TUESDAY, April 29 (HealthDay News) -- Secondhand smoke not only damages the delicate cells that line blood vessels but also disrupts the body's natural repair mechanism for those cells, a new study shows.

The research was done because there still are skeptics who doubt the health value of public smoking bans, said study co-author Stanton A. Glantz, professor of medicine at the University of California, San Francisco, Center for Tobacco Control Research and Education.

"There still are some people out there saying these effects [from smoking bans], seen in terms of reduced heart attacks and an immediate drop in heart attacks, are just not feasible," Glantz said.

The findings were expected to be published in the May 6 issue of the Journal of the American College of Cardiology.

The new study tested the arterial effects of 30 minutes exposure to secondhand smoke on 10 young adult nonsmokers. The concentration of ambient smoke used was "about the level you would get in a bar," Glantz said.

The researchers did a number of detailed tests to measure the impact of that exposure on the endothelial cells that line blood vessels. These cells line the entire circulatory system and serve as a kind of interface between circulating blood and the interior of the vessel wall.

That endothelial cells are damaged by secondhand smoke was already known, Glantz said. However, "Everybody asks how long that effect persists, but nobody had studied that question," he said.

The answer, according to the study, is that "most of the effects persist for at least a day," Glantz said. "We only did 24 hours, because we thought they would be gone after 24 hours. They weren't."

There was also a clear negative effect on endothelial progenitor cells, which are produced in the bone marrow and circulate through the body. The progenitor cells' job is to seek out and repair endothelial damage.

Secondhand smoke exposure interfered with chemical signals that bring these progenitor cells to the sites of damage, Glantz said. "It wiped out the chemotaxis [direction signaling] for at least a day," he said. "We don't know how long the effect persists."

It's a "fascinating" study, said Dr. Norman H. Edelman, chief medical officer of the American Lung Association.

"We already know that exposure to secondhand smoke can cause endothelial changes," Edelman said. "The beginning of arterial disease is endothelial damage. What this study shows is that the cells that are essential in the repair of the endothelium are also affected by secondhand smoke."

The study comes as Atlantic City becomes the latest American community to ban smoking in public places, Edelman noted.

"The good news is that a little more than half of the country is now smoke-free," Glantz said. "The bad news is that a little more than half of the country is not smoke-free."

More information

A fact sheet on secondhand smoke is available from the American Lung Association  .

TUESDAY, April 29 (HealthDay News) -- Increased levels of exercise can reduce but not eliminate the risk of heart disease in overweight and obese women, a U.S. study finds.

The researchers analyzed data from 38,987 women who took part in the recently completed Women's Health Study. At the start of the study in 1992, information was gathered about the women's height and weight, the average amount of time per week they were physically active, other health habits, and medical history. The women were then followed for an average of 10.9 years.

At the start of the study, 34 percent of the women were considered physically active, 31 percent were overweight, and 18 percent were obese.

During the follow-up, 948 of the women developed coronary artery disease. Both body-mass index (BMI) and physical activity levels were individually associated with the risk of heart disease. The risk was lowest for normal weight women who were active, slightly higher for inactive normal-weight women, higher still for active women who were overweight or obese, and highest for inactive overweight or obese women.

Dr. Amy R. Weinstein, of Beth Israel Deaconess Medical Center in Boston, and colleagues noted that fat cells (adipocytes) release chemicals that may harm the heart by accelerating the hardening of the arteries and increasing inflammation, clotting and dysfunction of the blood vessels.

"We postulate that the beneficial effect of physical activity may directly reduce and combat the ill effect of the prothrombotic factors released by adipocytes," the researchers wrote.

But they noted that exercise didn't eliminate the effects of being overweight.

"Even high quantities of physical activity are unlikely to fully reverse the risk of coronary heart disease in overweight and obese women without concurrent weight loss," the study authors concluded. "Regardless of body weight, these data highlight the importance of counseling all women to participate in increasing amounts of regular physical activity and maintaining a healthy weight to reduce the risks of coronary heart disease."

The study was published in the April 28 issue of the Archives of Internal Medicine.

More information

The U.S. National Women's Health Information Center has more about heart disease.

MONDAY, April 28 (HealthDay News) -- Pneumonia, irregular heart beat, and obstructed blood flow to the heart are the most common reasons for hospitalization for heart failure in the United States, researchers say.

A team at the University of California, Los Angeles analyzed data from a heart failure patient registry called the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF). Between March 2003 and December 2004, the registry enrolled almost 49,000 patients from 259 hospitals across the United States.

The factors that most often led to hospital admission for heart failure patients were: pneumonia or respiratory ailments (15.3 percent); obstructed blood flow to the heart (14.7 percent); irregular heart beat or arrhythmia (13.5 percent); uncontrolled hypertension (10.7 percent); not taking medications (8.9 percent); worsening kidney function (6.8 percent); and not adhering to a special diet (5.2 percent).

"Over 60 percent of hospitalized heart failure patients had at least one of these precipitating factors at hospital admission," study first author Dr. Gregg C. Fonarow, UCLA's Eliot Corday Chair in Cardiovascular Medicine and Science and director of the Ahmanson-UCLA Cardiomyopathy Center, said in a prepared statement.

Fonarow and colleagues also found that patients with none of these factors had lower in-hospital death rates than those with one or more of the factors. Pneumonia, obstructed blood flow to the heart (ischemia), and worsening kidney function were associated with higher in-hospital death rates and longer hospital stays.

"Understanding the factors that can exacerbate heart failure and lead to hospitalizations -- especially the ones that are avoidable -- are invaluable to help us improve management of heart failure," Fonarow said.

He said this study "offers important insight and points to where we can intervene early, such as making sure patients with heart failure are immunized against flu and pneumonia."

The study was published in the April 28 issue of the journal Archives of Internal Medicine.

"In future studies, we plan to target how specific interventions based on these precipitating factors, such as flu vaccinations, may help this high-risk heart failure population," Fonarow said.

More information

The American Heart Association has more about heart failure  .

THURSDAY, April 24 (HealthDay News) -- High levels of C-reactive protein, an inflammatory marker that may warn of impending heart disease, are tied to variations in genes that control metabolism, two new studies show.

The studies identify "new genes that are of potential importance for either the treatment of cardiovascular disease or potentially screening individuals who may be at higher risk of developing cardiovascular disease," said Dr. Alexander Reiner, of the University of Washington, Seattle, who authored one of the reports.

Still unresolved, however, is the exact nature of the relationship between C-reactive protein (CRP) levels and cardiovascular disease.

"That's an absolutely crucial piece of evidence that we don't have, and until we have it, we cannot know whether any of these new [genetic variants] will predict disease," said Dr. James Scott of Imperial College London, who was not involved in either study.

The reports are published in the May issue of The American Journal of Human Genetics.

Researchers have known for some time that blood CRP levels can predict one's risk of heart disease and stroke. Like the swelling that occurs when someone cuts a finger, cardiovascular disease is, to a large extent, an inflammatory condition. CRP is an indicator of that inflammation. Not surprisingly, environmental risk factors such as smoking, diet and exercise strongly influence CRP levels. But genetics also play a role -- accounting for about 40 percent elevated CRP levels, Reiner said.

"The genetic side of this is rather straightforward," explained Dr. Paul Ridker of Harvard Medical School and Brigham and Women's Hospital in Boston, who led the second study. "If we know people with high CRP levels are at risk, what governs CRP levels? There's a high environmental risk -- people who don't exercise, who smoke, who are overweight, tend to have higher CRP levels than thin, athletic people. But some thin, athletic people have high CRP levels anyway."

Some genetic factors (including variants in the CRP gene itself) had already been identified. But they accounted for only a small percentage of the variance in these levels; researchers wanted to find the other players. In separate efforts, Reiner and Ridker led research teams to see if they could locate them.

Using genetic material and data stemming from three separate cardiovascular studies that comprised more than 12,000 individuals, the groups scanned for genetic differences that correlated with elevated CRP levels. Their tools were DNA microarrays -- glass slides, about the length and width of a stick of gum, which can probe more than 300,000 individual genetic variants per individual. Reiner's team also employed a candidate gene approach, looking specifically at polymorphisms in specific genes the scientists thought might play a role.

The teams found seven genomic regions that appeared to be strongly correlated with CRP levels. Six of those regions contained genes associated in one way or another with metabolic syndrome; the seventh contained no known genes. These six genomic locations read like a Who's Who of cardiovascular disease and metabolic disorder, genes such as HNF1A, which regulates the CRP gene; the leptin receptor, which regulates weight; a regulator of glucose metabolism; and apolipoprotein E.

"I think it's quite interesting that genes involved with traits of metabolic syndrome are also associated with CRP," said Dr. Caroline Fox, medical officer of the National Heart, Lung, and Blood Institute. "I think that's the most fascinating aspect of this paper."

"From our perspective, it's an incredibly satisfying finding," said Ridker. "Often when you do genome-wide association studies, you get genes that you don't understand. In this case, we found a gene cluster that makes perfect sense."

Scott, who has performed similar (albeit unpublished) analyses, said he believed the findings. "We basically replicate all of those loci, the headline loci anyways," he said. "I'm sure it's right, absolutely."

According to Ridker, "The 'Aha' moment was recognizing that these six or seven genes are all interrelated to these metabolic pathways. The question is, I know CRP predicts heart attack and stroke, and these genes are related to CRP. Do these provide clues to what the proper interventions might be? And we think the answer is yes."

Indeed, given the link between CRP and cardiovascular disease, researchers have instigated clinical trials to determine whether individuals with elevated CRP levels, but low cholesterol, should be treated proactively. Ridker heads one of those trials, called JUPITER, which involves the use of a cholesterol-lowering statin called Crestor. On March 31, AstraZeneca announced it was closing JUPITER, "because there is unequivocal evidence of a reduction in cardiovascular morbidity and mortality amongst patients who received CRESTOR when compared to placebo."

But Scott cautioned that fundamental questions must be addressed before any drugs or therapies targeting the loci identified in these two studies can be developed.

"Is it [CRP] merely a response to inflammation, or does it make the inflammation worse?" he asked. "Until that question is addressed, these genes are not a valid drug target."

Metabolic syndrome comprises a collection of risk factors that often lead to cardiovascular disease, including abdominal obesity, elevated blood sugar, elevated blood pressure and abnormal lipids, said Fox. According to the American Heart Association, the syndrome affects almost 50 million Americans.

More information

For more on metabolic syndrome, visit the American Heart Association  .