Category: Stroke

A stroke can weaken one side of the body, raising the dangerous possibility of unstable walking and debilitating falls. Physical therapy can help patients learn to shift their body weight slightly to the weaker, stroke-affected side to help regain balance, but for some patients, the weakness returns after their therapy ends.

University of Illinois at Chicago physical therapy professor Alexander Aruin has developed an inexpensive, simple way to deal with the problem, training the brain to rebalance body weight using a simple shoe insole he calls a "compelled body weight shift." It slightly lifts and tilts the body toward the stroke-affected side, restoring balance without the patient having to think about it.

Aruin along with colleagues at UIC and Marianjoy Rehabilitation Hospital in Wheaton, Ill., studied two patient groups: one group at UIC who just had strokes, and one at Marianjoy who had strokes over a year ago.

"We tried a purely biomechanical approach," Aruin said. "We mechanically lifted the healthy side so the patient cannot resist. The mechanics force body weight to where it is distributed almost 50/50. When patients ambulate in such a condition, they learn how to bear weight equally through both extremities. It's quite simple."

The two test groups followed slightly different protocols and were tested for various lengths of time. Their results were measured against those of control groups, who did not get the small therapeutic shoe insole, which measures less than half an inch thick. patients in all groups also received standard post-stroke physical therapy.

After the testing period ended, patients stopped using the insole. About three months afterward they were tested again to see if they retained the ability to keep their balance. Aruin and his colleagues found that physical therapy helped both the insole-user and control groups, but the insole group got an added boost.

"They showed more symmetrical body weight distribution and bore more weight on their affected side, and their gait velocity improved," he said. "The outcome looks promising. The technique is very simple and inexpensive and has potential, which is exciting."

Aruin hopes other physical therapists use the simple devices on stroke patients to see if they too benefit from it. His associates are also considering ways to use the insole to improve posture in post-stroke patients.

Results are published in two journals: ISRN Rehabilitation, and in a forthcoming issue of Topics in Stroke Rehabilitation.

Co-authors of the ISRN Rehabilitation article include Sambit Mohapatra, Aileen Eviota, Keir Ringquist and Sri Ranjini Muthukrishnan of UIC. Co-authors of the Topics in Stroke Rehabilitation article include Noel Rao, Asha Sharma and Gouri Chaudhuri of Marianjoy Rehabilitation Hospital.

The research was supported by a grant from the National Institutes of Health.

 It is a cellular component so scarce, some scientists even doubted its existence, and many others gave up searching for its molecular structure. Now a team led by researchers at Johns Hopkins has defined the protein structural composition of mitoKATP, a potassium channel in the mitochondria of the heart and other organs that is known to protect against tissue damage due to a heart attack or stroke. Importantly, the newly found channel strongly improves heart cell survival, demonstrating an essential life-saving role.

In a report to be published in the journal Circulation Research online July 17, the O'Rourke group and colleagues from Portland State University in Oregon describe their successful efforts to pinpoint and identify mitoKATP, which is an opening, or "pore," responsible for potassium uptake into mitochondria, the powerhouses of the heart cell. This particular potassium channel is a key player in the heart's intrinsic 4ability to protect itself from a loss of blood flow, speeding recovery from heart attacks and preventing cell death and scar tissue formation. Unexpectedly, the protein structure of mitoKATP matched that of another, much more plentiful and well-known potassium channel in the kidney, called ROMK.

Senior study investigator Brian O'Rourke, Ph.D., professor at the Johns Hopkins University School of Medicine's Heart and Vascular Institute and director of the Bernard Laboratory of Fundamental Research in Preventive Cardiology, says the team's discovery solves a 20-year mystery among cardiologists, physiologists and protein biochemists. Although there was abundant evidence that enhancing the ability of the mitochondria to take up potassium ions strongly protects against myocardial infarction, the channel behind this protective effect had escaped detection.

Noting that other scientists had failed to pin down mitoKATP among other known heart potassium channels and mitochondrial proteins, the Hopkins team broadened the search for new, presumably unknown heart mitochondrial proteins. Using cow hearts, chosen because their large size offered more mitochondrial starting material, lead author and protein biochemist, D. Brian Foster, Ph.D., used mass spectrometry to identify 20 million peptide signatures that yielded over 900 potential mitochondrial proteins — only one of which stood out as a tantalizing candidate for mitoKATP. Surprisingly, this candidate, ROMK, was a channel known to be found in the kidney, but had never been previously detected in mitochondria.

Foster and study co-lead investigator, Alice S. Ho, a Ph.D. candidate in biomedical engineering at Hopkins, then set up a series of experiments to determine if the mitochondrial version of ROMK (mitoROMK) was indeed a key component of mitoKATP and had similar heart protective qualities. Using cultured heart-derived cells, she showed that ROMK is localized to mitochondria. Next, Ho perfected an assay for mitoROMK activity, by monitoring mitochondrial uptake of thallium, which has a similar size and electrical charge as potassium. In cells in which mitoROMK was depleted, thallium uptake was decreased by more than 70 percent.

Additional supporting evidence came from experiments using Tertiapin Q, a honeybee toxin known to block ROMK. Co-investigator Keith Garlid, M.D., and his research team in Oregon, employing a classic assay for mitoKATP, showed that treating mitochondria with Tertiapin Q potently inhibited potassium-dependent mitochondrial swelling. The honeybee toxin also inhibited mitoKATP activity using the thallium assay.

A final set of experiments demonstrated mitoROMK's protective effects in cells; increasing mitoROMK levels led to increased rat heart cell survival and less damage after exposure to increasing amounts of tert-butyl hydroperoxide, an oxidizing chemical that mimics heart attack damage. Moreover, heart cells with depleted mitoROMK levels had a higher death rate with the same treatment.

O'Rourke says this study provides the first molecular key to unlocking the pore structure of the cardioprotective mitoKATP channel. More work will be required to fully understand the role of mitoROMK in protecting against cell injury and death in intact animals and humans during heart disease. However, since mitoROMK is expressed in organs such as the brain and liver too, the work uncovers a new avenue for therapies targeting mitochondria and opens the door for discovering more potent and specific drugs that activate mitoKATP.

Funding for the study was provided by the U.S. National Institutes of Health, specifically corresponding grant numbers P01-HL081427, R01-HL108917 and P01-HL36573.

In addition to O'Rourke, Foster and Ho, other researchers involved in this study were Jasma Rucker, B.Sc., and Ling Chen, M.S., all at Johns Hopkins; and Anders Garlid, B.Sc.; Agnieszka Sidor, Ph.D.; and Keith Garlid, M.D., Ph.D., all at Portland State University, in Oregon.

Stroke patients treated who received hormonal treatment, combined with rehabilitation, performed better on functioning and reasoning tests than patients who received rehabilitative therapy alone, a new clinical study from Italy shows.

The results were presented Monday at The Endocrine Society’s 94th Annual Meeting in Houston.

In the United States, stroke is the fourth-leading cause of death. The disease occurs when a blood vessel to the brain either ruptures (hemorrhagic stroke), or is obstructed by a clot during an ischemic stroke, which is the most common type. Inadequate blood flow prevents oxygen from reaching parts of the brain, which can lead to tissue death and serious long-term disability.

The hormone, relaxin, or RLX, is a naturally occurring protein produced by the reproductive organs in men and women, although only women have circulating hormone in the blood, both during ovulation and pregnancy. For years after its discovery in 1926 by the renowned zoologist and reproductive endocrinologist Frederick Hisaw, the hormone’s primary role was thought to be that of relaxing the uterus and pelvis for childbirth.

More recently, however, research from this study’s investigators, as well as others, has demonstrated that the hormone also helps many different organs and bodily processes prepare for pregnancy. These include the heart and blood vessels, or cardiovascular system; lungs; kidneys; mammary glands; as well as the immune system.

“Considering the present clinical results and our previous experimental studies, we believe that RLX is a very important, if not the most important, cardiovascular hormone,” said study author Mario Bigazzi, M.D. an internist at Prosperius Institute, in Florence, Italy. “We believe that the presence of relaxin in women’s blood at each ovulation represents the still-undiscovered factor protecting them from cardiovascular diseases during the fertile span of life until the menopause. This may assure their well-known longer survival time than men.”

Twenty days after beginning treatment, patients who received relaxin performed comparably to non-recipients on a test measuring daily-task ability. On a similar test 40 days after initial treatment, however, relaxin patients performed better than their non-relaxin counterparts. Both groups also received rehabilitative therapy.

Similarly, relaxin recipients scored higher than other patients on tests of reasoning and overall functioning, both at 20 and 40 days after starting treatment. No side effects associated with relaxin were reported during the study.

According to Bigazzi, these results demonstrate relaxin’s tremendous promise to treat, and even prevent, heart and blood-vessel diseases, including stroke. “We anticipate that, in the near future RLX, will represent an essential tool in the therapy and primary and secondary prevention of ischemic cardiovascular disease,” he said.

Thirty-six patients who had suffered a stroke participated in the study. Patients ranged in age from 64 to 79 years, and 53 percent were male.

Each participant was randomly assigned to receive daily treatment with oral relaxin, combined with physical rehabilitation, or physical rehabilitation alone. Investigators then used standardized tests to determine patients’ functioning in three domains, including daily activity, reasoning, and overall functioning. These assessments occurred on the first day of the study, then again at 20 and 40 days.

The RRCAA Foundation (Foundation for Research on Relaxin in Cardiovascular Disease and other Diseases), Prosperius Tiberino in Umbertide (Perugia-Italy ), and Prosperius Institute (Florence, Italy) funded the study.

The hot flashes and night sweats that most women experience early in menopause are not linked to increased levels of cardiovascular disease risk markers unless the symptoms persist or start many years after menopause begins. These new study results were presented June 23 at The Endocrine Society's 94th Annual Meeting in Houston.

"Our study provides reassurance that the common experience of menopausal symptoms in early menopause is not associated with increases in blood pressure or other risk markers for cardiovascular disease," said lead researcher Emily Szmuilowicz, MD, an assistant professor at Northwestern University's medical school in Chicago.

Researchers have questioned whether vasomotor menopausal symptoms such as hot flashes and night sweats reflect poor cardiovascular health. However, a 2011 study by Szmuilowicz and co-workers found that women who experienced menopausal symptoms only at the onset of menopause were less likely to have a stroke or heart attack or to die than were women who experienced hot flashes late in menopause or who did not have hot flashes at all.

Their new study focused on markers in the body that have been linked to a raised risk of cardiovascular disease. The risk markers examined were blood pressure, cholesterol, insulin, glucose (blood sugar) and blood markers of abnormal blood vessel function. Because inflammation is common in people with heart disease or stroke, the group also looked at blood markers of inflammation, including white blood cell count — the number of disease-fighting cells.

This study used retrospective data from nearly 60,000 postmenopausal women who participated in the Women's Health Initiative Observational Study. The ongoing study, funded by the National Institutes of Health, is examining the relationships between health outcomes and new risk indicators for disease.

The researchers grouped women into four categories based on timing of their menopausal symptoms of hot flashes and night sweats: only at the start of menopause (early-onset menopausal symptoms), only years later in menopause (late-onset menopausal symptoms), both time periods (persistent menopausal symptoms), and not at all.

The investigators found no association between early-onset vasomotor menopausal symptoms and increased levels of any cardiovascular risk markers. However, both persistent and late-onset menopausal symptoms were associated with higher blood pressure and higher white blood cell count compared with women without menopausal symptoms, they reported. Persistent menopausal symptoms also correlated with higher levels of glucose and insulin, which are markers for diabetes.

It is unclear why women who experience menopausal symptoms at different stages of menopause may have differing levels of cardiovascular disease risk, Szmuilowicz said She speculated that "if menopausal symptoms occur long after menopause begins, this may signal a blood vessel abnormality that could also affect cardiovascular health."

A heart attack doesn't just damage heart muscle tissue by cutting off its blood supply, it also sets off an inflammatory cascade that worsens underlying atherosclerosis, actively increasing the risk for a future heart attack. These findings from a study receiving advance online publication in Nature suggest an important new therapeutic strategy for preventing heart attacks and strokes, both of which are caused when atherosclerotic plaques rupture and block important blood vessels.

"We have known for a long time that heart attack patients are at increased risk for a second heart attack or a stroke, and now we know why," says Matthias Nahrendorf, MD, PhD, of the MGH Center for Systems Biology, senior author of the report from a team of researchers from the USA, Canada, Germany and the Netherlands. "The immune response to the infarct — tissue damaged by lack of oxygen — can accelerate the underlying disease by actually increasing the size and inflammation of the atherosclerotic plaque."

The study was designed to test the hypothesis that systemic inflammation caused by heart muscle damage would worsen pre-existing atherosclerosis. Using a mouse model genetically programmed to develop atherosclerosis, the researchers conducted a series of experiments showing that experimentally induced heart attacks led to the following:

• increased activity, in atherosclerotic plaques at a distance from the induced heart attack, of enzymes that break down the fibrous plaque cap, possibly leading to future rupture,

• accumulation of monocytes and other inflammatory immune cells in those atherosclerotic plaques,

• increased generation in the spleen of monocyte progenitors, along with changes in the function of those immune cells,

• increased release from the bone marrow of blood stem cells, which traveled to the spleen, triggered by increased activation of the sympathetic nervous system.

"The ancient fight-or-flight responses to injury stimulate immune cell activities that are involved in wound healing. But when the 'wound' is in the heart and caused by atherosclerosis, that increased activity actually accelerates the underlying disease," Nahrendorf explains. "While most of this work was done in mice, we have hints that something similar may happen in human patients — for example, we found increased numbers of blood stem cells in the spleens of patients who had died shortly after a heart attack. "

Ralph Weissleder, MD, PhD, a corresponding author of this study and director of the MGH Center for Systems Biology where the work was performed, adds that these findings set the stage for a totally novel approach to cardiovascular disease. Therapies directed to the sites of white blood cell production, including the bone marrow or the spleen, may be able to prevent immune-system exacerbation of atherosclerosis. "This gives us potential new therapeutic targets that we had not thought about before. Clinically, we focus on reducing risk factors such as elevated cholesterol and blood pressure, but not inflammation. We hope our work can help change that," he says.

Weissleder is a professor of Radiology, and Nahrendorf an assistant professor of Radiology at Harvard Medical School. Co-lead authors of the Nature paper are Partha Dutta, PhD, and Gabriel Courties, PhD, of the MGH Center for Systems Biology. Collaborators include Filip Swirski, PhD, MGH Center for Systems Biology, and Peter Libby, MD, chief of Cardiology at Brigham and Women's Hospital, where the clinical data were analyzed. The study was primarily supported by grants from the National Institutes of Health.

Living alone was associated with an increased risk of death and cardiovascular death in an international study of stable outpatients at risk of or with arterial vascular disease (such as coronary disease or peripheral vascular disease), according to a report published Online First by Archives of Internal Medicine, a JAMA Network publication.

Social isolation may be associated with poor health consequences, and the risk associated with living alone is relevant because about 1 in 7 American adults lives alone. Epidemiological evidence suggests that social isolation may alter neurohormonal-mediated emotional stress, influence health behavior and effect access to health care, which may result in association with or acquisition of, cardiovascular risk, according to the study background.

Jacob A. Udell, M.D., M.P.H., of Brigham and Women's Hospital, Harvard Medical School, Boston, and colleagues examined whether living alone was associated with increased mortality and cardiovascular (CV) risk in the global REduction of Atherothrombosis for Continued Health (REACH) Registry. Among 44,573 REACH participants, 8,594 (19 percent) lived alone.

Living alone was associated with higher four-year mortality (14.1 percent vs. 11.1 percent) and cardiovascular death (8.6 percent vs. 6.8 percent), according to the study results.

Based on age, living alone was associated with an increased risk of death among those patients 45 to 65 years old compared with those living with others (7.7 percent vs. 5.7 percent) , and among those participants 66 to 80 years old (13.2 percent vs. 12.3 percent). However, among patients older than 80 years, living alone was not associated with an increased risk of mortality compared with those living with others (24.6 percent vs. 28.4 percent), the results indicate.

"In conclusion, living alone was independently associated with an increased risk of mortality and CV death in an international cohort of stable middle-aged outpatients with or at risk of atherothrombosis," the authors conclude. "Younger individuals who live alone may have a less favorable course than all but the most elderly individuals following development of CV disease, and this observation warrants confirmation in further studies."

One of the top suspects behind killer vascular diseases is the victim of mistaken identity, according to researchers from the University of California, Berkeley, who used genetic tracing to help hunt down the real culprit.

The guilty party is not the smooth muscle cells within blood vessel walls, which for decades was thought to combine with cholesterol and fat that can clog arteries. Blocked vessels can eventually lead to heart attacks and strokes, which account for one in three deaths in the United States.

Instead, a previously unknown type of stem cell — a multipotent vascular stem cell — is to blame, and it should now be the focus in the search for new treatments, the scientists report in a new study appearing June 6 in the journal Nature Communications.

"For the first time, we are showing evidence that vascular diseases are actually a kind of stem cell disease," said principal investigator Song Li, professor of bioengineering and a researcher at the Berkeley Stem Cell Center. "This work should revolutionize therapies for vascular diseases because we now know that stem cells rather than smooth muscle cells are the correct therapeutic target."

The finding that a stem cell population contributes to artery-hardening diseases, such as atherosclerosis, provides a promising new direction for future research, the study authors said.

"This is groundbreaking and provocative work, as it challenges existing dogma," said Dr. Deepak Srivastava, who directs cardiovascular and stem cell research at the Gladstone Institutes in San Francisco, and who provided some of the mouse vascular tissues used by the researchers. "Targeting the vascular stem cells rather than the existing smooth muscle in the vessel wall might be much more effective in treating vascular disease."

It is generally accepted that the buildup of artery-blocking plaque stems from the body's immune response to vessel damage caused by low-density lipoproteins, the bad cholesterol many people try to eliminate from their diets. Such damage attracts legions of white blood cells and can spur the formation of fibrous scar tissue that accumulates within the vessel, narrowing the blood flow.

The scar tissue, known as neointima, has certain characteristics of smooth muscle, the dominant type of tissue in the blood vessel wall. Because mature smooth muscle cells no longer multiply and grow, it was theorized that in the course of the inflammatory response, they revert, or de-differentiate, into an earlier state where they can proliferate and form matrices that contribute to plaque buildup.

However, no experiments published have directly demonstrated this de-differentiation process, so Li and his research team remained skeptical. They turned to transgenic mice with a gene that caused their mature smooth muscle cells to glow green under a microscope.

In analyzing the cells from cross sections of the blood vessels, they found that more than 90 percent of the cells in the blood vessels were mature smooth muscle cells. They then isolated and cultured the cells taken from the middle layer of the mouse blood vessels.

After one month of cell expansion, the researchers saw a threefold increase in the size of the cell nucleus and the spreading area, along with an increase in stress fibers. Notably, none of the new, proliferating cells glowed green, which meant that their lineage could not be traced back to the mature smooth muscle cells originally isolated from the blood vessels.

"Not only was there a lack of green markers in the cell cultures, but we noticed that another type of cell isolated from the blood vessels exhibited progenitor traits for different types of tissue, not just smooth muscle cells," said Zhenyu Tang, co-lead author of the study and a Ph.D. student in the UC Berkeley-UCSF Graduate Program in Bioengineering.

The other co-lead author of the study, Aijun Wang, was a post-doctoral researcher in Li's lab.

"The different phenotypes gave us the clue that stem cells were involved," said Wang, who is now an assistant professor and the co-director of the Surgical Bioengineering Laboratory at the UC Davis Medical Center. "We did further tests and detected proteins and transcriptional factors that are only found in stem cells. No one knew that these cells existed in the blood vessel walls because no one looked for them before."

Further experiments determined that the newly discovered vascular stem cells were multipotent, or capable of differentiating into various specialized cell types, including smooth muscle, nerve, cartilage, bone and fat cells. This would explain why previous studies misidentified the cells involved in vessel clogs as de-differentiated smooth muscle cells after vascular injury.

"In the later stages of vascular disease, the soft vessels become hardened and more brittle," said Li. "Previously, there was controversy about how soft tissue would become hard. The ability of stem cells to form bone or cartilage could explain this calcification of the blood vessels."

Other tests in the study showed that the multipotent stem cells were dormant under normal physiological conditions. When the blood vessel walls were damaged, the stem cells rather than the mature smooth muscle cells became activated and started to multiply.

The researchers analyzed human carotid arteries to confirm that the same type of multipotent vascular stem cells are found in human blood vessels.

"If your target is wrong, then your treatment can't be very effective," said Dr. Shu Chien, director of the Institute of Engineering in Medicine at UC San Diego, and Li's former adviser. "These new findings give us the right target and should speed up the discovery of novel treatments for vascular diseases."

Grants from the National Institutes of Health and the California Institute for Regenerative Medicine helped support this research.

In a step towards improving rehabilitation for patients with walking impairments, researchers from the Kennedy Krieger Institute found that non-invasive stimulation of the cerebellum, an area of the brain known to be essential in adaptive learning, helped healthy individuals learn a new walking pattern more rapidly. The findings suggest that cerebellar transcranial direct current stimulation (tDCS) may be a valuable therapy tool to aid people relearning how to walk following a stroke or other brain injury.

Previous studies in the lab of Amy Bastian, PhD, PT, director of the Motion Analysis Laboratory at Kennedy Krieger Institute, have shown that the cerebellum, a part of the brain involved in movement coordination, is essential for walking adaptation. In this new study, Dr. Bastian and her colleagues explored the impact of stimulation over the cerebellum on adaptive learning of a new walking pattern. Specifically, her team tested how anode (positive), cathode (negative) or sham (none) stimulation affected this learning process.

"We've known that the cerebellum is essential to adaptive learning mechanisms like reaching, walking, balance and eye movements," says Dr. Bastian. "In this study, we wanted to examine the effects of direct stimulation of the cerebellum on locomotor learning utilizing a split-belt treadmill that separately controls the legs."

The study, published June 1 in the Journal of Neurophysiology, found that by placing electrodes on the scalp over the cerebellum and applying very low levels of current, the rate of walking adaptation could be increased or decreased. Dr. Bastian's team studied 53 healthy adults in a series of split-belt treadmill walking tests. Rather than a single belt, a split-belt treadmill consists of two belts that can move at different speeds. During split-belt walking, one leg is set to move faster than the other. This initially disrupts coordination between the legs so the user is not walking symmetrically, however over time the user learns to adapt to the disturbance.

The main experiment consisted of a two-minute baseline period of walking with both belts at the same slow speed, followed by a 15-minute period with the belts at two separate speeds. While people were on the treadmill, researchers stimulated one side of the cerebellum to assess the impact on the rate of re-adjustment to a symmetric walking pattern.

Dr. Bastian's team found not only that cerebellar tDCS can change the rate of cerebellum-dependent locomotor learning, but specifically that the anode speeds up learning and the cathode slows it down. It was also surprising that the side of the cerebellum that was stimulated mattered; only stimulation of the side that controls the leg walking on the faster treadmill belt changed adaptation rate.

"It is important to demonstrate that we can make learning faster or slower, as it suggests that we are not merely interfering with brain function," says Dr. Bastian. "Our findings also suggest that tDCS can be selectively used to assess and understand motor learning."

The results from this study present an exciting opportunity to test cerebellar tDCS as a rehabilitation tool. Dr. Bastian says, "If anodal tDCS prompts faster learning, this may help reduce the amount of time needed for stroke patients to relearn to walk evenly. It may also be possible to use tDCS to help sustain gains made in therapy, so patients can retain and practice improved walking patterns for a longer period of time. We are currently testing these ideas in individuals who have had a stroke."

Other co-authors on this study were Pablo Celnik and Gowri Jayaram, Johns Hopkins University School of Medicine; and Byron Tang, Rani Pallegadda, and Erin V.L Vasudevan, Kennedy Krieger Institute.

The study was funded by the National Institutes of Health and the Johns Hopkins Brain Sciences Institute.

Older women who have been diagnosed with an irregular heartbeat are at higher risk of stroke than men. A new study led by the Research Institute of the McGill University Health Centre (RI MUHC) shows that warfarin, the most common anticoagulant therapy used to prevent stroke in patients with Atrial fibrillation (AF) may not be as effective in women, 75 years or older, as in men. The results of the study are published in the Journal of the American Medical Association (JAMA).

"Our results suggest that elderly women with AF may need to be targeted for more effective stroke prevention therapy," says Dr. Louise Pilote, corresponding author of the study, researcher in epidemiology at the RI MUHC and Professor at McGill University's Department of Medicine. "Knowing the stroke risk is higher in women is something that both physicians and patients should be focusing on."

Atrial fibrillation (AF) affects approximately 350,000 Canadians and is the most common cardiac arrhythmia, a condition involving an irregular heart rhythm. Generally, the risk of developing AF increases with age and with other risk factors such as diabetes, high blood pressure, and underlying heart disease. People with AF have a risk of stroke that is 5 times greater than those in the general population

"We found that women had a 14 % higher risk of stroke then men," says Dr. Meytal Avgil Tsadok, first author of the study and Post-Doctoral Fellow funded by the Canadian Institutes of Health Research (CIHR) in the Division of Clinical Epidemiology at the MUHC. "Even though the adherence to warfarin was the same in both sexes the follow up and the level of anticoagulation may not be as high in women compared to men. Other reasons could be a combination of uncontrolled hypertension and some other vascular factors."

Researchers compared the incidence of stroke and warfarin use among 39,398 men and 44,115 women with AF in Quebec between 1998 and 2007. They used administrative data with linkage between hospital discharge, physicians and prescriptions drug claims databases.

"Physicians should put more emphasis on female sex as a risk factor in deciding to start anti coagulation treatment for stroke," says Dr. Pilote who is also director of the Division of General Internal Medicine at McGill and the MUHC. "Because study results in men do not always apply to women, we need women to participate in our studies in order to develop new strategies to effectively prevent stroke equally in both sexes."

Researchers from Cleveland Clinic's Wellness Institute and Harvard University have found that greater consumption of sugar-sweetened and low-calorie sodas is associated with a higher risk of stroke. Conversely, consumption of caffeinated or decaffeinated coffee was associated with a lower risk.

The study — recently published in the American Journal of Clinical Nutrition — is the first to examine soda's affect on stroke risk. Previous research has linked sugar-sweetened beverage consumption with weight gain, diabetes, high blood pressure, high cholesterol, gout and coronary artery disease.

"Soda remains the largest source of added sugar in the diet," said Adam Bernstein, MD, ScD, study author and Research Director at Cleveland Clinic's Wellness Institute. "What we're beginning to understand is that regular intake of these beverages sets off a chain reaction in the body that can potentially lead to many diseases — including stroke."

The research analyzed soda consumption among 43,371 men who participated in the Health Professionals Follow-Up Study between 1986 and 2008, and 84,085 women who participated in the Nurses' Health Study between 1980 and 2008. During that time, 2,938 strokes were documented in women while 1,416 strokes were documented in men.

In sugar-sweetened sodas, the sugar load may lead to rapid increases in blood glucose and insulin which, over time, may lead to glucose intolerance, insulin resistance, and inflammation. These physiologic changes influence atherosclerosis, plaque stability and thrombosis — all of which are risk factors of ischemic stroke. This risk for stroke appears higher in women than in men.

In comparison, coffee contains chlorogenic acids, lignans and magnesium, all of which act as antioxidants and may reduce stroke risk. When compared with one serving of sugar-sweetened soda, one serving of decaffeinated coffee was associated with a 10 percent lower risk of stroke.

In addition, study findings show that men and women who consumed more than one serving of sugar-sweetened soda per day had higher rates of high blood pressure and high blood cholesterol and lower physical activity rates. Those who drank soda more frequently were also more likely to eat red meat and whole-fat dairy products. Men and women who consumed low-calorie soda had a higher incidence of chronic disease and a higher body mass index (BMI). The investigators controlled for these other factors in their analysis to determine the independent association of soda consumption on stroke risk.

"According to research from the USDA, sugar-sweetened beverage consumption has increased dramatically in the United States over the past three decades, and it's affecting our health," said Dr. Bernstein. "These findings reiterate the importance of encouraging individuals to substitute alternate beverages for soda."