Until last Friday, cardiologists thought they were on the verge of a new frontier in treating heart disease. Three companies were conducting large clinical trials on experimental drugs that slash levels of a blood protein, Lp(a), thought to cause heart attacks and stroke. When Novartis, the first company to complete its trial, announced its results, cardiologists were shocked. The drug could lower Lp(a) levels by 80 percent, but it did not prevent heart attacks and strokes.

“There’s something we don’t understand here,” said Dr. John Alexander, a cardiologist at Duke. About 20 percent of Americans have elevated Lp(a) levels; people with the highest levels can have double or triple the risk of a heart attack. But the failure raised an uncomfortable possibility: Maybe Lp(a) is not a cause but a marker of heart disease risk.

“That is the nagging question we are all pondering,” said Dr. David Maron, president of the American Society for Preventive Cardiology. Some researchers are not ready to discard the hypothesis, suggesting other explanations, such as testing the wrong patients or insufficient lowering. The full data will be presented at the American Heart Association meeting in November.

“We still have a lot to learn,” said Dr. Sadiya Khan of Northwestern University. Dr. Harlan Krumholz of Yale noted that high Lp(a) levels are genetic and fixed, so lowering them in adulthood might be too late.