A study that had much of its impetus at the University of Utah Hospital and then expanded into a national effort has discovered that a new drug can save many lives of victims of chronic heart failure.
The drug is carvedilol, and the study results were published in Thursday's edition of the New England Journal of Medicine. One of the principal authors is Dr. Edward M. Gilbert of University Hospital.Carvedilol, developed by the companies SmithKline Beecham and Boehringer Mannheim Corp., reduced the risk of death from the disease during a two-year study by an astonishing 65 percent.
A pilot study of the effects of carvedilol, tested on 60 patients at University Hospital, was published in the Journal of the American College of Cardiology in May 1985. The results showed the drug was beneficial for the heart's pumping action and other symptoms.
Soon, "similar results were confirmed by two other centers, one in Italy and one in New York," Gilbert told the Deseret News Thursday. "That led to the multicenter study," reported in the latest medical article.
In the study, 1,094 patients with chronic heart failure were treated, about 35 of them at University Hospital. Some got carvedilol and others got a harmless placebo (a substitute that did nothing).
"The overall mortality rate was 7.8 percent in the placebo group and 3.2 percent in the carvedilol group; the reduction in risk attributable to carvedilol was 65 percent," says the study.
It was so successful that random testing was halted on Feb. 3, 1995, when it became obvious that carvedilol significantly improved survival. From then on, the drug was used as an accepted treatment.
Carvedilol also reduced the risk of hospitalization for patients who were receiving other treatments.
Gilbert emphasized that nobody was put at risk by the study, which continued from 1993 to February 1995. Giving either carvedilol or a placebo happened only in addition to the patient receiving the best medical therapy available.
"Even with good background therapy, we were able to see a dramatic improvement," he said.
Carvedilol is a beta-blocker, a drug that inhibits the effects of adrenalin and related substances that are excreted by nerves in the heart. The material stimulates heart cells to work harder.
Although the effects of adrenalin will make the patient feel better temporarily as circulation improves, this is somewhat illusory.
"Long-term, this probably leads to damage to the heart," said Gilbert. An analogy that he cited is if a person is driving a "lousy little car" along the freeway in second gear. That might work for a while, but in the long-run, it would burn out the gear.
"There's over 3 million patients in the country with heart failure, and heart failure is a very expensive disease," he said. An estimated $7 billion is spent yearly on hospitalization for heart failure. Reducing the financial toll is important, in addition to the drug's value in lessening suffering and death.
While the Journal of Medicine article doesn't describe this finding, Gilbert said, in four of five ways used to assess patient well-being, carvedilol caused improvements.
In the fifth way tested, called the Minnesota Living with Heart Failure Questionnaire, the results did not show a statistically-significant improvement. But they also did not show any harm.
Areas where carvedilol showed improvements were the patient's ability to do more, having less shortness of breath, a great activity area, and a reduction in condition deterioration.
Only 5 percent of those with carvedilol reported a worsening of overall feelings of well-being, while 15 percent in the placebo reported that kind of downturn.