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It's hard to find anything good to say about angina pectoris, the brief
but often intense chest pain that strikes when the heart muscle is temporarily
deprived of adequate blood and oxygen. This pain is most often due to atherosclerosis,
which narrows the coronary arteries and increases the risk for heart attack.
Not only that, but on a day-to-day basis anginal pain can interfere with
such varied activities as climbing stairs, catching the bus, or making love.
But there is growing evidence that people who have a certain type of angina
in the days or weeks before a heart attack may be better off than those
who have no such warning. A series of studies now suggests that people who
suffer from this condition before a heart attack may respond better to initial
treatment and have less heart muscle damage.
In an editorial in the january 4, 1996, issue of the New England Journal
of Medicine, Harvard cardiologist Eugene Braunwald described how unstable
angina seems to "prepare" the heart for myocardial infarction.
This type of angina is characterized by pain that becomes more frequent
and severe, lasts longer, and is increasingly common at rest.
There are several possible explanations for why people who have pain like
this generally do better than those with "unheralded" heart attacks,
says Braunwald, chief of medicine at Boston's Brigham and Women's Hospital.
The latest answer comes from the same issue of the New England Journal
of Medicine, where British and Italian researchers describe the results
of a study comparing patients who had unstable angina during the week before
their heart attack with those who had no warning signs. All patients were
treated with an intravenous infusion of the clot-buster t-PA (recombinant
tissue plasminogen activator) within six hours after they developed continuous
chest pain. There was a striking difference in reperfusion time,
the mean time for restoring blood flow to the heart. For those with preinfarction
angina it was 27 minutes; it was 48 minutes for those who didn't have pain
beforehand.
When the researchers measured blood levels of enzymes that indicate the
size of the infarct (the killed portion of the heart muscle) they
found that significantly less harm had been done in patients with preinfarction
angina. This was true even when the size of the blockage involved, or the
length of time that the artery had been occluded, did not differ. Although
these results are not definitive, they hint that thrombolytic treatment
may work best in people who experience intermittent chest pain before a
heart attack, whereas mechanically removing the blockage with angioplasty
may be a better approach for patients without preinfarction pain.
Cardiologists have long known that when atherosclerotic deposits partly
block a coronary artery, blood often pushes into smaller vessels in the
same area, using them as a temporary route to the portion of the heart muscle
that would otherwise be starved for oxygen. If this collateral circulation
is sufficiently well developed, it may be able to prevent a heart attack
or contain damage to the heart muscle by providing a detour around the occluded
artery.
One theory about the benefits of unstable angina is that it repeatedly puts
pressure on the collaterals, opening them up and increasing their carrying
capacity before the heart attack happens.
Other researchers speculate that people with preinfarction angina have smaller
heart attacks due to a phenomenon called ischemic preconditioning.
Just as Olympians who trained in hot and humid settings expected to do better
in Atlanta than those who trained in more temperate climates, myocardial
tissue that is accustomed to intermittent shortages of blood and oxygen
may fare better when a heart attack blocks the supply for a longer time.
In a 1995 article in Circulation, Italian researchers compared the
extent of post-infarction damage in a dozen people with unstable angina
and in 13 with no advance symptoms during the 24 hours before a heart attack.
All were treated with t-PA, there was no significant difference in their
reperfusion time, and there was no evidence that blood flow was circumventing
the blockage through collaterals.
Despite these similarities, infarcts were significantly smaller in the patients
who had experienced unstable angina than in those who had not. In experimental
animals, ischemic preconditioning appears to delay cell death in the blood-deprived
portion of the heart muscle; something similar apparently happens in humans
as well.
Another consideration is that many people who have unstable angina immediately
before a heart attack have experienced such symptoms before and routinely
take aspirin, heparin, or other drugs that lessen their risk. Although myocardial
infarctions still happen in these people, their occlusive clots may break
up more easily than blockages in people who haven't been using protective
medications.
In the spectrum of cardiovascular disease, unstable angina lies between
garden-variety angina pectoris and acute myocardial infarction. When episodes
of new chest pain strike and get worse over days or weeks, when old chest
pain changes in frequency or severity, when angina occurs at rest, or when
pain that feels like a heart attack occurs, don't wait: seek immediate medical
attention. A brief stay in the hospital may be needed to pin down the diagnosis,
initiate treatment, and stop disaster in its tracks.