Bacteria & Cardiovascular Disease
Insulin resistance and diseases
Fragile X Syndrome, and stem cell research
Bacteria & Cardiovascular Disease
STEM CELLs--Scientific American
Serotonin--a detailed overview
Hedgehog genes & embryo development
DNA Repair--Mechanism Revealed
Immune response to cancer observed
CANCER, Classification of cell types
INTRONS, vital roles revealed
Sex-linked Brain Differences--Scientific American
Gene For Diabetes Found
Why People Have Different Blood Types
Dupuytren's Contracture: most common connective tissue disease
New Technique for observing superoxides

Cardiovascular Connections


Cardiovascular Connectons:  David M. Ojcius, Toni Darville, & Partik. M. Davoil,

Scientific American, May 2005,p.78


C. PNEUMONIAS turned up in the atherosclerotic coronary arteries of 54 percent of the 272 patients surveyed for a study published in 2000.  
One of several similar findings for a connection between bacteria and cardiovascular disease.  This ties into the related relationship between carbon monoxide and arteriosclerosis.--jk

The picture is complex with significant contributions being made by bacteria, carbon moxide (and certain other reactive chemicals), diet, genes, diabetes, and exercise to name the princple--jk. 

Colds, bronchitis and pneumonia may not be the sole concern for people who have inhaled the airborne species of Chlamydia. Recent evidence hints that C. pneumoniae infections may also contribute to strokes and heart attacks. Such a link may have an upside, however—doctors might eventually be able to prescribe antibiotics to fight both the infection and the heart disease.


Atherosclerosis—a narrowing of the coronary arteries that leads to most strokes and heart attacks—causes approximately half of all adult deaths in the Western world. But traditional risk factors, such as elevated cholesterol and cigarette smoking, account for only about half of that total. Scientists searching for a reason behind the other 50 percent began to consider infections once it became clear that inflammation—a generalized immune response against any perceived invader—also underlies the growth and destructive ruptures of the fat-laden deposits that constrict coronary arteries [see "Atherosclerosis: The New View," by Peter Libby; scientific american, May 2002].


C. pneumoniae became a prime suspect in the condition shortly after it was identified as a separate chlamydial species in 1983. It drew suspicion because of its ubiquity—more than 60 percent of adults world wide carry antibodies against it (a sign of past or ongoing infection). Support forthe hunch emerged in 1988, when physicians in Finland reported a positive correlation between the presence of these antibodies and the risk of developing coronary artery disease; other researchers identified the bacterium in clogged human arteries five years later. Since then, organizations such as the National Institutes of Health and the American Heart Association have invested millions of dollars to study the relation between C. pneumoniae and atherosclerosis.


Animal studies conducted within the past five years or so have provided some of the most convincing evidence for a link. One demonstrated, for example, that chlamydial bacteria can move from the lungs of mice to other parts of the body within white blood cells, the agents responsible for inflammation. Other research has shown that C. pneumoniae infections accelerate atherosclerosis in both mice and rabbits and that antichlamydial antibiotics can preventthat acceleration.


Experimental results such as these, though tentative, were enough to justify a handful of small clinical trials in humans. Five of these trials showed that one to three months of antibiotic treatment had a statistically significant benefit against the progression of atherosclerosis. But results were mixed as to whet her the antibiotics could actually prevent serious cardiac events. The promise for longer-term treatment was also dealt a blow by the negative outcomes of two large trials completed in 2004, each involving 4,000 volunteers who received antibiotics for one to two years.


Establishing whether a clear connection exists between C. pneumoniae infection and atherosclerosis in humans may prove difficult simply because so many other factors participate in heart disease. Exactly how troublesome such complications will be, however, remains to be seen.     —D.M.O., T.D. and P.M.B.







A new treatment paradigm

One of our more recent recommendations, AtheroGenics, is a biotech company that is taking a novel approach to CVD treatment—an approach we feel could pay very large dividends not only for their shareholders, but also for the CVD patient. Rather than targeting LDL or HDL, AG1X is approaching the treatment of CVD through the inhibition of inflammation (In fact, AGIX describes themselves as a company committed to developing treatments for chronic inflammatory diseases, not just CVD.) Inflammation has been shown to play a key role in the development of atherosclerosis, which, in turn, is a leading contributor to the development of CVD.  AGIX is doing this through the development of their V-Protectant technology, which is based upon the concept that the endothelial cells which line the interior wall of the blood vessel play an active role in recruiting white blood cells (which play an integral role in the inflammatory process) from the bloodstream to the site of chronic inflammation.  AGIX' v-protectants are drugs that block a class of signals, called oxidant signals, which are generated within endothelial cells. These oxidant signals activate genes, which produce inflammatory proteins. The protein products of these selected genes, including VCAM-1, attract white blood cells to the site of chronic inflammation. The v-protectants appear to have the ability to act as anti-oxidants, but also appear to be able to do this without impeding upon the body's ability to protect itself against infection.

Interestingly, a study was published this week which provides further evidence that inflammation is a key factor in the occurrence of strokes and heart attacks.  In this study which is part of the Women’s health Initiative, over 66,000 women had thei5r white blood cell counts measured once, and then they were followed for six years.  The results showed that the women wit the highest levels of white blood cells were found to be twice as likely to die from heart disease as women with the lowest levels.  In addition, high white blood cell counts were associated with a 40% higher risk for nonfatal heart attack, and a 46% higher risk for stroke.  While the results from this study do not say for sure whether lowering white blood cell counts will lead to a lower risk of heart attack or stroke, and while they may not change medical treatment guidelines any time soon, they should serve as an eye opener to doctors that heart disease is likely not due to cholesterol alone.


from MTSL No. 514 March 17, 2005, Medical Technology Stock Letter