WASHINGTON — Damping down inflammation in the body appears to be as important for fighting heart disease as lowering cholesterol, according to two new studies that provide the first direct evidence that curbing inflammation can independently protect the heart.

Patients who reduced inflammation were significantly less likely to have their heart disease worsen or to die from a heart attack, even if their cholesterol levels already were low, according to the studies, paid for by drug manufacturers.

The results suggest that doctors should consider routinely monitoring inflammation in the same way they test cholesterol and take steps to reduce inflammation in patients with high levels, especially in those already at high risk, researchers said.

The same steps that lower cholesterol — a healthful diet, exercise, weight loss, quitting smoking and cholesterol-lowering statin drugs — can help reduce inflammation. Researchers also are studying new drugs that may target inflammation specifically.

"For the first time, we have hard clinical evidence that lowering inflammation lowers the risk of heart attack and stroke and cardiovascular disease," said Paul Ridker, a cardiologist at Brigham and Women's Hospital in Boston, who led one of the studies being published in today's New England Journal of Medicine. "The magnitude of the benefit is at least as large as the magnitude of the benefit from cholesterol reduction. This is a radical change in our thinking about heart-disease prevention."

Doctors for years have thought coronary-artery disease occurs primarily when high cholesterol causes fatty buildups called plaques inside the arteries that supply blood to the heart, like clogging a drain. The theory holds that arteries slowly narrow and eventually are blocked, often by a blood clot, causing a heart attack.

But evidence has accumulated that inflammation, a usually beneficial response by the immune system for fighting infections and healing injuries, also plays a key role. Too much inflammation, perhaps from being overweight, having high cholesterol or suffering from a chronic low-level infection, appears to damage the lining of artery walls and contribute to the formation and rupture of plaques.

No one knows how many Americans have excess inflammation, which often produces no symptoms, but doctors can detect it by testing blood levels of a protein called C-reactive protein (CRP), which goes up and down as inflammation rises and falls.

Other researchers called for more study before recommending routine testing and treatment of inflammation based on the findings but said the research provides powerful support for the new way of thinking about heart disease, the nation's top killer.

In the first study, Ridker and his colleagues gave 3,745 patients who had a heart attack or severe chest pain either normal doses of the statin Pravachol or high doses of another statin called Lipitor, and measured their CRP levels.

Statins appear to reduce inflammation, leading scientists to speculate that at least some of their benefit stems from their anti-inflammatory powers. The new studies were aimed at teasing apart their separate effects on cholesterol and inflammation.

Those whose CRP levels dropped the most were the least likely to suffer or die from another heart attack, researchers found. In fact, cutting CRP was just as important as cutting levels of LDL, the so-called bad cholesterol, and those with low CRP levels did better regardless of whether their LDL was high or low. That indicates that CRP was an independent risk factor. Patients with the lowest risk had the lowest levels of LDL and CRP.

The findings may explain why many patients with low cholesterol have heart attacks, Ridker said.

The second study, led by cardiologist Steven Nissen of the Cleveland Clinic, involved 502 patients with heart disease, half of whom received moderate statin therapy while the others received high doses. Researchers then measured their CRP levels. Patients whose CRP levels dropped most had the least progression of heart disease, again independent of cholesterol levels.

"We saw a very, very strong relationship between the degree in reduction in CRP and the degree of disease progression," Nissen said. "It has the same magnitude of effect as LDL but had an additive effect. This is a very compelling finding."

Some other experts agreed.

"This is an amazing vindication of the concept that inflammation is related to atherosclerosis," said Peter Libby, a professor of medicine at Harvard Medical School. "I would change my practice based on these data."

But other researchers said it is too early to recommend routine CRP testing or increasing statin doses specifically to lower CRP.

" ... I think we need more proof," said David Gordon of the National Heart Lung and Blood Institute.

Mark Pepys of London's Royal Free & University College Medical School was more skeptical:

"There's no good evidence that lowering CRP will lower the risk. The evidence is not there that you must measure CRP in everybody and give statins to people with normal cholesterol. There's just no evidence for that."

The studies were paid for by Bristol-Myers Squibb, which makes Pravachol, and Pfizer, which makes Lipitor.