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BOSTON – An experimental drug has shown a striking efficacy in prolonging the lives of people with heart failure and could replace what has been the bedrock treatment for more than 20 years, researchers said Saturday.

The drug, which is being developed by the Swiss company Novartis, reduced both the risk of dying from cardiovascular causes and the risk of being hospitalized for worsening heart failure by about 20 percent in a large clinical trial.

“I think that when physicians see these data, they will find it compelling, and what we will see is a paradigm shift,” said Dr. Milton Packer, a professor of clinical sciences at the University of Texas Southwestern Medical Center in Dallas and one of the two principal investigators in the study.

The results are being presented at the European Society of Cardiology congress in Barcelona, Spain, this weekend and were published Saturday by the New England Journal of Medicine.

Heart failure is a disease in which the heart cannot pump enough blood to the body’s organs, resulting in shortness of breath, fatigue and retention of fluids. It can be caused by a heart attack, uncontrolled hypertension or other problems.

Some 5 million to 6 million Americans, and an estimated 26 million people globally, have heart failure, and it is the leading cause of hospitalization in the United States and Europe, according to a recent paper in the Journal of the American College of Cardiology. Many patients die within a few years of diagnosis.

Some doctors not involved in the study agreed the results were compelling.

“They are not just positive, they are remarkably positive and positive in every dimension,” said Dr. Clyde W. Yancy, chief of the cardiology division at Northwestern University’s Feinberg School of Medicine. “Patients with heart failure are eager, if not desperate to have better options.”

Novartis executives say the company will file for approval of the drug, known by the code name LCZ696, in the United States by the end of the year and in Europe in the first quarter of 2015. That means the drug could get to patients as early as next year.

Novartis had announced in March that the study was being ended early because the drug had been better than the comparator drug. But until Saturday, it was not known exactly how much better.

That is important not only for doctors but also for Wall Street analysts, who are trying to predict the drug’s future sales, expected to be billions of dollars annually.

As a proprietary drug, LCZ696 is likely to be expensive. Existing drugs are generic, and insurers might balk at paying for the new drug unless the evidence that it is more effective is compelling.

The study, sponsored by Novartis, involved more than 8,400 patients in 47 countries who were randomized to receive either LCZ696 or enalapril, one of a class of drugs called ACE inhibitors that have been the standard treatment for heart failure.

More than 90 percent of the patients in both arms of the trial also used a drug called a beta blocker, and many used other drugs, as their doctors saw fit. Some also had implanted defibrillators.

The patients were followed for a median of 27 months before the trial was stopped. By that point, 21.8 percent of those who received LCZ696 had died from a cardiovascular cause or had been hospitalized for worsening heart failure. That figure was 26.5 percent for those receiving enalapril. That represents a 20 percent relative reduction in risk using a statistical measure called the hazard ratio.

There was a 20 percent relative risk reduction for cardiovascular death alone, and a 21 percent reduction for first hospitalization for heart failure. About 17 percent of patients getting LCZ696 died from any cause, compared to 19.8 percent of those in the control group, a relative risk reduction of 16 percent. About 32 patients had to be treated with LCZ696 to prevent one death.

LCZ696 was relatively well tolerated, though patients who clearly could not tolerate the specified doses of either LCZ696 or enalapril were eliminated from the trial in advance. LCZ696 caused more hypotension, or too-low blood pressure, than enalapril but fewer kidney problems.

Dr. Marc A. Pfeffer, a cardiologist at Brigham & Women’s Hospital and Harvard Medical School who was not involved in the trial but has done research funded by Novartis, said it was impressive that LCZ696 could improve on existing therapy.

“It really is an advance, and we haven’t had one in a long time because the bar really is high,” he said.

Yancy of Northwestern said one caution was that only about 5 percent of patients in the study were of African descent, even though in the United States blacks suffer disproportionately from heart failure.

He said that about a decade ago, Bristol-Myers Squibb gave up on a drug somewhat similar to LCZ696 in part because it caused a serious side effect called angioedema, mainly in African-Americans. He said, however, that LCZ696 does not seem to pose that risk.

LCZ696 is a combination of two drugs. One is valsartan, the blockbuster heart drug that Novartis sells as Diovan. It is an angiotensin receptor blocker, a drug that acts somewhat like an ACE inhibitor in relaxing blood vessels. The other component is an inhibitor of an enzyme called neprilysin.

Novartis could use a hit to help compensate for declining sales of Diovan, which has lost patent protection. A success with LCZ696, which is for chronic heart failure, would help offset the recent failure of the company to win regulatory approval for serelaxin, a drug for acute heart failure.