecting dangerous atherosclerosis in the large fraction of people whose lipid levels look too good to justify treatment. Recent findings suggest that blood tests combining lipid testing with monitoring of a substance called C-reactive protein might improve detection.
Toward Early Detection
THE PRESENCE of C-reactive protein in the blood signifies that inflammation is occurring somewhere in the body; highly elevated levels, even in the presence of LDL values too low to prompt treatment under current guidelines, indicate an increased risk of heart attack or stroke. What is more, in at least one study, delivery of statins to people with below-average LDL concentrations but high C-reactive protein levels reduced the incidence of heart attack relative to the rate in a matched group of patients who received no treatment. Such results need to be confirmed in a much larger trial before doctors can confidently treat patients on the basis of the combined test, although some physicians already incorporate tests of Creactive protein in their practices.
Noninvasive methods for specifically identifying vulnerable plaques might also help pinpoint individuals who lack strong warning signs of risk for heart attack or stroke but who nonetheless are destined for disaster. Ideas include measuring the heat of blood vessels (because heat should accompany inflammation) and altering existing imaging technologies, such as MRI or CT scans, to improve their ability to visualize material inside vessel walls. Geneticists, meanwhile, hunt for gene variants that render some people more vulnerable to chronic inflammation and to atherosclerosis and its complications, so that individuals most prone to these disorders can seek more aggressive monitoring and treatment.
For most of human history, inflammation’s ability to ward off infection outweighed its drawbacks. Today, as we live longer, exercise less, eat too much and smoke, many of us suffer from inflammation’s dark side—including its ability to contribute to atherosclerosis and other chronic disorders. Scientists continue to pursue a deeper understanding of inflammation’s role in atherosclerosis and to decipher the devilishly intricate interactions that ignite and drive the inflammatory processes in the arteries. These insights should enable us to make further inroads against a disease of growing worldwide importance that causes extensive disability and takes far too many lives.
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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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