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Senior Citizen Health & Medicine
Day after President Ford gets Pacemaker Researchers
say They are on Track to Make the Device Unnecessary
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larger view - Read more below about pacemakers below news. |
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August 22, 2006 Only a day after a cardiac
pacemaker was inserted in former President Gerald R. Ford, researchers
at UC Davis say they have successfully used a custom designed protein
and gene delivery system to restore normal heart rhythms in pigs on
electronic pacemakers, reducing their dependence on the implanted
devices. They suggest that this puts them one step closer to making
bioengineering a reality in treating the more than 2.2 million Americans
affected by irregular heartbeats.
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The UC Davis study, which was co-authored by an
international team that included scientists from the University of Hong
Kong and Johns Hopkins University, is published in the current issue of
the journal Circulation, (which is available online and will appear in
print on September 5). The same issue also includes a similar but
independent research effort by scientists from Columbia University and
State University of New York at Stony Brook.
"Our study offers positive and direct evidence in
living models that bioengineered cells can replace the electronic
pacemaker," said Ronald Li, who leads the research team and is an
associate professor of cell biology and human anatomy at the UC Davis
School of Medicine.
More than 250,000 people in the United States get
artificial pacemakers implanted each year. Researchers believe this
biological approach would provide a more permanent, reliable and less
invasive alternative to implanted electronic devices. "Our hope is to
one day replace electronic pacemakers in people," Li said.
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"Former President Gerald R. Ford has completed an evaluation and
series of tests resulting in the implantation of a cardiac
pacemaker to enhance his heart's performance.
"The procedure this afternoon went smoothly and without
incident. President Ford is resting comfortably with his wife
and children and is expected to continue his recuperation at
Mayo Clinic for the next several days."
- Statement from his office
President Ford, the 38th President, is the oldest living
President at 93.
Click to Ford Foundation, Library and Museum |
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Li and his colleagues have been working for years
to develop biological alternatives to drugs and electronic devices for
treating heart arrhythmias heartbeats that are irregular in rhythm,
rate or sequence. The sinoatrial (SA) node, a patch of cells called the
pacemaker, generates cardiac rhythms for coordinated contractions and
blood pumping. Malfunctions due to aging or diseases can lead to a range
of potentially lethal arrhythmias, such as slow heart rates or rhythms
called bradycardias.
In the current study, the researchers delivered a
gene encoding a bioengineered cell-surface protein to heart muscle cells
of pigs. This protein mimics the combined action of several proteins
called HCN ion channels, which play a critical role in maintaining a
normal, evenly paced heartbeat. These channels control the flow of
sodium and potassium ions in and out of cells that regulate the
electrical impulses of the heart.
"These channels are critical to normal heart
function. We were able to make one protein that codes for a single
channel that does the work normally required by several," Li explained.
By getting heart muscle cells to produce
bioengineered HCN channels, Li and his colleagues were able to
reconstruct the SA node of the heart in pigs with implanted electronic
pacemakers. The SA node is normally located on the right atrium, the
upper right chamber of the heart that receives deoxygenated blood from
the body.
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About Pacemakers |
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A pacemaker is a small, battery-powered device that is implanted
permanently into the body. The pacemaker monitors the electrical
impulses in the heart and, when needed, delivers electrical
stimuli to make the heart beat (contract) in a more normal
rhythm.
A pacemaker is used when the heart beats too slowly (bradycardia)
or has other abnormal rhythms (arrhythmias). In some cases,
pacemakers are also used to treat the symptoms of heart failure.
A pacemaker consists of a battery and electrical circuitry
(pulse generator). The battery powers the pacemaker. The
circuitry checks the heart rate and produces tiny electrical
pulses that keep the heart beating at the correct pace.
The pacemaker is connected to the heart through one to three
insulated wires (leads) that are attached directly to the
heart's chambers.
Some pacemakers can be customized to meet specific needs.
● Rate-Responsive Pacemakers These pacemakers may be
programmed to increase or decrease heart rate to match your
activities (i.e. resting or walking).
● Single-Chambered Pacemakers These pacemakers use only one
lead placed into the right upper chamber of the heart (right
atrium) or the right lower chamber (right ventricle).
● Dual-Chambered Pacemakers These pacemakers have two leads.
One is placed in the right atrium, the other in the right
ventricle.
● Cardiac Resynchronization Therapy Pacemakers These
pacemakers have three leads. One is in the right atrium, one is
in the right ventricle, and one is placed through the hearts
veins to the left ventricle.
A pacemaker can restore a normal heart rate so that the heart
can pump more effectively. This can reduce or stop the symptoms
of abnormal heartbeats (arrhythmias), such as dizziness,
confusion, fainting, or fatigue.
FDA Heart Health Online
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"We were even able to create new pacemaker regions
on the left atrium," Li said.
According to Li, the current study moves research
beyond using animal models such as mice and rats, whose hearts can beat
up to 600 times per minute. Large animals such as pigs make for far more
realistic models because their anatomy and physiology, including average
heart rates of about 70 to 80 beats per minute, are similar to humans.
In the current study, researchers used
radiofrequency ablation to remove the SA nodes in pigs' hearts. This is
the same minimally invasive technique cardiologists use in clinics to
destroy the heart cells that cause abnormal electrical discharges and
rapid heart rates in their patients. To restore the SA node function and
evaluate the bioengineered cells, Li's team then implanted electronic
cardiac pacemakers like those used in humans and injected an adenovirus
carrying a gene encoding for the engineered HCN protein into the heart
muscle. Adenovirus has the ability to deliver its own genes into a host
cell and hijack its protein-synthesizing machinery. Scientists use this
ability to deliver genes of interest into cells.
In a matter of days following the gene transfer,
the pigs' hearts had generated bioartificial nodes at the injection
sites. Li explained that, through gene expression, normal muscle cells
of the heart were converted into pacemaker cells by a process called
transdifferentiation. Studies done two weeks after the injections showed
the new nodes were able to take over pacemaking function from the
electronic devices. The results also have implications for future stem
cell research.
Li and his colleagues are now preparing to do
long-term, follow-up experiments. UC Davis offers a unique environment
for this work to be continued through eventual testing in humans, Li
said.
"It is a place where we can do the basic laboratory
science, test in animal models, utilize the only non-human primate
facility in California and eventually partner with physicians at the UC
Davis Health System to treat patients," he said.
Li and his team previously generated the first
genetically engineered human heart cells from human embryonic stem
cells, and demonstrated that they can be transplanted into a recipient
heart and function normally. Li plans to combine stem cells and
protein/cell engineering approaches to the treatment of heart
arrhythmias.
"Heart cells do not normally regenerate, but we now
have the technologies to make new human heart cells using stem cells.
And, we can also customize these cells to treat diseases," he said.
Notes:
Co-authors on the paper include UC Davis' Tian Xue;
Hung-Fat Tse, Chu-Pak Lau, Chung-Wah Siu, Kai Wang, Qing-Yong Zhang from
the University of Hong Kong; and Gordon Tomaselli and Fadi Akar from
Johns Hopkins University.
This work was supported by grants from the National
Institutes of Health and the Hong Kong Research Grant Council.
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