The State of the Heart

Monday, Nov. 27, 2000 By ALICE PARK

Article Tools

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.