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Until now no guidelines existed for one of the more difficult questions in medicine — what to do with a heart-assisting device, such as an implanted defibrillator, in a patient’s final days of life?

An implanted defibrillator delivers a potentially life-saving electric shock to restart a heart that stops beating. However, the shock can cause acute discomfort in the last days of life, when the goal is to minimize pain, and in this case continued use of the devices may conflict with a patient’s wishes.

Now, expert guidelines announced Friday at the meeting of the Heart Rhythm Society in Denver suggest that, whenever possible, terminally ill patients should be free to make their own decisions as to whether they’d like the devices removed.

“This is a situation we face more and more often,” noted Dr. Rachel Lampert, associate professor of cardiology at Yale University School of Medicine. “As the population in hospices grows, the issue of how to manage defibrillators becomes more important.”

Lampert is co-chair of a committee scheduled to present a consensus statement on the management of pacemakers, defibrillators and other cardiovascular implantable electronic devices. The statement will also be published in the July issue of HeartRhythm.

Few medical institutions have policies about deactivating electronic heart devices. A recent study of more than 400 hospices found that just 10 percent had guidelines about disconnecting implanted defibrillators.

“At Yale, we looked at our own population and found that up to 20 percent of patients with defibrillators got shocked in the weeks before death,” Lampert said.

She worked with Dr. David Hayes of the Mayo Clinic, Rochester, Minn., in assembling a committee to consider guidelines for the issue. “We put together a group of individuals with expertise in different areas,” Lampert said. “It included an ethicist, a lawyer, a nurse and a psychiatrist.”

The purpose of the statement “is to carry out a patient’s wish to provide or withdraw therapy as the patient desires,” said Dr. Richard Page, professor and chair of medicine at the University of Wisconsin and president of the Heart Rhythm Society.

Removing an implanted defibrillator near the end of life, “is not physician-assisted suicide or euthanasia,” he stressed.

The statement, developed in cooperation with other organizations, including the American College of Cardiology and the American Heart Association, recommends above all that all patients with implanted electronic devices be encouraged to make advance directives.

“Ideally, you have the conversation and make the patient aware of his or her empowerment and what decision should be made before you get to this point,” Page said.

Other provisions of the consensus statement:
All adult patients are assumed to be competent to make decisions on continuing or stopping treatment. When a patient lacks capacity, the decision can be made by a designated health care proxy.
Physicians or other caregivers cannot be compelled to carry out a procedure that conflicts with their ethical values. In such a case, the issue can be passed to a colleague who is willing to carry out the task.
The recommendations will give physicians and institutions a frame of reference, experts said. “At least now you have a consensus statement based on a number of perspectives and a literature review to provide guidance,” Page said.

SOURCES: Rachel Lampert, M.D., F.H.R.S., associate professor, cardiology, Yale University, New Haven, Conn.; Richard Page, M.D., professor and chair, medicine, University of Wisconsin, Madison, and President, Heart Rhythm Society; May 14, 2010, Heart Rhythm Society annual meeting, Denver;

Patients who get the clot-busting drug alteplase (tPA) within 4.5 hours of having a stroke fare better than patients who are given the drug later, Scottish doctors report.

It has been known that treating a stroke earlier is better than later, but this study shows for the first time that there is significant harm done with starting tPA after 4.5 hours, the researchers noted.

“The benefit of giving this treatment for stroke continues if we start it as late as 4.5 hours,” said lead researcher Dr. Kennedy R. Lees, from the University Department of Medicine and Therapeutics of the Gardiner Institute at the Western Infirmary in Glasgow.

“There is no net benefit to patients if you start the treatment after 4.5 hours. But if you start treatment after 4.5 hours, you will have more patients who die,” he added.

“Starting at an hour is much better than starting at two hours, and that’s better than three hours, and that’s better than 4.5 hours,” Lees explained.

The benefit derived from early tPA treatment is a long-term benefit, Lees pointed out.

“It’s a benefit that we can measure three months later,” he said. “So, what we are getting is long-term improved function. They are more likely to have no symptoms and more likely, if they do have symptoms, to be able to do things for themselves, or need less help. A whole range of disability is reduced, by just starting tPA a few minutes earlier.”

The report is published in the May 15 issue of The Lancet.

For the study, the research team collected data on 3,670 patients in eight trials that investigated how the benefits and risks of tPA changed based on the time the drug was given after the onset of a stroke.

The investigators found that when tPA was given within 4.5 hours, the chances of a positive outcome were good. However, when the drug was given later, the chances of a strong recovery rapidly declined.

In fact, patients given tPA within 90 minutes after suffering a stroke were more than 2.5 times more likely to have a good recovery, compared with similar patients who did not get the drug. Moreover, patients who got tPA 4.5 hours after their stroke had only a 22 percent chance of a good recovery, compared with patients who never got tPA, the researchers found.

Lees and colleagues also found that patients given the drug after 4.5 hours of the onset of a stroke were more likely to die.

These findings mean that patients have more time to get to the hospital, Lees said. “The message for the doctors is we can’t waste a moment once the patient has arrived in starting treatment, so there is more time for the patients and less time for the doctors.”

Dr. Steven R. Levine, a professor of neurology at Mount Sinai School of Medicine in New York City and co-author of an accompanying journal editorial, agreed that “the sooner you get treatment for your stroke, the more likely you are to have minimal or no disability from it.”

For every 90 minutes you wait to get treated, you reduce your chances of a good recovery by a factor of two, he noted. “For every 10 minutes you wait, that’s about 20 million brain cells that are dying,” Levine said.

Everybody needs to know about stroke and what to do, Levine said. The first thing is to call 911, he said.

“Time is brain. That’s really the message,” he said.

Another expert, Dr. Larry B. Goldstein, director of the Duke Stroke Center at Duke University, said that “this combined analysis is consistent with the prior analysis based on a smaller number of trials and reinforces the benefit of treatment with tPA on carefully selected patients with acute ischemic stroke.”

It also reinforces the need to begin treatment as soon as possible after symptom onset, Goldstein added.

“Even though selected patients may derive benefit up to 4.5 hours after symptom onset, the likelihood of benefit is much greater if treatment can begin sooner. Primary stroke centers are organized to evaluate and treat stroke patients in an expedited fashion. Time saved is brain saved,” he said.

SOURCES: Kennedy R. Lees, M.D., University Department of Medicine and Therapeutics, Gardiner Institute, Western Infirmary, Glasgow, U.K.; Steven R. Levine, M.D., professor, neurology, Mount Sinai School of Medicine, New York City; Larry B. Goldstein, M.D., professor and director, Duke Stroke Center, Duke University, Durham, N.C.

After hip replacement surgery, a compression device works as well as medication — and is safer — for preventing blood clots, a new study suggests.

“This device is as useful as blood thinners for the reduction of blood clots after hip replacement, and it’s superior in safety,” said study co-author Dr. Douglas E. Padgett, chief of adult reconstruction and joint replacement at the Hospital for Special Surgery in New York City, in a statement. “This has the potential to change the paradigm as to how we prevent blood clots after hip replacement. The efficacy is the same, the safety is markedly better and the cost is comparable.”

An estimated 30 percent to 50 percent of hip or knee replacement surgery patients will develop blood clots if preventive measures, such as taking blood thinning medication, aren’t taken.

In the study, researchers looked at a compression device that wraps around the leg and pumps it, helping to prevent clots. Typically, these devices are only used in hospitals because they’re big and restrict movement, but a new, smaller device can be used outside the hospital.

Researchers randomly assigned 410 hip replacement patients to get a blood thinner or use the compression device. Ultrasound examinations 10 to 12 days after surgery found major bleeding in 6 percent of those who took the blood thinner, but in none who used the device.

The study is published in the March issue of Journal of Bone & Joint Surgery.

A new drug called mipomersen reduced low-density lipoprotein (LDL) “bad” cholesterol by nearly 25 percent when added to current therapy in people with a rare genetic condition that causes extremely high cholesterol, a new study finds.

Mipomersen is designed to decrease the formation of apolipoprotein B (the main structural protein in LDL cholesterol) and its release from the liver or intestine. This reduces circulating LDL cholesterol concentrations.

Inherited high cholesterol (homozygous familial hypercholesterolemia) affects one in every one million people. Patients with the disorder have severely elevated LDL cholesterol and a high risk of early cardiovascular disease. If untreated, these patients rarely live past the age of 30.

This phase 3 clinical trial included 51 patients with homozygous FH who were already taking lipid-lowering drugs, including high-dose statins. The patients were randomly selected to receive either 200 milligrams of mipomersen or placebo per week for 26 weeks.

At the end of the treatment period, LDL cholesterol levels had decreased 24.7 percent in the mipomersen group, compared with 3.3 percent in the placebo group.

“Mipomersen could be a valuable addition to the drugs used in the management of homozygous FH and should prove useful in the management of other forms of severe refractory hypercholesterolemia,” wrote an international team of researchers led by Frederick Raal of the University of Witwatersrand, Johannesburg, South Africa.

The study was published online March 13 in advance of print publication this week in The Lancet, and was slated to be presented Saturday at the annual meeting of the American College of Cardiology in Atlanta.

SOURCE: The Lancet, news release.

Better health translates into better sex lives, with healthy people more likely to engage in sex (and good sex at that) and to express an interest in sex, new research finds.

This association held firm into middle-age and later life as well, according to the study by University of Chicago researchers.

The authors of the study, published in the March 10 issue of BMJ, also created a novel measure called “sexually active life expectancy.” According to this new measure, men aged 55 could expect another 15 years of sex while women of the same age could expect 10.6 more active years.

Overall, however, more men reported a satisfying sex life than women, a chasm that widened as people aged.

The findings shine light on a little discussed topic.

“The really important thing about this study is just that it was done,” said Dr. Eva Ritvo, vice chair of psychiatry at the University of Miami Miller School of Medicine. “People don’t look at sexual activity in a scientific way very often but it’s so very fundamental to our existence. The focus has always been on illness, but health is about well-being, looking at sexual functioning as an important part of well-being.”

Dr. Margaret E. Wierman, professor of medicine at the University of Colorado Denver, said the new study “points out that, over time, as a society women and men are becoming more comfortable talking about sex. Having a good sex life is critical to their overall quality of life.”

But the fact that men are doing better than women is something that needs attention, Ritvo stated. “Why should men be having better sex than women? Viagra came out for men. Where’s the female equivalent? For whatever reason women are not as satisfied as men and that needs to be addressed,” she said.

The study authors looked at two different samples of people, one involving over 3,000 adults aged 25 to 74, and another with more than 3,000 adults aged 57 to 85. An equal number of men and women were in each group.

Men were more likely to report positive experiences with sex than women. This gender gap was most noticeable among 75-to-85-year olds, with 38.9 percent of men, compared to 16.8 percent of women, reporting being sexually active. Almost 71 percent of men in this age group reported a good sex life, versus only half of the women.

And more men today are reporting an interest in sex than in 2000.

“This probably is related to new medications in therapy, so now men who before never could even think about having sex can have sex,” Weirman said.

Also, she added, “as people age, the unhealthy men die off so these are the healthiest men in that cohort.”

Study lead author Dr. Stacy Tessler Lindau, director of the University of Chicago’s Program in Integrative Sexual Medicine, said the “major reason why the picture looks better for men than women is that women tend to outlive their marriages and relationships, so there are more women in the adult population without partners. But if you look at women who have partners, the proportion who say they’re sexually active is about the same as men who have a partner.”

On the other hand, men’s sex lives do seem to suffer more from poorer health.

“At age 55, men have, on average, 15 years of sexually active life expectancy and women about 11 years,” Lindau explained. “Men who are in excellent or good health gain an additional five to seven years. What this says is that men benefit more from good health. Men in poor health lose more years of sexually active life expectancy than do women.”

People with partners were more likely to be having sex and more men than women reported having partners, especially in later life, the study found.

SOURCES: Stacy Tessler Lindau, M.D., director, Program in Integrative Sexual Medicine, University of Chicago; Eva Ritvo, M.D., vice chair of psychiatry, University of Miami Miller School of Medicine, and co-author, The Beauty Prescription; Margaret E. Wierman, M.D., professor of medicine, University of Colorado Denver; BMJ

Though hormone therapy has proven useful in treating late-stage prostate cancer, it often results in the development of fatal secondary tumors that are resistant to such therapy.

Now, however, researchers working with mice believe they have uncovered a mechanism by which the secondary tumors gain their resistance — a finding that eventually might help prolong the lives of men with prostate cancer.

Substances secreted during the body’s inflammatory response to the hormone therapy appear to play a role in creating resistance to hormone therapy, according to the study, published in the March 11 issue of Nature.

Doctors might be able to delay the onset of hormone-resistant tumors by two to three years if subsequent research finds a way to control the effects of inflammation, according to the research team, which included scientists from the University of California, San Diego (UCSD), the Scripps Research Institute in Florida and the Engelhardt Institute of Molecular Biology in Moscow.

Hormone therapy for prostate cancer, also known as androgen deprivation therapy or androgen ablation therapy, involves the reduction of male hormones in the body, according to the American Cancer Society. These male hormones, called androgens, promote the growth of prostate cancer cells. Reducing androgen levels can cause prostate tumors to shrink or can retard their growth, making them easier to remove surgically or treat with radiation.

“That therapy usually works, but in too many patients it leads to the appearance of castration-resistant cancer — cancer that no longer responds to androgen ablation therapy,” said Michael Karin, one of the UCSD researchers. “That form of prostate cancer is more aggressive, more metastatic and more difficult to treat with traditional chemotherapy and radiation therapy.”

By studying prostate cancer in mice, the researchers figured out that, as the prostate tumor shrinks, the dying cancer cells apparently send off signals that activate the body’s immune response.

“What we think is going on is, when you kill the tumor, the body doesn’t know it’s the tumor being killed,” Karin said. “It responds to it like there is tissue injury, a wound or something like that.”

White blood cells called B-cells infiltrate the tumor and release a substance called lymphotoxin, a protein that kills infected cells. The research team found that exposure to lymphotoxin promoted the development of cancer cells resistant to hormone therapy. Interfering with the inflammatory response delayed the development of castration-resistant cancer.

“It’s somewhat counterintuitive, that the death of these androgen-resistant cells somehow contributes to androgen resistance,” said Dr. Durado Brooks, director of prostate and colorectal cancer for the American Cancer Society.

The finding could be key in developing a means to delay or stop the development of therapy-resistant secondary tumors. Until now, research into this resistance has focused on the role that the cells’ androgen receptors play in the process. But researchers now can also consider controlling inflammation as another way to delay resistance.

Don’t expect anything useful for humans anytime soon. Researchers will have to first make sure that human prostate cancer responds in the same way that the cancer did in mice.

“There’s going to have to be a lot more work done to clarify that the mechanisms in humans are the same as those they have identified in mouse prostate cancer,” Brooks said. “It’s going to be quite a while before this mouse model moves to the bedside and actual clinical practice, if it ever does.”

But if the findings do transfer to humans, this new understanding of the role of inflammation in prostate cancer treatment could help extend lives.

“Androgen resistance is often one of the complications that occurs in later stages of prostate cancer management that often precedes death related to prostate cancer,” Brooks said. “If there was a way to prolong the time between treatment and development of androgen resistance, we could prolong a man’s life.”

SOURCES: Michael Karin, Ph.D., professor, pharmacology, University of California, San Diego; Durado Brooks, M.D., director, prostate and colorectal cancer, American Cancer Society, Atlanta;  2010, Nature

Strength training improves hand grip and arm function in people who have suffered a stroke without causing increased muscle spasticity or pain, according to combined data from multiple studies.

Stroke commonly weakens muscles and may temporarily cause muscle spasm and pain.

There is some controversy surrounding strength training in stroke patients, as some rehabilitation groups feel that strengthening stroke-weakened muscles will also increase spasticity and pain. But that’s not what Dr. Janice J. Eng and Dr. Jocelyn E. Harris, of University of British Columbia in Vancouver, Canada, found.

They pooled results from 13 studies that recorded how strength training exercises, versus no strengthening intervention, affected overall arm strength and function in 517 stroke patients with mild to moderately impaired movement of the upper limbs.

On average, strength training lasted for about one hour on 2 to 3 days a week for 4 weeks, although some of the training periods extended as long as 19 weeks. Most interventions used small weights, resistance bands, and gym-type pulley weights to build muscle.

The combined results suggest, “strengthening does not increase spasticity on a permanent basis,” Eng told Reuters Health in an email. Rather, strengthening may actually reduce muscle spasticity, she added.

None of the studies analyzed reported side effects and those that measured spasticity prior to strength training reported no increase in spasticity over the course of training.

In six studies (a total of 306 participants), strength training led to moderate or large improvement in hand grip strength, Eng and Harris report.

In 11 studies (a total of 465 participants) training resulted in a small improvement in arm function.

However, five studies involving 210 participants showed no improvement in activities of daily living, for example picking up a small object. This finding, Eng said, calls for a re-examination of stroke rehabilitation efforts to “ensure that strength training not only improves function, but also activities of daily living.”

SOURCE: Stroke

Scientists have linked a chemical used in consumer goods like non-stick pans and water-resistant fabrics with thyroid disease, raising questions about the potential health risks of exposure to the substance.

A study by British researchers found that people with high levels of the chemical perfluorooctanoic acid (PFOA) in their blood have higher rates of thyroid diseases — conditions which affect the body’s metabolism.

PFOA is a common chemical, used in industrial and consumer products including non-stick cooking pans, stain-proof carpet coatings and waterproofing for fabrics.

The study, published in the Environmental Health Perspectives journal, did not establish whether PFOA was causing higher levels of thyroid disease.

The researchers said the link might be complex and indirect, and added that their work highlighted a need for further studies of the human health effects of low-level exposures to chemicals like PFOA.

“We need to know what they (these chemicals) are doing,” said Tamara Galloway, a professor of ecotoxicology at Exeter University, who led the research.

Previous studies of people living near sites where PFOA is manufactured have not found an association between exposure to these chemicals and thyroid function, and some other scientists advised caution about drawing conclusions from the study.

INDIRECT LINK?

“Studies like this cannot tell us that the two things are definitely linked,” said Ashley Grossman, professor of neuroendocrinology at Queen Mary, University of London.

“We also don’t know whether this chemical is directly affecting the thyroid. Thyroid disease is often caused by the body’s own immune system attacking the thyroid gland so perhaps this chemical is having some effect on the immune system, rather than directly on the thyroid.”

The thyroid, located in the neck, is a kind of master gland, secreting hormones affecting metabolism. People with low thyroid function may lose hair, gain weight and feel sluggish, while those with overactive thyroids may lose weight and feel their hearts race. Both conditions can be treated.

The British researchers looked at 3966 American adults aged 20 and above whose blood serum was sampled between 1999 and 2006 for PFOA. They found that those with the highest PFOA concentrations (above 5.7 nanograms per milliliter) were more than twice as likely to report current thyroid disease than individuals with the lowest levels (below 4.0ng/ml).

Thyroid diseases are much more common in women than men, but in terms of the link between PFOA and thyroid disease, the researchers found no difference between the sexes.

Galloway and colleagues stressed the need for more work but said their study suggested it is “plausible that the compounds could disrupt binding of thyroid hormones in the blood or alter their metabolism in the liver.”

“This new evidence does not rule out the possibility that having thyroid disease changes the way the body handles PFOA,” they added, and its presence “might also prove to be simply a marker for some other factor associated with thyroid disease.”

A nationwide program to get faster treatment for people with the most severe kind of heart attack has dramatically reduced the time between hospital arrival and lifesaving angioplasty.

More than three-quarters of people with STEMI heart attacks — so called because of the electrocardiogram pattern that shows major blockage of a heart artery — were receiving artery-opening angioplasty within 90 minutes of reaching a hospital in 2008, said a report released online Wednesday in advance of print publication Dec. 15 in the Journal of the American College of Cardiology.

Before the campaign began, in 2005, only half of those patients met the 90-minute deadline recommended for emergency angioplasty.

“It is a remarkable leap in performance, a tangible improvement in how people are being treated around the country,” said Dr. Harlan M. Krumholz, professor of medicine at Yale University School of Medicine and an author of the journal report.

When the American College of Cardiology and 38 partner organizations set up what is called the Door-to-Balloon (D2B) Alliance, there were doubts that it could succeed, Krumholz said. The name is based on the angioplasty procedure, in which a thin, balloon-tipped catheter is threaded into a blocked heart artery, and the balloon is expanded to restore blood flow.

“There were warnings that we were setting up a situation where we all could fail,” Krumholz said. “But all of a sudden people were saying, ‘We can do this.’”

The report on 831 hospitals showed the 90-minute door-to-balloon deadline for STEMI heart attacks being met in 52.5 percent of cases in 2005. That number increased to 76.4 percent of cases in 2008.

And the improvement has continued, said the American College of Cardiology. Its most recent data, from June 2009, shows 81.7 percent of patients getting 90-minute door-to-balloon time. Also, the average time for start of angioplasty decreased from 121 minutes in 2005 to 80 minutes in 2009.

“I think we can say that in this country, the speed with which you are treated for a heart attack has improved no matter where you are,” said Elizabeth H. Bradley, professor of public health at Yale and lead author of the journal report.

And while the study does not measure the effect of quicker treatment on outcome, “in the past couple of years, several studies have shown that reduction of door-to-balloon time is associated with improved patient survival,” Bradley said.

Most of the changes prompted by the program were simple: Having ambulance attendants call the hospital to alert them that a heart attack victim was on the way, alerting the catheterization laboratory where angioplasty is done and the interventional cardiologists who do the procedure to be ready to go to work, and getting the patient to the catheter laboratory as quickly as possible, Bradley said.

But a key ingredient was a change in the mindset of the hospital personnel dealing with heart attacks, Krumholz said. “The important thing is that everyone felt they were working hard and fast before this,” he said. “But the numbers showed they weren’t. Then people came together and reworked the process by which these procedures were done.”

Data on how much the program has improved survival might not be easy to obtain, because statistics do not separate out STEMI heart attacks — “the crushing heart attacks that kill you,” Bradley said.

But overall figures show “a marked reduction in heart attack mortality over this period,” Krumholz said, and it can be assumed that the D2B program has a role in that reduction.