The State of the Heart

By Alice Park

As recently as five years ago, doctors thought they had a pretty clear picture of what causes a heart attack. They saw it as a plumbing problem: too much fat in the diet builds up in the blood vessels that feed the heart, creating stoppages that starve the heart of oxygen. It was an elegant model and one that patients could understand. But it's not that simple. Cholesterol, it turns out, is just the starting point of a cascade of interlocking events. Underlying the new research presented at the American Heart Association meeting last week was a clear message: this isn't your father's heart disease anymore.

INFLAMMATION

For years now, heart doctors have urged their patients to reduce the fat in their diet. But half of all heart attacks in the U.S. occur in people with normal cholesterol levels. Cardiologists knew something other than cholesterol was involved in heart disease; they just didn't know what.

Now some of the other candidates have begun to emerge. One of the most important is inflammation. It appears that the same all-out war that the body's immune system launches against the joints in arthritis may also be waged in the blood vessels of the heart. No one knows exactly what sets off the immune system in heart patients; it could be fatty deposits or bacteria or the toxins in cigarette smoke or even the physical strain caused by high blood pressure. But once the immune system locks on a target, it attacks relentlessly. White blood cells, clotting factors and a host of other soldiers of the body's defense system swarm in and begin to pile up inside the vessel wall, forming plaques. The most dangerous plaques are those prone to rupture; the explosive release of clotting factors and other cells into the blood can cause a heart attack.

So much for the theory. What was stirring excitement among heart specialists last week is that they now have a reliable way to track and measure the inflammation process. C-reactive protein (CRP), produced wherever there is inflammation, is consistently high in the blood of people who go on to have a heart attack. The latest data show that those with low levels of "bad" cholesterol (LDL) but high levels of CRP, as measured by a new supersensitive test, suffered the same rate of heart attacks as those with high levels of LDL and low CRP. "CRP testing should by no means replace cholesterol testing," says Dr. Paul Ridker of Brigham and Women's Hospital and a pioneer in the CRP field. "Lipids tell us how much plaque has built up in an artery, and CRP tells us how likely that plaque is to rupture and cause a heart attack."

The good news for patients is that doctors have some powerful medications to keep inflammation in check. Aspirin, for one, may protect against heart disease not only by keeping clots from forming but also by controlling inflammation. And the newest studies show that even some of the statin drugs, such as pravastatin (Pravachol) and lovastatin (Mevacor), which do such a good job of lowering cholesterol, are good for bringing down CRP levels as well.

MORE ON STATINS

Statins were much in the news last week. They are so successful in preventing heart attacks that researchers are furiously investigating all the other things these drugs might be doing for the heart besides lowering cholesterol levels. It turns out that the noncholesterol effects of statins, such as controlling clotting and inflammation, may be as important as the cholesterol effects. In a study of patients given atorvastatin (Lipitor) as soon as they arrived at a hospital complaining of chest pain, it was found that those who took the drug for four weeks after their cardiac event were significantly less likely to be rehospitalized or feel increased chest pains than patients who did not take the statin. However, another study that looked at the effect of a different statin taken immediately after a heart attack showed no benefit in giving early treatment. Apparently not all statins are alike, at least in terms of protecting patients in emergency care.

TO BE OR NOT TO BE

Folic acid, already known to prevent certain types of birth defects, is emerging as the leader of the vitamin pack in protecting against heart disease. A member of the B-vitamin family, folic acid lowers levels of homocysteine, an amino acid that has been linked to greater risk of heart disease. While scientists are still trying to explain why--it may have something to do with homocysteine's tendency to promote blood clots and eat away the lining of blood-vessel walls--the newest research suggests that taking more folic acid can lower homocysteine levels and reduce the risk of coronary disease by half.

Meanwhile, an English study reports that it may take about twice the current U.S. Dietary Reference Intake of folic acid--in other words, 0.8 mg a day--to lower homocysteine levels enough to ward off a heart attack.

SEEING IS BELIEVING

Until quite recently, most cardiologists put little value on pictures of the heart. They assumed that it was impossible to get a truly accurate image of an organ in constant motion. But with improvement in the technology for snapping freeze-frames of the beating heart, physicians have started to rely more and more on images of the heart not just for looking at problem areas but also for predicting the likelihood of future heart trouble.

The whizziest new device, an ultrafast form of computer scanning called electron-beam computer tomography (EBCT), picks up the presence of tiny deposits of calcium in the heart. One study based on the scan showed that patients who build up 20% or more calcium each year have an 18-fold greater chance of suffering a heart attack than those with less calcium in their hearts.

Although it is not yet clear whether calcium deposits spotted by EBCT can accurately predict who will go on to have a heart attack, at the very least it's one more test that cardiologists can use to decide how aggressively to treat a patient who is at risk.