http://bmj.com/cgi/content/full/324/7330/133/a
BMJ 2002;324:133 ( 19 January )
Scott Gottlieb New York
Greater exposure to bacteria and viruses seems to be related to the acceleration
of atherosclerosis, the degeneration of the inner lining of the walls of blood
vessels in heart disease, and a worse prognosis, the latest research shows. The
findings add to growing evidence that inflammation and infection have a key
role in the development of heart disease.
The study (Circulation 2002;105:15-21), led by Dr Christine
Espinola-Klein from the Mainz University Clinic, Germany, looked at 572
patients who were admitted to the hospital for cardiac catheterisation. All the
patients were tested for antibodies to several bacteria and viruses, including
herpes simplex viruses 1 and 2, cytomegalovirus, Epstein-Barr virus, Haemophilus
influenzae, Chlamydia pneumoniae, Mycoplasma pneumoniae, and Helicobacter
pylori.
The patients were then followed for an average of 3.2 years, over which time
the extent of atherosclerosis was determined by coronary angiography, carotid
duplex sonography, and evaluation of the ankle brachial pressure index.
Patients who had four or five past infections were 1.8 times as likely to have
advanced atherosclerosis as people with fewer infections. Patients with 6-8
past infections were 2.5 times as likely to have advanced heart disease as
people with fewer infections. After the follow up period, cardiovascular mortality
was 7% in patients with advanced atherosclerosis and seropositive for 0-3
pathogens, compared with 20% in patients seropositive for 6-8 pathogens.
The researchers conclude, "We demonstrated that increasing numbers of
infectious pathogens were significantly related to the extent of
atherosclerosis and to adverse long-term outcome. Our results are compatible
with the concept that infections are involved in the development of
atherosclerosis and that infections with multiple pathogens may augment the risk
conveyed by one pathogen."
Previous research looking at some of these and other infectious agents
individually had conflicting results. This study is the first to look at the
impact of a range of infectious diseases.
However, the study cannot prove that the infections are the cause of the
advanced atherosclerosis, Dr Paul M Ridker from Brigham and Women’s Hospital,
Boston, comments in an editorial in Circulation (2002;105:2-4). Indeed,
other studies that looked at C pneumoniae and H pylori infections
in particular found little or no association with atherosclerosis, he notes.
"Only a few years ago, there was virtually no clinical evidence that
inflammation played a fundamental role in atherothrombosis. It will take
several years more to discern what the triggers of that inflammation are and
whether infection is a key determinant of that response," Dr Ridker
writes.
Dr Ridker noted that all the study’s participants had heart disease and that
the infections could have come after the onset of heart disease, or people with
arterial disease might be more prone to infection.
Dr Espinola-Klein acknowledged that other factors could skew the results but
said that, even after adjustment for age, sex, cardiovascular risk, and other
kinds of inflammation, the association between infection and development of
atherosclerosis remained significant. In fact, the association was strongest
with the four bacterial infections and much less so with the viral infection,
she said.
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