(Circulation. 1997;96:12-14.)
© 1997 American Heart Association, Inc.
Articles |
Genetics of Interventional Cardiology
Old Principles, New Frontiers
From the Department of Medicine, Brigham and Women's Hospital, Boston, Mass.
Correspondence to Klaus Lindpaintner, MD, Department of Medicine, Brigham and Women's Hospital, 75 Francis St, Thorn 1103, Boston, MA 02115-6195.
Key Words: Editorials • genetics • epidemiology • stents • angiotensin • enzymes
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Introduction |
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The Master said, "By nature, men are nearly alike; by practice, they get to be wide apart."
—Confucius, Analects
The origin of
cardiovascular disorders, as of all disease, lies in
the duality of inborn predisposition, or susceptibility, and the
exposure to external (environmental) influences. We apply this
knowledge in our daily clinical practice as we consider anamnestic data
from a patient's family history as well as from his or her lifestyle
and occupation in our assessment of cardiovascular
risk. We also commonly draw a connection between these two etiologic
domains, simplistic as it may be, by estimating a proportionately
higher risk in the presence of "positive" findings from both
categories. At the same time, we are keenly aware of how vague and
inaccurate prognostications remain that are based on these recognized
risk factors and how little specific guidance for the management of
individual patients they offer. Is it possible that more detailed
knowledge of the genetic component of a patient's "risk profile"
might raise the precision and specificity of our risk assessment and
thus improve the success rate of intervention? To the geneticist, the
specific, not simply additive, interaction between inherited
characteristics and environmental factors is a well-appreciated
phenomenon: neither exposure to dietary phenylalanine nor a defect in
the gene encoding phenylalanine hydroxylase is by itself associated
with disease, yet the combination of the two results in the severe
syndrome of pronounced mental retardation and associated somatic
abnormalities typical of phenylketonuria. We may expect that in other
diseases
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