In the first study, Ridker and his colleagues gave 3,745 patients who had already suffered 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.
The widely used 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.
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Those whose CRP levels dropped the lowest were the least likely to suffer or die from another heart attack, the researchers found. In fact, cutting CRP was just as important as cutting levels of LDL cholesterol, 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, the researchers said. The patients with the lowest risk had the lowest levels of both LDL and CRP.
The findings may explain why many patients with low cholesterol still suffer heart attacks, Ridker said.
"These data provide overwhelming confirmation for the role inflammation plays in heart disease independent of cholesterol," he said. "It's no longer enough to simply monitor cholesterol. If we want to do the best for our patients, we now need to measure both cholesterol and CRP."
The second study, led by cardiologist Steven E. Nissen of the Cleveland Clinic, involved 502 patients with heart disease, half of whom received moderate statin therapy while the other half got high doses. The researchers then examined the inside of their arteries with a special ultrasound technique and measured their CRP levels. The patients whose CRP levels dropped the most had the least progression of their 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 of 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.
"The paradigm is shifting, but it doesn't shift overnight. I think we need more proof," said David Gordon of the National Heart, Lung, and Blood Institute.
Mark Pepys of the Royal Free & University College Medical School in London 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 being reported today were funded by Bristol-Myers Squibb, which makes Pravachol, and Pfizer Inc., which makes Lipitor.