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Gene
Increases Heart
Disease Risk in Blacks
NEW
YORK (Reuters Health) - A specific version of a gene involved
in blood clotting greatly increases the risk of heart disease
in African Americans, but does not increase risk among whites.
Blacks who
have the gene have six times the risk of heart disease compared
with those who have another version of the gene, which controls
the production of a molecule found on cells lining the blood vessels.
``Our findings
underscore the importance of studying genetic risk factors by
ethnic group,'' Dr. Kenneth Wu from the University of Texas-Houston
Health Science Center said in a statement released by the American
Heart Association. ``They also provide a genetic basis for differential
risk factors of heart attacks between African-Americans and whites.''
The study appears in the April 24th issue of the journal Circulation:
Journal of the American Heart Association.
Wu and associates
conducted blood tests on heart attack patients and healthy individuals,
looking for a particular form of the gene necessary for the manufacture
of the protein thrombomodulin. Thrombomodulin is found on cells
lining blood vessels, and is important because it converts the
clot-producing protein, thrombin, to an anti-clotting agent. Thrombomodulin
may also protect blood vessels from damage.
The ``V''
form of the gene, in which one of the protein's amino-acid building
blocks is switched, has been linked to raised risk for heart attack.
In general, people have two copies of the gene--one inherited
from each parent.
Heart attack
patients, in general, were 60% more likely than those without
heart disease to have at least one copy of the V form of the gene,
the authors report, whereas healthy individuals were more likely
to have two copies of the ``A'' form of the gene.
This difference
was most marked among black individuals. After adjustments for
other heart disease risk factors, blacks with the V gene were
6.1 times more likely to have heart disease than were blacks who
had only the A form of the gene. This did not seem to be true
for whites.
The researchers
have not yet discovered why this simple genetic difference has
such a profound effect on heart disease risk. Perhaps, they suggest,
subtle differences in the way blacks with the V gene respond to
inflammation prevents their thrombomodulin from working effectively.
Or perhaps other unidentified risk factors give thrombomodulin
a greater role in the development of heart disease in blacks.
Whatever the
mechanism, doctors now have another way of estimating the risk
of heart disease in African Americans, the authors conclude.
The researchers
caution, however, that larger studies need to confirm their results
before genetic testing for thrombomodulin becomes part of the
routine assessment of heart disease risk.
SOURCE:
Circulation:Journal of the American Heart Association
Reference
Source 89
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