Health
Lowering CRP reduces second heart attack risk
■ Statin drugs can lower cardiovascular disease risk by reducing inflammation as well as cholesterol levels.
By Victoria Stagg Elliott — Posted Jan. 31, 2005
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Physicians should consider monitoring C-reactive protein as well as cholesterol levels in patients who have already experienced a cardiovascular event and are taking statin drugs to prevent a subsequent one, according to the authors of two studies in the Jan. 6 New England Journal of Medicine.
"Strategies to lower cardiovascular risk with statins should include monitoring CRP as well as cholesterol," wrote researchers from Brigham and Women's Hospital in Boston.
That study concluded that patients with low CRP levels had better outcomes than those with higher levels, regardless of the cholesterol numbers.
The second study, conducted by researchers at the Cleveland Clinic, found that patients who reduced both cholesterol and CRP levels with statin therapy did better than those who only reduced one factor or the other. CRP was also independently associated with progression of disease.
Testing CRP levels has long been debated as a possible strategy for monitoring heart disease risk. Most guidelines, however, recommend against its populationwide use.
In primary prevention situations, physicians do use it to determine strategies for those who are at moderate risk. But integration into medical care has been hampered by a lack of evidence delineating effective strategies for lowering CRP levels as well as a deficiency of studies supporting the idea that lowering it is beneficial.
"Although we have known for several years that elevated CRP was a risk factor for heart disease, until now we did not have evidence that targeting CRP could reduce disease burden," said Steven Nissen, MD, lead author for the Cleveland Clinic study and vice chair of the clinic's department of cardiovascular medicine. "These two trials strongly suggest that we should target statin therapy at reducing CRP, not just cholesterol."
An accompanying editorial suggested that these studies could lead to therapies that more directly target the inflammation associated with cardiovascular disease.