The Cholesterol Paradox

Study finds higher levels may actually help heart failure patients

TUESDAY, Dec. 2, 2003 (HealthDayNews) -- A new study turns common sense on its head by suggesting high cholesterol levels may actually help people with heart failure.

Despite the fact that high blood cholesterol has been linked to increased risk for ailments such as coronary vascular disease and blocked arteries, especially in combination with other risk factors, the finding that higher levels may help this group have researchers scratching their heads.

"On the face of it, the result seems quite surprising, given the strong association between cholesterol and vascular disease. However, we have been developing for some time the notion that heart failure is a metabolically stressful illness," says Dr. Andrew L. Clark of Castle Hill Hospital and the University of Hull in England. Clark is co-author of the study, which appears in the Dec. 3 issue of the Journal of the American College of Cardiology.

"A high cholesterol level can be seen as good in that it indicates a greater reserve to deal with metabolic stresses. And this is supported by some of the other studies. . . showing a greater survival with increasing body weight in heart failure and following heart surgery," Clark adds.

Researchers from Castle Hill Hospital, along with colleagues in London and Berlin, studied 417 patients with chronic heart failure and found the chance of survival increased 25 percent for each 39-milligram-per-deciliter (mg/dl) increment in total cholesterol.

On average, patients with a total cholesterol level of 232 mg/dl had a 25 percent higher survival rate than heart failure patients with a total cholesterol level of 193 mg/dl. Experts say a total cholesterol figure under 200 mg/dl is desirable.

Although the results of this study go against the usual "lower cholesterol is better" advice, they reinforce findings in several previous studies that linked lower cholesterol with poorer prognosis in heart failure patients, the study says.

Clark says two hypotheses may explain the paradoxical relationship.

"Lipoproteins are good at absorbing bacterial endotoxin. An intriguing notion is that the reason for the immune system activation seen in heart failure patients is related to bowel wall edema, allowing bacterial translocation into the body. It may be that lipoproteins mediate a beneficial effect by mopping up any bacterial proteins before they cause immune system activation," he says. "I tend to like the lipoprotein idea."

But he cautions on the use of cholesterol-lower statins for chronic heart failure patients.

"If [health professionals] are using cholesterol-lowering statins, they are doing that without evidence that what they are doing is correct. What we say to them is get those patients, those with chronic heart failure, to clinical trials so it can be studied further," Clark says.

However, some caution that lower cholesterol may not necessarily be the cause of the higher mortality in heart failure patients, but may be a indicator of other factors that might be linked.

Dr. Robert Doughty, a research fellow at the University of Auckland in New Zealand, who was not connected with the study but reviewed the data, emphasized the results cannot determine that low cholesterol was the cause of worse outcomes in the heart failure patients.

"We have to be careful about this data. Don't get me wrong, and it is very interesting data," Doughty says. "But we should not automatically extrapolate this group of patients who may be at the endgame of their disease, and don't forget -- chronic heart failure patients are at the end stages of their disease."

"Just because there is association doesn't mean there is causality. This study is important, but there is more work needed to be done for that group which has progressed further along with heart failure due to coronary heart disease," he adds.

More information

Get the lowdown on cholesterol figures from the National Heart, Lung and Blood Institute. The American Heart Association has a primer on heart failure.

SOURCES: Andrew L. Clark, M.D., Department of Academic Cardiology, University of Hull, Hull, England; Robert Doughty, M.D., research fellow, University of Auckland, New Zealand; Dec. 3, 2003, Journal of the American College of Cardiology
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