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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.