WEDNESDAY, Nov. 7 (HealthDay News) -- Exercise boosts the number of progenitor cells in people with heart failure, and those cells in turn repair and rebuild weakened muscle and blood vessels, researchers report.

According to two studies that were to be presented Wednesday at the American Heart Association annual meeting in Orlando, Fla., that response can dramatically enhance patients' ability to move and work out.

"Both studies point to the beneficial effect of exercise on patients with heart failure," said Dr. Sidney Smith, past president of the American Heart Association and director of the Center for Cardiovascular Science and Medicine at the University of North Carolina School of Medicine.

"These observations provide some understanding into the mechanisms which [make exercise helpful]," Smith said.

More than 5 million people in the United States have heart failure, a condition that affects the heart's ability to pump blood throughout the body.

However, researchers are beginning to understand that heart failure woes come not only from this pumping disorder but from changes in the legs and other parts of the body.

"The muscle of the leg starts to shrink, so there is less muscle mass," explained Dr. Axel Linke, a co-author on both studies and assistant professor of medicine at the University of Leipzig in Germany. "The endothelium and the vessels supplying blood to the muscles deteriorate, so they are less flexible, elasticity is reduced," he said. The endothelium is a layer of cells that lines blood vessels.

However, exercise opens up the vessels and improves their flexibility and elasticity.

In the first study, investigators looked at whether exercise training could activate progenitor cells -- immature cells that can divide into other cells and help repair tissue.

Fifty men with moderate-to-severe heart failure were randomized to receive either six months of exercise training under the supervision of a physician, or to be sent to a control group that remained inactive.

Exercise consisted of riding a stationary bicycle at least 30 minutes a day (usually in two sessions).

At the end of six months, biopsies of the patients' thigh quadriceps revealed that the number of progenitor cells in the exercise group increased by 109 percent, progenitor cells turning into muscle cells increased by 166 percent, and progenitor cells actively dividing to form new cells and repair damage to the muscle increased sixfold.

For the second study, 37 men with severe heart failure were randomly assigned to receive three months of exercise or to remain inactive.

The exercisers experienced dramatic changes: Circulating progenitor cells increased 47 percent, progenitor cells beginning to mature into endothelial cells increased almost 200 percent, and the density of capillaries in skeletal tissue increased 17 percent. There were no changes in the control group.

When they began, the exercising patients had peak oxygen uptake in the range of other patients needing heart transplants. But regular exercise was linked to an average 35 percent increase in exercise capacity, giving the men about 75 percent of the capacity seen in healthy people of the same age.

"Your heart is like an engine with six cylinders, and when we started the exercise program in those patients, about 3.5 cylinders were just not working," Linke explained. "After three to six months of exercise training, two of the cylinders started working again."

"It's a tremendous improvement, and no medication is able to do it," he noted.

But patients with heart failure should only embark on an exercise regimen under the supervision of a physician, Linke added.

"We recommend exercise once a day for up to 20 minutes five days a week for patients with heart failure, but clearly an exercise program should be initiated in in-hospital conditions or an outpatient setting, because you never know how an individual patient might react to initiation of a training program," he explained.

More information

For more on exercise and fitness, head to the American Heart Association  .

WEDNESDAY, Nov. 7 (HealthDay News) -- Brain development is delayed in babies born with certain heart defects, new research shows.

The slowdown in brain development is similar to the delay found in premature infants, the researchers added.

Babies who require heart surgery have long been known to experience developmental delays, but whether the delays were due to the surgery or other factors has been in debate.

Now, a study published in the Nov. 8 issue of the New England Journal of Medicine shows that these brain abnormalities exist before the surgery.

"This is one of the first studies to say they have a true difference [in brain development] before they have surgery," says pediatric cardiologist Vidu Garg, assistant professor of pediatrics and molecular biology at the University of Texas Southwestern Medical Center and a pediatric cardiologist at Children's Medical Center, Dallas.

"It's been known that kids don't do well after open heart surgery. The relationship between congenital heart defects and brain development has not been known but has been hypothesized," said Garg, who was not involved in the study.

According to the U.S. National Institutes of Health, congenital heart defects cause more deaths among newborns than any other birth defects. Slightly less than one percent of American babies, or about 35,000 annually, have a congenital heart defect, according to the American Heart Association.

In the study, a team from the University of California, San Francisco, and at the University of British Columbia, Vancouver, examined 41 infants born with congenital heart disease. Twenty-nine had transposition of the great arteries and 12 had single-ventricle physiology. The researchers used magnetic resonance imaging (MRI) to analyze measures of brain development in each infant, including diffusivity and white-matter tracts.

White matter is the tissue through which nerve cells in the brain and nervous system communicate. Although the babies in the study had the same amount of white matter as babies without heart defects, the white matter was less mature and therefore at greater risk of injury, due to stressors like reduced blood oxygen levels. White-matter injury was observed in 13 of the 41 infants.

The team also found a decrease of 10 percent in the ratio of N-acetylaspartate (NAA) to choline, and an increase of 28 percent in the ratio of lactate to choline. These are surrogate measures for metabolic brain development, explained study co-researcher Dr. Patrick McQuillen. McQuillen practices Pediatric Critical Care Medicine and Pediatrics in San Francisco, California.

Previous studies have shown that lower levels of NAA and higher levels of lactate were associated with an increased risk of neurodevelopmental impairment in infancy and childhood.

The researchers also found an increase of 4 percent in what's knows as diffusivity, a measure of brain tissue structure. According to Miller, as a brain develops more complex tissues, there are usually more barriers to water diffusing through tissues, which means that diffusivity decreases with maturity.

Finally, babies with heart defects also displayed a decrease of 12 percent in white-matter fractional anisotropy, meaning the brain's white matter was less mature.

"White matter injury, the characteristic pattern of injury in the premature newborn, was surprisingly common in the newborns with heart disease that we studied," said study lead author Dr. Steven Miller, assistant professor of pediatrics at the University of British Columbia.

White matter does have some capacity to heal itself following injury, a process known as remyelination, which may involve injured cells repairing themselves or new cells being produced, the researchers said.

"It is very important to note that babies with heart disease have the potential for ongoing brain development and even recovery if there is injury," said McQuillen.

Better imaging technologies are helping identify babies with heart defects in utero, which means parents can plan for the birth at a facility that provides care and surgery to these infants. Many times, congenital heart defects are diagnosed soon after birth, said McQuillen. However, some infants still go home and become very ill before their condition is recognized, he added.

"Although we don't know the exact cause of delayed brain development, it is likely to relate to the way blood flows to the brain in fetal life. In babies with the two types of heart disease that we studied, the brain receives blood with lower oxygen," said McQuillen.

But questions remain, Garg said. Even though the study confirms that brain development delays exist prior to surgery, it does not settle the question of cause and effect, he said.

It's possible for heart defects and brain abnormalities to exist in the same population but not necessarily be related to each other, Garg argued.

"In the paper, they describe the abnormalities that have been seen. The question is whether [heart defects are] related to that. It's an association. Also, the kids have these abnormalities on MRI, but does this lead to later abnormalities? Further studies need to be done in terms of linking the two brain abnormalities," said Garg.

The researchers said further investigation is needed to find ways of minimizing brain development delays in utero and as a result of heart surgery.

Garg acknowledged that the new information may help physicians protect babies' brains before and during heart surgery, but those steps could have hazards of their own.

"We do a lot of interventions that can lead to neurologic problems. You have multiple hits, so how do you know what caused the developmental delay? That's what's tricky about it," Garg said.

The researchers did not compare the infants' brain development to that of other infants who are ill at birth, he added, and long-term studies of the impact of these brain abnormalities are needed.

"Babies with a fetal diagnosis may also be studied with MRI to learn more about how the brain develops when there is congenital heart disease. This will be especially important as cardiologists begin to consider interventions to treat heart conditions before birth -- something that is only being studied at this time," said McQuillen.

The researchers stressed that both of the congenital heart defects in the study required surgery. Parents who have been told their child has a heart murmur but does not need surgery should not worry about related developmental delays, McQuillen and Miller said.

More information

There's more on congenital heart defects at the American Heart Association  .

TUESDAY, Nov. 6 (HealthDay News) -- Heart failure patients treated with a device that synchronizes pumping in the heart's ventricles showed no improvement in exercise capacity, researchers report.

The results were presented Tuesday at a late-breaking clinical trial session at the American Heart Association's annual meeting, in Orlando, Fla., and were expected to be published in the Dec. 13 print issue of the New England Journal of Medicine.

Cardiac Resynchronization Therapy (CRT) devices are surgically implanted and deliver electrical impulses to both ventricles at the same time, making both chambers contract simultaneously and thereby improving pumping efficiency.

While current guidelines support using CRT in patients with moderate to severe heart failure, this study aimed to see if the device could benefit patients outside those recommended parameters.

For this trial, 172 heart failure patients were randomly assigned to receive treatment with CRT or not.

Those treated with CRT showed no significant improvement in exercise capacity as measured by peak oxygen consumption. Some symptoms did improve, but quality-of-life scores and results of the six-minute hall walk test did not change significantly, the researchers reported.

"There was no significant difference in the change in peak oxygen consumption between the treatment group and the control group during cardiopulmonary testing," Dr. John Beshai, study lead author and director of pacemaker and defibrillator services in the division of cardiology at the University of Chicago, said at a news conference Tuesday. "Further research is necessary," he said.

The trial was funded by St. Jude Medical, which makes the CRT device.

More information

There's more on heart failure at the American Heart Association  .

TUESDAY, Nov. 6 (HealthDay News) -- Treatment with cholesterol-lowering statin drugs after coronary artery bypass graft (CABG) surgery reduces a patient's risk of stroke, U.S. researchers report.

The study, from the Cleveland Clinic, included more than 5,200 patients who underwent bypass between early 1993 and late 2005. The overall incidence of post-operative stroke one year after surgery was 3.3 percent (181 strokes).

"Patients discharged on statin therapy were more likely to have a lower low-density cholesterol (LDL or "bad" cholesterol) and were significantly less likely to suffer a post-operative stroke at one year," the researchers wrote.

They also said that age, peripheral vascular disease and kidney disease were independent predictors of stroke, heart attack or death. The use of both statin and ACE inhibitors significantly reduced risk, they found.

"These data suggest that a discharge regimen including statin therapy may reduce post-operative morbidity and warrants prospective validation," the researchers concluded.

The study was to be presented Tuesday at the American Heart Association annual meeting, in Orlando, Fla.

More information

The Society of Thoracic Surgeons has more about CABG  .