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Cardiovascular disease accounts for nearly fifty percent of
deaths in both the developed world and in developing countries.
Indeed, the risk of dying from heart disease is greater than the
risk from AIDS and all forms of cancer combined. (Source: WHO) Worldwide,
cardiovascular diseases cause 12 million deaths in the world each
year. It is the leading cause of death in the US, killing some 950,000
people each year. It also accounts for a significant amount of disability
and diminished quality of life.
The news is not all bad. The incidence of some forms of heart
disease appears to be declining. New screening tools are allowing
cardiologists to recognize problems earlier and new treatments are
slowing the course of life and improving the quality of life of
millions of people. Lifestyle education efforts and the use of aspirin
to prevent heart attacks is also improving the public health outlook.
In the research fast lane, everything from the human genome project,
stem cell research and the recent implantation of the world's first
completely implantable artificial
heart indicate significant progress on many fronts. (link to
oz)
Sean Henahan got an update on the battle against heart disease
in an interview with Dr. Rose Marie Robertson, former president
of the American Heart Association and director for the Women's Heart
Health Institute at Vanderbilt University Medical Center.
Q: What is the status of the battle against cardiovascular
disease, how are we doing?
A: Oddly enough, the trends are moving in two directions at once.
Some 60 million people in the US have heart disease, including hypertension,
stroke and coronary artery disease. As the population ages there
are more people who have heart disease. However, the death rates
from many forms of heart diseases are actually falling. We have
become much better at treating patients who have had a heart attack,
in some cases stopping a heart attack in its tracks. We have gotten
better at treating people with heart rhythm problems, or heart failure.
So we can give people many more years of high quality life even
though they have heart disease. Also, we now know many ways to prevent
heart disease.
Q: How are we doing in terms of improving diagnosis and screening
for ethnic minorities, poorer populations, and women?
A: We are not doing as well there. Heart disease is a big problem
for women, and it is a problem they don't recognize. In fact if
you look at mortality rates from heart disease in this country,
almost all of the benefit is seen in men. For example, the number
of men dying each year from heart attacks has been steadily decreasing
each year since 1979. Over that same time period, the number of
fatal heart attacks among women has gone up. Since 1979, every year
but one, more women have died from heart attacks than men. Most
women don't realize the risks of heart disease. When we survey women,
the great majority fear and worry about breast cancer or cervical
cancer. We've done a good job of encouraging screening there. But
very few women conceive that heart disease might be a problem. The
statistics tell us that 1 in 27 women will die of breast cancer,
but nearly one in every two women will die of cardiovascular disease.
We are also not doing as well as we should with our diverse population.
The American Heart Association, the Surgeon General, the CDC, the
National Heart Lung and Blood Institute are all involved in efforts
to reduce disparities in health care so that every one has appropriate
access to both preventive and therapeutic medical care.
Q: Let's start with atherosclerosis,
or hardening of the arteries. How have basic and clinical
research improved our understanding of this aspect of heart disease?
A: We have seen tremendous progress in our understanding in this
area. For a long time we have understood that atherosclerotic plaque-
i.e. fatty deposits in the coronary arteries, were the basis of
coronary artery disease and heart attack, and that rupture (cracking)
of those plaques was a critical feature when patients have a heart
attack. We have learned a lot more about the factors that make those
plaques rupture, so that we can now look at plaque and say, this
plaque is a vulnerable plaque. That is important. For many years
people would go to the doctor's office and have an exercise test
or another screening test, appear to be fine, and then days or weeks
later, have a heart attack.
 This
is easier to understand when we know that plaque is not something
that is gradually laid down until it finally fills up a blood vessel,
then you have a heart attack. In fact, it turns out that plaque
is laid down in very different ways from one person to the next.
In some people it is laid down in a soft fatty component in a very
thin cap over the cholesterol or fat deposit. In that case that
cap is quite liable to rupture, so if the artery is subjected to
undue stress, e.g. a sudden surge in blood pressure, that plaque
is much more likely to rupture than one that is more stable. We
know that harder plaque with a lot fibrous tissue is less likely
to crack. Once the plaque cracks it is extremely thrombogenic (that
is, it encourages the formation of blood clots).
Another thing we've learned is that inflammation or infection seems
to release compounds that make patients more likely to lay down
plaques that are vulnerable. We are still in the early days of understanding
that phenomenon. There are markers of inflammation we can measure
in the blood that seem to correlate with the development of atherosclerosis
and adverse outcomes.
The question of how to intervene in this process is more difficult
to answer. We have a number of trials looking at the question of
whether infection of blood vessels or endothelial cells or elsewhere
in the body can be treated with antibiotics to reduce the incidence
of heart attacks.
Q: Are we getting to the point where it is becoming possible
to screen at risk populations genetically, to identify those who
might have a genetic predisposition to atherosclerotic disease?
A: We are identifying many different kinds of markers of coronary
disease risk. This area is just exploding as the Human Genome Project
has come to completion. As one of the scientists involved with Human
Genome Project said, it wasn't a race to the finish line, it was
a race to the starting line. It was race to say 'here is information'.
Now we have to take that information and go back into populations
and individuals and say 'here is a gene that could cause a problem,
let's see if this is so'.
Graphic:
Cross section illustration of artery with plaque build-up
 For
example, researchers recently identified a genetic marker for obesity.
You could say this marker is present in 25% of a given ethnic population.
And individuals with that marker, given the same intake and lifestyle,
are more prone to be more obese. Obesity is an independent risk
factor for coronary disease. That is a rather high tech way to find
a risk factor. If the individual with that risk factor engages in
the kinds of activities we recommend, i.e. 30 minutes of exercise
four or five times per week, they could completely overcome the
effect of that genetic marker. We'll be able to use genetic markers
to select those at increased risk. Some times we will use traditional
means to try and reduce that risk. Other times, if we know which
gene is involved it will let us be very specific about a particular
treatment.
Q: Let's talk about cholesterol, something that is associated
with the atherosclerotic process. There has been a positive association
between heart disease and elevated cholesterol for some time, yet
some patients with normal cholesterol levels develop heart disease,
while others with elevated cholesterol do not. Are genetics helping
us sort this out?
A: Yes, genetics and biochemistry are helping us to sort that out.
For any risk factor, there are those who will have a great resistance
to that risk factor, people who say 'my uncle Joe smoked until he
was 90 and it didn't do him any trouble', or 'overweight runs in
my family, but we don't have heart disease'. But there will also
be many more patients who are particularly susceptible to a risk
factor.
Sometimes a gene will have a very specific effect. It will cause
a protein to be made or not to be made and you will have a specific
disease. For example, there are some patients who have an increased
heart rate when they stand up, this is not uncommon among younger
patients We now know that some of these patients have a specific
problem with the receptor on the nerve that pulls norepinephrine
(one of the so-called stress hormones) back into the nerve. So when
they get a stimulus to release norepinephrine, they get a lot of
it out there, and don't sop it up very quickly, so they have a much
more profound response to a stimulus. Knowing exactly what the problem
is, we can be very specific about our treatment.
Other times there will be genes or clusters of genes that don't
do anything by themselves, but make you susceptible to a problem.
So a gene that wouldn't have any effect if you were eating a healthy
diet might put you at risk if you eat a standard high fat Western
diet.
Genetics may also help us to understand situations where people
do not have the usual risk factors. This is not a common patient,
but we look at these to identify alternative risk factors, things
like, homocysteine
or Lp(a)
or markers of inflammation like C-reactive
protein.
Q: One of the huge cardiology stories in the past decade has
been treatment of elevated cholesterol with 'statin' drugs. What
are learning about these drugs?
Do they have effects beyond simply lowering cholesterol?
A: We now have ample evidence that lowering cholesterol either
with diet and lifestyle modification, or with drugs, can make a
big difference We've seen something very interesting as we give
these 'statin' medications. The beneficial effect seems to happen
much earlier than we would have expected if this was just a matter
of reducing cholesterol. Once the plaque is there in an atherosclerotic
artery, even if you reduce the cholesterol, it takes a while to
change that plaque. Some may never change, others may change only
very slowly over months and years. But the effect of the statins
was seen in a period only weeks or months. It seems reasonable to
believe the statin is somehow involved in reducing the vulnerability
of the plaque by reducing inflammation, or by other mechanisms.
Click here to continue to Part 2 of this
inteview
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