Is your
daily aspirin falling down on the job?
Not everyone gets the full effect of aspirin.
A test can show if it’s working for you.
(This article was first printed in the May
2004 issue of the Harvard Heart Letter.
For more information or to order, please go
to www.health.harvard.edu/heart.)
You might bristle a bit if someone told you
that you were just like everyone else. Yet the
idea that we all respond in much the same way
to medications lurks behind drug therapy for
most conditions.
Take aspirin as an example. Almost everyone
with heart disease (see Who needs aspirin?)
is urged to take an aspirin a day to prevent
a future heart attack or stroke, as are some
otherwise healthy people at high risk. This strategy
works in the population as a whole. But does
it work for every person who takes aspirin?
It’s relatively easy to check how well
some drugs work. Before-and-after cholesterol
tests can show whether a cholesterol-lowering
drug is doing what it should. Blood pressure
measurements will do the same for an antihypertensive
medication. Not so with aspirin — we’ve
had to take on faith that it is doing its job.
That’s changing. Tests are being developed
to measure how well aspirin works in individuals.
They show that some people who take aspirin don’t
get the full protection it can offer.
Experts call this “aspirin nonresponsiveness.” It’s
a big problem, says Harvard Medical School’s
Dr. Daniel I. Simon, the associate director of
interventional cardiology at Brigham and Women’s
Hospital. “The millions of people with
heart disease need to know if the aspirin they
take each day is working for them.”
Who needs
aspirin?
Some doctors have a different kind of
aspirin nonresponsiveness. Guidelines from
nearly every major medical group urge doctors
to prescribe aspirin for people with heart
disease or at high risk for it. Yet up
to one in five people who should be taking
aspirin don’t, either because it
wasn’t prescribed or they don’t
follow their doctors’ recommendations.
Unless you are allergic to aspirin or
it causes you problems, you should take
it if you
- have had a heart attack
- have had an ischemic (clot-caused)
stroke or a mini-stroke (transient ischemic
attack)
- have angina (chest pain)
- have had a coronary artery bypass or
angioplasty
- have diabetes
- are at high risk for heart disease.
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When aspirin doesn’t work
The discovery that aspirin affects an important
step in the formation of artery-blocking blood
clots transformed it from a fever reliever and
pain quencher into a key weapon against heart
attacks and strokes.
Aspirin keeps the body from making a substance
called thromboxane A2. This is a chemical signal
that acts on small pieces of blood cells called
platelets.
Normally, platelets slide past each other as
they careen around the bloodstream. Thromboxane
A2 makes them latch onto each other, Velcro-like,
and begin to clump. By blocking thromboxane A2,
aspirin makes platelets less “sticky.” This
helps prevent clots that can block arteries that
feed the heart or brain.
Researchers are using different tests to identify
people for whom aspirin has little or no effect
on platelets. So far, this work indicates that
- Aspirin fails to affect platelets’ tendency
to clump, or does it only partially, in 5%–40%
of people who take it.
- The body’s response to aspirin can
change over time.
- People who don’t respond to aspirin
have a higher chance of suffering a heart attack
or stroke than those who do.
Why does aspirin act differently in different
people? There are many possible reasons. Some
people have trouble absorbing aspirin from the
digestive tract. Smoking blunts the effect of
aspirin on platelets, as do being overweight
and having high cholesterol or high blood pressure.
Drugs such as ibuprofen can block aspirin from
fitting into a receptor on cell surfaces. And
a variety of genes influence how the body responds
to aspirin.
Testing aspirin’s effectiveness
There are two basic ways to measure how well
aspirin works for an individual. One is a two-day
lab test that measures how much thromboxane is
in the urine. Low thromboxane is a signal that
aspirin is working. The second is an FDA-approved
device called the Ultegra aspirin assay. This
10-minute test uses light to “see” how
quickly platelets in a small sample of blood
begin clumping in response to a chemical signal.
Many doctors either aren’t aware of aspirin
nonresponsiveness or are waiting for more evidence
that it’s real before ordering these tests.
Given its importance in preventing heart attacks,
if you take aspirin it’s not too early
to talk with your doctor about being tested for
aspirin responsiveness. “We are entering
a new era of personalized medicine,” says
Dr. Simon, “and this test is an important
step in that direction.”
Even if aspirin doesn’t fully block your
platelets from clumping, don’t stop
taking it. Aspirin probably works in other
ways besides acting on platelets to prevent heart
attacks. Instead, talk with your doctor about
adding clopidogrel (Plavix), which can complement
or take the place of aspirin.
(This article was first printed in the May
2004 issue of the Harvard Heart Letter.
For more information or to order, please go
to www.health.harvard.edu/heart.)
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