The sound -- called a carotid bruit (pronounced brew-ee) -- is caused by turbulent blood flow due to buildup of fatty deposits in one of the two arteries that carry blood to the front and middle part of the brain. It is usually regarded as a possible indicator of increased risk of stroke.

Now an analysis of 22 studies finds that people with carotid bruits are more than twice as likely to have heart attacks or to die of cardiovascular disease. "The presence of a carotid bruit should heighten clinician concern for coronary heart disease," said the report by physicians at Walter Reed Army Medical Center in Washington, D.C.

The studies included 17,295 people who were followed for an average of four years. "In the four studies in which direct comparison of patients with and without bruits were possible, the odds ratio for myocardial infarction [heart attack] was 2.15 and for cardiovascular death 2.27," the report said.

The findings are published in the May 10 issue of The Lancet.

Using the presence of a bruit as an indicator of cardiovascular risk could be helpful, but "there are some unresolved questions about the usefulness of carotid bruit and prognosis," said Dr. Victor Aboyans, a cardiologist at Dupuytren University Hospital in Limoges, France, and co-author of an accompanying editorial in the journal.

"First, many of the patients who were studied already had cardiovascular disease, so what is the additional value of carotid bruit in such a case?" Aboyans asked. "The second issue is that some patients who don't have carotid bruit may have other evidence of cardiovascular disease."

Several studies have shown that starting preventive measures for stroke on the basis of screening for carotid bruit aren't useful, Aboyans said. Nevertheless, presence of carotid bruit could prompt physicians to be more aggressive in recommending measures to reduce the risk of cardiovascular disease, such as cholesterol reduction, he said.

Dr. Deepak Bhatt, associate director of the Cleveland Clinic Cardiovascular Coordinating Center, said, "The [study authors'] recommendation that they be even more aggressive with risk modification, that is good clinical judgment."

Physicians routinely listen for possible carotid bruits when doing a physical examination of people who are middle-aged or older, Bhatt noted.

Studies have shown that there's a link between the risk of stroke and of coronary heart disease, Bhatt said. "The core knowledge already exists," he said. "This study helps put a number on how high the risk is."

But the study raises some practical issues, Bhatt added. "One is whether, if a carotid bruit is found, to go ahead and do an ultrasound examination," he said. "I would say yes, but it is controversial. The U.S. Preventive Task Force recommends against routine ultrasound in general."

More information

Learn what a carotid bruit is and what it might mean from the American Heart Association.

They said their findings could lead to the development of new, genetically targeted therapies to treat and prevent fatal arrhythmias. The study was published online Thursday in The Journal of Clinical Investigation.

"We are still struggling to understand why arrhythmia causes sudden cardiac death in some patients, but not others, and what underlying molecular mechanisms or abnormalities may be at play," study senior author Dr. Gideon Koren, director of the cardiovascular research center at Rhode Island Hospital and a professor of medicine at Brown University's medical school, said in a prepared statement.

He and his team developed animal models of long QT syndrome (LQTS) -- a disorder of the heart's electrical system that causes fast, chaotic heartbeats -- to study the various mechanisms that cause arrhythmia. The animal models included the two most common genetic forms of LQTS in humans -- LQT1 and LQT2.

In both forms, faulty genes lead to production of abnormal ion channels, the proteins responsible for moving potassium in and out of heart cells so they can contract. In LQT1, the mutation is in the KvLQT1 gene, while in LQT2, the mutation is in the HERG gene.

The animals with LQT2 exhibited spontaneous arrhythmias, and some of them died suddenly, while there was no spontaneous arrhythmia or sudden death among the animals with LQT1.

The researchers believe that the electrical cause for the deadly arrhythmias in the LQT2 group is increased spatial dispersion of repolarization across the front of the outside layers of cardiac muscle. The LQT1 group did not have increased dispersion.

Koren and his team also believe that HERG and KvLQT1 may interact, and that a mutation of either one of these genes could affect the other.

"While results from animal models are not always applicable to humans, we believe our findings are a first step toward gaining a better understanding of how and why arrhythmias cause sudden cardiac death. However, there is much more that we still don't know," Koren said.

More information

The American Academy of Family Physicians has more about arrhythmia.

When stroke patients are too weak to walk on their own, physical therapists fit the patients in a harness, put them on a treadmill and help them move. Because this can be physically demanding, robotic devices have been developed as an alternative.

"We wanted to know whether using a robotic device that guides the limb in a symmetrical walking pattern would facilitate greater improvements in walking speed and symmetry than more traditional walking interventions with a physical therapist," study author T. George Hornby, an assistant professor in the physical therapy department, said in a prepared statement.

The study included 48 people who'd suffered strokes at least six months earlier and still had moderate to severe trouble walking due to weakness on one side of the body. The patients were randomly assigned to receive physical therapist-assisted or robotic-assisted locomotor therapy. All the patients received a dozen 30-minute therapy sessions during the four to five weeks of the study.

"We found that stroke patients improved their walking whether they had the robotic device or the therapist helping them. However, the amount of improvement was greater in the therapist-assisted group," Hornby said.

Patients in the therapist-assisted group showed greater improvements in walking speed and in the amount of time spent on the weak leg during therapy. Among patients who had severe walking deficits, those in the therapist-assisted group -- but not those in the robotic-assisted group -- felt their quality of life improved after therapy because they had fewer physical limitations.

The fact that therapist-assisted training allows for patient error, while the robotic device controls movement and minimizes errors, may explain the differences between the two groups.

"When learning to walk again, if people can make mistakes and realize their errors and change their behavior based on those errors, they may learn better," Hornby said. "We also think that patients work harder and therefore improve more with therapists because the robotic device moved patients' legs for them throughout the therapy. Therapists only help as needed."

The study appears in the current issue of Stroke.

Hornby and colleagues suggested that robotic-assisted therapy may be best for stroke patients who have no ability to walk on their own, while therapist-assisted training is best for those who can walk independently, even at very slow speeds.

More information

The U.S. National Institute of Neurological Disorders and Stroke has more about stroke rehabilitation.

The latest findings from the Multiethnic Study of Atherosclerosis (MESA) are believed to provide the first large scale of evidence of such a link and give the estimated 72 million obese American adults another reason to change their lifestyle.

"The biological effects of obesity on the heart are profound. Even if obese people feel otherwise healthy, there are measurable and early chemical signs of damage to their heart, beyond the well-known implications for diabetes and high blood pressure," senior study investigator Dr. Joao Lima, a professor of medicine and radiology at the Johns Hopkins University School of Medicine and its Heart Institute, said in a prepared statement.

There is "now even more reason for (obese people) to lose weight, increase their physical activity and improve their eating habits," Lima said.

He and his colleagues tracked the development of heart failure in an ethnically diverse group of nearly 7,000 people, ages 45 to 84, who enrolled in the MESA study, starting in 2000. Of the 79 participants who've developed congestive heart failure so far, 35 (44 percent) were physically obese (body mass index of 30 or greater).

On average, obese participants were found to have higher blood levels of key immune system proteins involved in inflammation (interleukin 6, C-reactive protein, and fibrinogen) than non-obese participants. A near doubling of average interleukin 6 levels alone was associated with an 84 percent increased risk of heart failure.

"Our results showed that when the effects of other known disease risk factors -- including race, age, sex, diabetes, high blood pressure, smoking, family history and blood cholesterol levels -- were statistically removed from the analysis, inflammatory chemicals in the blood of obese participants stood out as key predictors of who got heart failure," Lima said.

He added that doctors "need to monitor their obese patients for early signs of inflammation in the heart and to use this information in determining how aggressively to treat the condition."

Lima and colleagues also found a link between inflammation and metabolic syndrome, which doubles a person's chances of developing heart failure. Metabolic syndrome is a collection of risk factors -- obesity, high blood pressure, elevated blood glucose levels, excess abdominal fat, and abnormal cholesterol levels -- that increase the risk of heart disease and diabetes.

The study was published in the May 6 issue of the Journal of the American College of Cardiology. The MESA study was expected to continue tracking patients through 2012.

More information

The American Heart Association has more about heart failure.

The risks of dying from other conditions also decline after quitting, although the time frame varies depending on the disease.

"The harms of smoking are reversible and can decline to the level of nonsmokers," said study author Stacey Kenfield, whose report is in the May 7 issue of the Journal of the American Medical Association. "For some conditions like chronic obstructive pulmonary disease, it can take more than 20 years, but there is a rapid reduction for others."

"It's never too early to stop, and it's never too late to stop," added Kenfield, who is a postdoctoral research fellow in the department of epidemiology at the Harvard School of Public Health in Boston.

Smoking is still the leading preventable cause of death in the United States. Not only does tobacco smoke cause lung cancer, it is also implicated in heart disease, other cancers and respiratory diseases.

According to the World Health Organization, an estimated 3 million people in industrialized countries will have died as a result of tobacco use by 2030, and an additional 7 million people in developing countries face the same fate.

This research is a continued follow-up on the Nurses' Health Study, a large trial involving more than 100,000 women. Scientists now have 22 years of data on the participants.

Current smokers had almost triple the risk of overall death compared with women who had never smoked.

Current smokers also had a 63 percent increased risk for colon cancer compared with never-smokers, while former smokers had a 23 percent increased risk. There was no significant association between smoking and ovarian cancer.

And women who started smoking earlier in life were at a higher risk for overall mortality, of dying from respiratory disease and from any smoking-related disease.

However, a smoker's overall risk of dying returned to the level of a never-smoker 20 years after quitting. The overall risk declined 13 percent within the first five years of abstaining.

Most of the excess risk of dying from coronary heart disease vanished within five years of quitting.

For chronic obstructive pulmonary disease, the return to normal took almost 20 years, although there was an 18 percent reduction in the risk of death seen within five to 10 years after quitting.

And the risk for lung cancer didn't return to normal for 30 years after quitting, although there was a 21 percent reduction in risk within the first five years compared with women who continued to smoke.

Many previous studies on tobacco use had focused on men and on lung cancer, the authors stated. They also only looked at smoking status at the beginning of the study. "We got smoking information every two years, so we feel we have a more accurate estimate of current and past smoking," Kenfield said. "We saw increased risks for current smokers [than previous studies], and we think that's because we know who the current smokers are."

"This shows the power of quitting smoking," said Dr. Jay Brooks, chairman of hematology/oncology at Ochsner Health System in Baton Rouge, La. "We've known this for a number of years, but the beauty of this study is it is a very large and well-studied group of people. When I tell people to quit smoking, I say the effect of the heart precedes that of the lungs. If you've smoked, you need to be cognizant that you're still at an increased risk of lung cancer."

More information

Visit the American Lung Association for more on women and smoking.