Heart failure generally results from a weakening of the heart muscle so that the heart can no longer pump enough blood to supply the body's needs. The disease be caused by a heart attack, high blood pressure or it can be inherited. Often, the cause is unknown.
The OPTIMIZER II is an implantable device, similar in size and shape to an artificial heart pacemaker, but that's where the similarity ends. An artificial pacemaker makes sure the heartbeat doesn't go too slow by initiating contractions when there's a missed beat. In contrast, the OPTIMIZER II senses when a beat has already started, then sends an electrical signal to strengthen the heart's contraction.
Last year, the U.S. Food and Drug Administration approved devices that deliver a different form of heart failure treatment called "cardiac resychronization therapy," or CRT, for treating a subgroup of patients with heart failure, said Daniel Burkhoff, M.D., Ph.D., a co-author of the report and a consultant to the maker of OPTIMIZER II.
"CRT appears to be useful in about 20 percent to 30 percent of people with heart failure who also have an abnormality in the timing heart chamber contractractions," said Burkhoff, an associate professor of medicine at Columbia University's College of Physicians and Surgeons in New York City.
"Our goal is to develop a treatment for the greater number of heart failure patients who don't necessarily have a problem with synchrony," he said.
The researchers enrolled 25 patients with moderately severe heart failure from medical centers in Austria, Germany and Italy. Their average age was 62 years, and 23 were men. To be eligible for the study, patients had to have a heart ejection fraction of less than 35 percent. Ejection fraction is the percentage of blood the heart expels during contractions. A normal ejection fraction is 60 percent, Burkhoff said.
Also, the patients had poor exercise tolerance; they could only walk short distances before becoming fatigued.
During the implantation procedure, which is similar to implanting a pacemaker, physicians tested the device to ensure that the patient's heart responded to the special signals the device delivered. Two patients did not respond, so the device was not implanted.
In the other 23 patients, the device was activated three hours a day for eight weeks. The patients returned periodically for tests.
At the end of the follow-up period, the patients' ejection fraction increased from an average of 22 percent to 28 percent, a statistically significant improvement.
"This improvement is comparable to those seen in prior studies of CRT. This encouraged us that the ultimate impact on patients' quality of life would also be similar to that achieved with CRT, with the hope that this treatment will be applicable to a larger percentage of the heart-failure population," Burkhoff said.
Indeed, the average distance patients could walk in six minutes increased from 411 meters to 465 meters (1,348 to 1,526 feet), also a statistically significant improvement. And participants reported that they had a better quality of life.
All the patients received appropriate medical treatment prior to enrolling in the trial, including beta-blockers, and continued to get treatment during the study, he said.
"The adverse events observed thus far seem to be similar to those encountered in patients with advanced heart failure and from normal pacemaker procedures," Burkhoff said.
"This is a very small study designed primarily to obtain some basic safety data, and in this regard the results are very encouraging. We are also encouraged by the efficacy findings, but we emphasize that this is merely a pilot study, and that patients knew they had gotten the device. Therefore, the efficacy findings could be influenced by a placebo effect," he said.
The team is now preparing a much larger trial of the device. Burkhoff and his colleagues have proposed that a large-scale patient trial be conducted primarily in the United States.
Some 550,000 new cases of heart failure are diagnosed each year and 51,500 people die from it annually, according to the American Heart Association.
"It is a very complex and long path to develop treatments for heart failure," said Burkhoff.
Co-authors are Guenter Stix, M.D.; Michael Wolzt, M.D.; Gabriele Vicedomini, M.D.; Salvatore Rosanio, M.D.; Martin Borggrefe, M.D.; Christian Wolpert, M.D.; Gerhard Hindricks, M.D.; Hans Kottkamp, M.D.; Dieter Horstkottre, M.D.; Barbara Lamp, M.D.; Dirk Böcker, M.D.; Thomas Wichter, M.D.; Yuval Mika, M.D.; Shlomo Ben-Haim, M.D. and Herwig Schmidinger, M.D.