' ctur Tel

Our St or y.

Dr. Steven
Lipshultz

with an open

heart model

Heart Health

Children's Hospital study may
lead to a breakthrough therapy.

ust in time for Heart Health
Month ... A recently published
study with major implica-
tions for ameliorating or preventing
gene-triggered hypertrophic cardiomy-
opathy, a chronic form of heart muscle
disease, suggests that pediatric cardi-
ologists may soon be able to use drug
therapy to block the onset of these
abnormalities.
Hypertrophic cardiomyopathy can
cause heart failure by stiffening the
heart muscle and interfering with
normal heart function. The condi-
tion sometimes causes sudden cardiac
death when abnormal muscle cells
and scar tissue lead to dangerous heart
rhythms. Hypertrophic cardiomy-
opathy is the most common genetic
disease of the heart, affecting 1 in
500 children, and is the most com-
mon cause of sudden cardiac death in
young people and athletes.
The new study — the first of
its kind and co-authored by the
Children's Hospital of Michigan
DMC Pediatrician-in-Chief, Steven
E. Lipshultz, M.D. — showed that in
many patients carrying these genes,
these abnormalities did not develop; or
if they did, they were better if treated
for one to three years with a calcium
channel-blocking drug called diltia-
zem. The drug helps block the effect of
these gene mutations on the growth of
heart muscle fibers.
"With this study, we are opening a
new chapter in the book about heart
care said Lipshultz, who also chairs
the Department of Pediatrics at the
Wayne State University School of
Medicine. "For the first time, we now
have convincing evidence that drug
therapy can protect patients from
genetic mutations that lead to the
abnormal heart development found in
hypertrophic cardiomyopathy, a set of
diseases that place affected children
at increased risk for heart failure and
sudden death.
"This study shows that if someone
is carrying a mutated gene for hyper-

j

trophic cardiomyopathy but hasn't yet
developed the disease, we can prevent
or delay the onset of the disease later
in life by administering the drug ther-
apy during the patient's earlier years.
Further, the drug may also reduce the
severity of associated diseases:'
"This proof-of-concept study,
funded by the United States National
Heart, Lung and Blood Institute of the
National Institutes of Health (NIH)
and published in the Journal of the

American College of Cardiology: Heart
Failure, is an important milestone
in the development of genetically
based therapies aimed at reducing the
harmful effects of cardiac mutations:'
Lipshultz said.
Describing the breakthrough, he
said, "The gene mutations that cause
the growth of too much heart muscle
(hypertrophy) in children or young
adults contribute to the leading cause
of sudden death in young adults in
the United States. But this study tells
us that if you can prevent the onset or
ameliorate the course of cardiomyopa-
thy in a child with a gene mutation,
you may be able prevent or reduce
the risk for heart failure and sudden
death that will occur in some affected
children.
"The first thing we aim for in pedi-
atrics is prevention, and this study
describes a truly exciting prospect —
the likelihood that we will soon begin
treating children with a heart failure-
causing gene mutation long before the
development of the muscle abnormal-
ity that causes the failure:'
Lipshultz, an internationally rec-
ognized expert on pediatric cardiac
care who 25 years ago led the effort to
found the nation's only NIH-funded
registry of pediatric cardiomyopathy
and who has published numerous
studies in pediatric cardiology and
pediatric oncology, described the study
as "a compelling example of how clini-
cal research can help children. Such
advancements continue to create a bet-
ter future for our patients:' ❑

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February 5 • 2015

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