You know that lowering “bad” cholesterol reduces your risk of heart disease. But have you heard that lowering inflammation might be just as important? Since 1999, researchers at Carolina’s Comprehensive Center for Inflammatory Disorders have been studying whether there is a link between heart disease and inflammation such as gum disease (see Endeavors, Winter 2004, “Disease that Invades from the Mouth.”)
Now two new studies published in the January 2005 issue of the New England Journal of Medicine have established a link. “These studies provide information about the role of inflammation and its predictive value in cardiovascular events,” says Sidney Smith, professor of medicine and coinvestigator on one study and member of the steering committee on the other.
Inflammation is your body’s response to injury. And while this self-protective mechanism is generally good, doctors have recognized for some time that inflammation has a down side. The buildup of cholesterol in the blood vessels — commonly seen in the development of heart disease — also provokes an inflammatory response. It’s the body’s misguided attempt to get rid of the buildup. But instead, this inflammation leads to blood clots, which occur in association with a splitting of the buildup. These clots can block the blood vessel and cause a heart attack. And worse, because the blood vessels become clogged up slowly, the inflammation can become chronic, which can contribute to narrowing and hardening of the blood vessels — atherosclerosis — and angina.
While the link between inflammation and heart disease is not fully understood, one protein has been slowly emerging as a key player: C-reactive protein (CRP).
So the first study measured LDL — “bad” cholesterol — as well as CRP, and related it to risk of a cardiovascular event. Patients who had had a heart attack or who had unstable angina were randomly assigned to one of two doses of statin therapy: high or low.
The low dose of statin was given to decrease LDL to one hundred, the level recommended by the American Heart Association. The higher statin dose aimed to lower LDL to seventy. Smith says this “is similar to what is seen in some parts of rural China where the incidence of heart disease is still relatively low.”
Patients who had an LDL level of seventy did much better than those who had lowered their cholesterol to only one hundred — the level the current guidelines recommend.
When the researchers looked at CRP levels, things really got interesting. “We learned that the best results were seen in patients who not only had their cholesterol level below seventy, but who also had a CRP that was low,” Smith says. “That is, their inflammatory activity was reduced.”
In patients who had lowered either LDL or CRP, but not both, the risk of suffering a further heart attack was about the same. This suggests that measuring inflammation may provide additional information about predicting your risk of heart attack.
The second study was designed to directly investigate the progression of heart disease by using ultrasound to measure plaque buildup in patients’ blood vessels. As in the first study, patients were randomized to either high or low doses of statins, and their LDL and CRP were measured. What the researchers saw was a significant correlation between the lowest LDL and CRP levels and the least plaque buildup and slowest progression of disease.
But before we all rush out and get our CRP levels checked, the researchers point out that there are still bits of the puzzle missing. They don’t know whether CRP serves simply as a marker of inflammation, or actually causes disease. So further studies are under way to demonstrate whether treatment based on CRP levels will improve the current care for patients with coronary heart disease.
But the good news is that a lower CRP level correlates with improved patient outcomes. And while increasing statin therapy is one way to reduce CRP, there are many other ways to do it that will not come as a surprise: stop smoking, lose weight, and exercise.
