New drug shows promise for saving lives from heart failure

November 09, 1999

ATLANTA, Nov. 10 -- A new drug for heart failure saves lives and reduces symptoms, according to a study presented today at the American Heart Association Scientific Sessions.

The new drug, called omapatrilat, is a member of a new class of compounds called vasopeptidase inhibitors.

The results of this study, combined with others, suggest that the use of omapatrilat may reduce deaths and hospitalizations from congestive heart failure by as much as 30 percent, says Jean-Lucien Rouleau, M.D., director of cardiology, Mount Sinai Hospital Association at the University Health Network of Toronto, Canada. "It's a potential breakthrough in the treatment of congestive heart failure."

Congestive heart failure is a condition in which the heart can't pump enough blood to meet the needs of other organs in the body. It occurs in hearts that are damaged or overworked after a heart attack, high blood pressure, heart valve disease, congenital defects or infection of the heart or its valves. Drugs used to treat heart failure include digitalis, which increases the heart's pumping action; diuretics, which help eliminate the buildup of fluid in the body's tissues; and vasodilators, which expand blood vessels, allowing blood to flow more easily and making the heart's work easier and more efficient.

Among the vasodilators is a class of drugs know as angiotensin converting enzyme (ACE) inhibitors, which interfere with the body's production of angiotensin, a chemical that causes arteries to constrict.

The problem with ACE inhibitors, according to Rouleau, is that they do not work on all substances in the body that promote abnormal constriction of arteries, which is characteristic of heart failure.

The new drug works in two ways. Like conventional ACE inhibitors, it blocks the action of angiotensin, inhibiting the constrictive action of this substance. But omapatrilat also neutralizes a substance called neutral endopeptidase, resulting in blood vessels relaxing.

"Omapatrilat is the first drug in this class and it may be better than the ACE-inhibitor class," says Rouleau. "It may end up replacing ACE inhibitors because it's an ACE inhibitor plus."

In the study, 289 patients received 40 mg of omapatrilat daily and 284 received 20 mg of lisinopril, an ACE inhibitor, for 24 weeks. The patients' average age was 64 years and 79 percent were male. All had mild to moderate congestive heart failure.

After 12 weeks of therapy, the patients' performance on treadmill tests, a test to measure heart function, improved similarly in both treatment groups. Measurements of cardiovascular and overall clinical function also improved. Side effects were minimal and included diarrhea and mild dizziness. But improvement was also seen in death rates and hospitalization for worsening heart failure. Only 16 patients in the omapatrilat group experienced any of these adverse events, while 29 did in the lisinopril group.

Rouleau says the study is encouraging because although a number of treatments for congestive heart failure have been developed, "death is still very high." The condition kills over 44,000 annually.

A new study of omapatrilat, OVERTURE (Omapatrilat versus enalapril randomized trial of utility in reducing event), has already started. Coordinated at the Columbia College of Physicians and Surgeons in New York, it will enroll 4,420 patients.

In addition to drug treatment, patients with congestive heart failure are urged to reduce salt consumption, eat a diet low in saturated fat and high in fruits and vegetables, and, exercise if they are able.

Co-authors are Marc A. Pfeffer, M.D., Ph.D.,Brigham and Women's Hospital, Boston; Duncan J.Stewart, M.D., St. Michael's Hospital, Toronto, Canada; Edmund K. Kerut, Heart Clinic of Louisiana Marrero; Charles B. Porter, M..D., Mid-American Cardiology Association, Kansas City, Mo; John O. Parker, Kingston General Hospital, Kingston, Canada; L. Kent Smith, The Arizona Heart Institute, Phoenix; Guy Prouix, Hospital Laval, Ste-Foy, Canada; and Chunlin Qian, Alan J. Block, Bristol-Meyers Squibb Pharmaceutical Research Institute, Princeton, N.J.
-end-
Media advisory: Dr. Rouleau can be reached at 416-340-3967 (Please do not publish number).

American Heart Association

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