Inflammatory findings
Gerald Thornell was 64 years old, with no family history of heart disease, good cholesterol and blood pressure numbers, and normal weight. He'd never smoked, was an avid runner, and had been taking half an aspirin a day for 10 years. Yet the Marion, Mass., college professor had a heart attack a few days before Thanksgiving. Christopher Cannon, his cardiologist at Brigham and Women's Hospital in Boston, blames inflammation.
Cannon is a coauthor of one of a pair of studies in the latest New England Journal of Medicine that make a case for tracking not only LDL (bad) and HDL (good) cholesterol in known and potential heart patients but also their C-reactive protein. Elevated CRP is a signal of inflammation, which most heart experts now agree is involved in coronary artery disease. Cannon, who first saw Thornell after his heart attack, notes that late in 2003 his CRP was 2.7 milligrams per liter. A safe blood level of CRP is considered to be below 1 mg/L; 3 mg/L and above is deemed risky. Thornell, says Cannon, "was doing all the right things, and he still had elevated CRP--so inflammation may literally have been the cause of his heart attack."
Statin drugs reduce heart attack risk by lowering LDL cholesterol. They also cut CRP. After mining data from two of their previously published clinical trials, Brigham and Women's cardiologist Paul Ridker and Cleveland Clinic cardiologist Steven Nissen, lead authors of the two new studies, concluded that reducing CRP is as important for patients with heart disease as is lowering their LDL.
Ridker's prior trial had tested two statins--a high dose of Lipitor and a moderate dose of Pravachol--on the rate of future heart attacks in patients who had already had one or who had severe chest pain. Lipitor yielded benefits so unexpectedly large that Ridker thought another explanation besides LDL was possible. Using an ultrasound device, Nissen's team had directly revealed that high-dose Lipitor in patients with heart disease stopped or shrank the fatty plaque building up in their coronary arteries; a moderate dose of Pravachol slowed the buildup but did not halt or reverse it. Nissen, too, was seeking a reason besides LDL.
They contend it is CRP. Ridker's new findings show that over a 2 1/2-year period, patients who achieved both low LDL (under 70 milligrams per deciliter) as well as low CRP (below 2 mg/L) did far better than patients who met one goal but not the other. And Nissen's data showed that plaque receded only when both CRP and LDL were slashed.
Get tough. Ridker says doctors should be far more aggressive in prescribing statins for heart attack patients and in dosing based on CRP as well as LDL. "The vast majority of patients on statins are on a very small dose," says Ridker. "Physicians are very conservative." Following his advice, he says, would save tens of thousands of lives. "I used to be a CRP skeptic," says Nissen. "I was wrong."
Not everyone considers the two studies a launching pad for a CRP initiative. David Siscovick, codirector of the cardiovascular health research unit at University of Washington Medical School, calls the conclusions a "small step," coming from after-the-fact analysis of previous work done for other reasons, not from a direct test of CRP as an independent risk factor. Siscovick also notes that both Ridker and Nissen receive funds from statin manufacturers and that Ridker is a coinventor of a laboratory process related to CRP measurement.
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