New Study Finds Inflammation a Bad Actor

Key protein puts those with valve disease at risk

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By
HealthDay Reporter

WEDNESDAY, Jan. 21, 2004 (HealthDayNews) -- Aortic valve disease has long been linked to an increased incidence of heart attacks and death from cardiovascular disease, but a new study says inflammation may really be the culprit.

While the study found people with aortic sclerosis -- a narrowing of the aortic valve in the heart that can lead to aortic stenosis -- were more than twice as likely to suffer a heart attack or to die, the authors believe aortic disease alone isn't to blame. Instead, a history of coronary artery disease or other heart disease, high levels of the inflammation marker C-reactive protein (CRP), and age were the highest risk factors for heart attack and death.

"In the past, aortic sclerosis was always associated with worse outcomes, but no one understood why," says study co-author Dr. William O'Neill, corporate chief of cardiology for Beaumont Hospital System in Royal Oak, Mich. "What we found was that when we measure CRP, those with the highest levels were the one with the worst outcomes."

O'Neill says these results suggest that anyone with aortic sclerosis should be screened for CRP and should actively try to reduce inflammation and cholesterol levels.

The findings appear in the Jan. 21 issue of the Journal of the American College of Cardiology.

For the study, O'Neill and his colleagues followed 425 people who had been treated in the emergency room at William Beaumont Hospital for chest pain. The average age of the study participants was 68, 54 percent were male, and 84 percent were white.

All of the patients were given electrocardiograms (ECG) and cardiac enzyme tests. They also had echocardiography, which is an ultrasound of the heart, to determine if they had aortic sclerosis. No one with aortic stenosis, a more severe narrowing of the aortic valve, was included in the study.

Forty-nine percent of the study participants had some degree of aortic sclerosis. The researchers found that people with aortic sclerosis were much more likely than people without the valve disease to have a heart attack or die in the year following the study -- 16.8 percent vs. 7.1 percent.

But, according to the study findings, having aortic sclerosis alone was not an independent predictor of a heart attack or death. What did affect the risk, according to the study, was a history of coronary artery disease, having had a heart attack at the start of the study, high levels of CRP, a history of congestive heart failure, and advanced age.

In an accompanying editorial in the same journal, Dr. Catherine Otto from the University of Washington in Seattle says other factors besides inflammation explain why people with aortic sclerosis have a higher risk for cardiovascular problems.

Dr. Dan Fisher, a cardiologist from New York University Medical Center, agrees. "We still have a lot to learn. CRP is a predictor of bad events, but we don't know if inflammation is part of the disease process or if it's merely a marker."

Fisher also points out there is a selection bias in this study because only people who came to the hospital with chest pain were studied.

O'Neill says there may well be other factors that contribute to heart disease. But he suggests CRP levels be monitored in people with aortic sclerosis because those with the highest levels were most likely to have problems.

"We had almost a 40 percent event rate for people with aortic sclerosis and a high level of CRP," says O'Neill.

More information

To learn more about how your heart works, got to the American Heart Association. For more information on aortic stenosis, a condition that can be caused by aortic sclerosis, visit the National Library of Medicine.

SOURCES: William O'Neill, M.D., corporate chief, cardiology, Beaumont Hospital System, Royal Oak, Mich.; Dan Fisher, M.D., cardiologist, New York University Medical Center, and clinical assistant professor, medicine, division of cardiology, New York University School of Medicine, New York City; Jan. 21, 2004, Journal of the American College of Cardiology

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