House Passes Health Care Reform Legislation, Obama’s Top Domestic Policy Close to Becoming Law
Late tonight, Sunday, March 21, 2010, the United States House of Representatives passed two bills to reform the health care delivery system.The first bill, H.R. 3590, the Patient Protection and Affordable Care Act, was the House’s concurrence with the health care reform legislation that the United States Senate passed on December 24, 2009.Analysis of the legislation indicates that H.R. 3590 will provide coverage for 32 million more Americans to reach 95% coverage in the United States.H.R. 3590 passed 219 to 212 and now will be sent to President Barack Obama for signature.To read APTA’s summary of this legislation, click here.
Following the passage of H.R. 3590, the Patient Protection and Affordable Care Act, the United States House of Representatives passed H.R. 4872, the Reconciliation Act of 2010 by a vote of 220-211.The Congressional Budget Office estimates that the health care reform legislation, addressed by reconciliation, will cost $940 billion but also cut the deficit by $138 billion over the next 10 years.This legislation modifies HR 3590 and must now be sent to the Senate for concurrence.If the Senate does not change the legislation and passes H.R. 4872 it will be sent to the President.To pass H.R. 4872, the Reconciliation Act of 2010, the Senate needs 51 votes.Earlier today, Senate Majority Leader Harry Reid indicated that the Democratic leadership has commitments from 52 Senators, not including Vice President Biden to pass H.R. 4872.Several procedural and parliamentarian hurdles will need to be clear in the Senate, but it is expected that the Senate will move this second piece of legislation making changes to the first in the coming weeks.APTA will be posting a summary of this legislation in the next week at www.apta.org/healthcarereform.
It should be noted that H.R. 3590 would extend the therapy cap exceptions process for the remainder of 2010, but would not prevent the 21.2% reduction in payments under the Medicare Physician Fee Schedule scheduled to go into effect on April 1, 2010.Congress will still need to pass legislation to avoid this cut in payments to physical therapists, physicians and other health care professionals.
As the final steps towards this top domestic policy priority of the President are completed, APTA will be providing its membership with resources and education on this legislation and its impact on physical therapy and the patients we serve.
March 9, 2010 (San Francisco, California) — Good news for coffee drinkers–new observational data presented last week at EPI|PNAM 2010, the Cardiovascular Disease Epidemiology and Prevention and Nutrition, Physical Activity, and Metabolism 2010 Conference, suggests that multiple cups of Joe are associated with a lower risk of arrhythmias. [1]
“A lot of people think they have palpitations from coffee, and doctors commonly tell people not to drink it, but there are very few actual data, and the data that are available suggest no relationship,” said lead investigator Dr Arthur Klatsky (Kaiser Permanente Division of Research, Oakland, CA). “We went into this study thinking there would be no association, but to our surprise, there was actually an inverse relationship. It could be protective, although one observational study doesn’t prove anything yet.”
To heartwire, Klatsky said his group has studied coffee off and on for many years and has published several studies, which have tended to vary in their results. These studies suggested a slightly increased risk of fatal and nonfatal MI, mostly in smokers, and no overall effect of coffee drinking on total mortality or cardiovascular mortality.
With these inconclusive findings, Klatsky said his group decided to look at some of the other major causes of cardiovascular disease, such as arrhythmias. They studied 130 054 participants in the Kaiser Permanente health plan, all of whom completed a questionnaire on coffee intake and other health habits.
After adjusting for multiple variables, including body-mass index, blood pressure, total cholesterol, and other measurements, the researchers found that coffee consumption was associated with a lower risk of hospitalization for arrhythmias and that the protective effect appeared to be additive. Individuals who drank more than four cups of coffee per day had an 18% lower risk of being hospitalized for any arrhythmia, and this reduction in risk was consistent among men and women, different ethnic groups, and smokers and nonsmokers.
Relative Risk (95% CI) of Arrhythmia Diagnosed by Coffee Intake
Arrhythmia
<1 cup/d
1–3 cups/d
>4 cups/d
Klatsky said that coffee is a complex substance and that it includes other ingredients that might be at work, including antioxidants, in reducing the risk of arrhythmias. However, they also performed an analysis looking at the relative reductions in risk among people who drank only decaffeinated coffee and found no protective effect, which suggests caffeine is the protective source.
Unknown Mechanisms
The mechanisms are still unknown at this stage, but Klatsky said that caffeine competes with adenosine in brain, so it might also compete with adenosine in the heart. Because adenosine affects conduction and recovery of heart muscle cells after depolarization, one of those effects, particularly the shortening of the refractory period, could provoke rhythm problems. By drinking coffee, the researchers speculate that this adverse effect is attenuated.
The data are observational and need to be confirmed in other studies. Moreover, the end point includes hospitalizations for arrhythmias, an end point that is easy to document, but future studies examining rhythm disturbances should include arrhythmias not severe enough for the patient to warrant a trip to the hospital, according to the researchers.
With the possibility of coffee protecting the heart and at minimum showing no risk of harm, Klatsky said it is possible for the popular drink to be tested in a randomized, controlled clinical trial, although the kinks of that study would need to be worked out.
“It might be a little tricky to get people to give up their coffee, and for those who aren’t coffee drinkers, it might be tough to get them to start drinking four cups per day,” said Klatsky.
March 8, 2010 (Savannah, Georgia) — Elderly adults who play brain fitness games that exercise global aspects of memory show improvements in the domain of delayed memory at 6 months compared with a slight decline in active controls, according to preliminary findings presented here at the American Association for Geriatric Psychiatry 2010 Annual Meeting.
Karen Miller, PhD, University of California at Los Angeles, reported that significant differences were observed at 6 months after randomization between the intervention group who were assigned to the Dakim BrainFitness computerized memory program vs active controls, even though after 2 months of training, “controls” were also given the same training as the intervention group.
Assessed by 4 different memory tests, the group who played the BrainFitness game for the full 6 months gained almost 2 points on memory scores, increasing from 10.4 at baseline to 12.1 at follow-up.
This is in contrast to controls, who, having played the same BrainFitness game from month 2 to month 6, had the same memory scores decrease slightly from 10.2 at baseline to 10.1 at follow-up (P = .001). A total of 38 elderly subjects completed the 6-month trial, 22 at an average age of 82 years in the intervention group and 16 at an average age of 83 years in the control group.
“By month 6, the intervention group had played more than double the number of sessions at 93 compared with only about 40 sessions played by active controls, so it’s the long-term use that improves overall memory. The maximum benefit comes when you keep on playing,” Dr. Miller told Medscape Psychiatry.
Pilot Study
Before launching the clinical trial, Dr. Miller and colleagues carried out a pilot study involving 22 elderly subjects, with an average age of 74 years, who were assigned to the Dakim BrainFitness computerized game or to an active control group.
Participants played the game 5 times a week, each session lasting 30 minutes, for 2 months. At the end of the 2-month pilot study, a modest effect size was seen on 1 memory test.
Realizing that this particular version of the BrainFitness game did not exercise traditional aspects of memory training, including encoding and long-term memory, UCLA investigators helped Dakim redesign the game. The version used in their latest clinical trial now exercises short-term memory, critical thinking, visual spatial skills, long-term memory, calculations, and language.
“There is also a variety of 300 to 400 games or events that cycles through each time a senior plays so they are not going through the same format each time,” Dr. Miller said.
“There are also 5 levels which can be preselected so this machine allows seniors to move up and down between levels, depending on how well they perform on different aspects of memory,” she added.
Dr. Miller also stressed that to see a training effect on memory, it is likely subjects will need to commit to regular memory training exercises, much in the same way people need to commit to other lifestyle behaviors, such as exercise and stress reduction.
She also believes computerized training will only be helpful in preventing memory decline in people whose memory is still relatively healthy.
Memory training devices, such as the program modified and used by the UCLA group, are also likely to benefit subjects with amnestic memory impairment and not those with impairment in multiple domains.
Dr. Miller noted that, in her experience, subjects with impairment in multiple domains continue to deteriorate relatively quickly even when they used the BrainFitness device on a regular basis.
“The longer a person is exposed to the BrainFitness program, the more likely they are to improve in verbal and visual memory. Even if you have no computer skills, you are able to use it,” said Dr. Miller.
Preliminary Results
Gary Small, MD, University of California at Los Angeles, told Medscape Psychiatry that these preliminary results are “encouraging” and that the Dakim BrainFitness program is a popular device in centers where it is been tested. “It is very much tailored to the older generation, with an easy-to-use touch screen, so seniors are enjoying it,” he added.
On the other hand, companies manufacturing these brain fitness games need to make sure the games are more than just fun and engaging and that they exercise all domains of memory, such as the Dakim BrainFitness program appears to do.
“The issue really is will these devices improve cognitive skills?” Dr. Small added that it is certainly feasible to incorporate the kinds of games and techniques into brain games that improve cognitive skills, as he himself has done it with training programs — companies just need the will to do so.
Dr. Miller and Dr. Small disclose a financial conflict of interest with Dakim. Dr. Small has received consulting and speaker’s fees from a number of pharmaceutical companies not relevant to his research with Dakim.
American Association for Geriatric Psychiatry’s (AAGP) 2010 Annual Meeting: Session 212. Presented March 6, 2010.
March 4, 2010 — Obesity and depression are closely linked in that each raises the risk for the other, a new meta-analysis confirms.
The study found that obese people have a 55% increased risk of developing depression, and those with depression have a 58% increased risk of becoming overweight over time.
These results should spur medical specialties to collaborate in an effort to prevent depression and obesity, each a condition that poses major health problems, said lead author Floriana S. Luppino, MD, Leiden University Medical Center, The Netherlands.
“The first step is to try to do the best we can, based on the facts we know now, and that would be for psychiatrists to monitor their patients’ weight and for internal medicine or general practitioners who see obese or overweight patients to check on their mental state to see if they’re on the way to developing a mood disorder which is mostly treatable.”
The study is published in the March issue of Archives of General Psychiatry.
For the analysis, researchers searched the literature for studies published in English up to March 2008. The studies had to have a follow-up period of at least 1 year, express weight as body mass index (BMI), and specify the way depression was assessed. The final analysis included 15 studies.
For the examination of the link between overweight (defined as a BMI between 25 and 29.99) or obesity (defined as a BMI of 30 or more) and depression, the total number of subjects was 55,387. For the inverse relationship, there were 7196 subjects. Some studies provided longitudinal data on both directions.
The pooled odds ratio (OR) was 1.55 (95% confidence interval [CI], 1.22 – 1.98; P < .001) for the 8 studies that examined the association between obesity at baseline and depression at follow-up.
Obesity and Depression Link Stronger in the United States?
The ORs for American studies differed significantly from European ones (P = .05), indicating that the association was stronger among Americans. The reason for this is not clear. However, according to the World Health Organization, the mean adult BMI is higher in the United States than in Europe. “If the mean BMI is higher in the US, and a higher BMI means more depression, that could explain it,” said Dr. Luppino.
A significant difference was also seen between ORs for depression outcome as a clinical diagnosis and as depressive symptoms (P = .05), suggesting that the effect of the association is stronger when depression is assessed by a diagnostic clinical interview rather than a self-report symptom list.
As for the inverse relationship — depression causing obesity — the pooled OR of the 9 studies examining the effect of depression on obesity was 1.58 (95% CI, 1.33 – 1.87; P < .001). Subgroup analysis did not show any significant differences.
The pooled OR for depression exposure on overweight was 1.20 (95% CI, 0.87 – 1.66; P = .26). Subgroup analysis found the association stronger with longer follow-up.
The stronger relationship between depression and obesity compared with that between depression and overweight suggests there is a “dose-response” element to the association, said Dr. Luppino.
Psychiatrists Should Monitor Weight
These new data suggest that psychiatrists should regularly monitor the weight of their depressed patients, something that is “easy to do,” said Dr. Luppino.
“If you think a patient is borderline overweight or obese, maybe there could be some kind of intervention, for example, sending that patient to a dietitian or someone involved in internal medicine, or to a general practitioner. This may help that patient take control, possibly preventing weight gain with lifestyle changes or dietary changes.”
Although previous research suggests that the relationship between depression and excess weight only applies to women, this study confirms it also exists in men.
The relatively long period of follow-up for the studies included in the analysis may be 1 possible explanation.
“In a short period of time, their different hormones could explain why women are more prone to becoming overweight or obese, but in time, other pathways may become involved, and this might explain why, in the end, the risk of obesity or overweight [in depressed patients] exists in both genders,” said Dr. Luppino.
The relationship between depression and obesity is likely multifactorial, involving more than 1 pathway — biological, psychological or both, she said.
Biological pathways could involve inflammation (linked to both depression and obesity), the hypothalamic-pituitary-adrenal axis (also linked to both conditions), and/or insulin resistance (obesity increases risks for diabetes and insulin resistance, which could induce alterations in the brain and increase the risk for depression).
Emphasis on Thinness
One psychological pathway could originate with Western society’s emphasis on thinness, with weight gain contributing to decreased self-esteem, a risk factor for depression, said Dr. Luppino.
The nature of the relationship between obesity and depression may vary from person to person. “For one person, it might be a biological system that’s not working the way it should, but in another person, it could be that self-esteem is low, and if that person is obese, it might be the last push for that person to get depressed.”
But perhaps elements of both a biological pathway and a psychological pathway are needed to create the obesity-depression link. “If one gets obese or overweight due to biological factors but self-esteem is great and you don’t have body dissatisfaction, you may not get depressed,” said Dr. Luppino.
Genes that increase vulnerability to depression can also play a role, said Dr. Luppino. “For a person with good self-esteem who is overweight or obese but who is not prone to depression, my best guess is that the chances for being depressed at the end are lower.”
Other explanatory factors could include unhealthy lifestyles, such as lack of physical activity and poor diet, and the use of antidepressants, all of which can lead to weight gain.
Future research should examine such things as the potential role of depression characteristics, medication use, physical activity, and dietary patterns, the study authors write.
Excellent Example
Reached for a comment, Michelle Riba, MD, associate chair for Integrated Medicine and Psychiatric Services, Department of Psychiatry, University of Michigan, Ann Arbor, and past president, American Psychiatric Association, said the study “is an excellent example of the use of a meta-analytic approach for 2 large public health problems — depression and obesity.”
But she did note some limitations of the analysis; for example, it only included adult studies. “We know many of these problems begin much earlier, in childhood, Dr. Riba told Medscape Psychiatry.
As well, important factors, such as sleep and sleep problems related to depression and obesity, and patients with diabetes or cardiovascular diseases were not included.
“We also don’t know about medications that patients might have been on to affect mood and obesity. Bipolar disorder, alcohol and substance abuse, socioeconomic issues, and health insurance are also not addressed,” she said.
The authors have disclosed no relevant financial relationships.
March 4, 2010 — An Alzheimer’s disease (AD) progression rate measure that can be calculated at the initial visit can reliably predict how quickly the individual patient will lose cognitive and other abilities.
Rachelle Doody, MD, PhD, and colleagues from Baylor College of Medicine in Houston, Texas, report initial results using the prognosis indicator with 597 patients followed up for 15 years published online February 23 in Alzheimer’s Research & Therapy.
“Patients and families frequently ask clinicians to predict expected rates of cognitive and functional decline, and clinicians currently have little basis for making such decisions,” Dr. Doody told Medscape Neurology.
“We’ve found that a simple, calculated progression rate at the initial visit gives reliable information regarding performance over time,” she said. “The slowest progression group also survives longer.”
Calculating AD Progression Rate
The preprogression rate is calculated using a standard assessment of symptom duration in years and the baseline Mini-Mental State Examination (MMSE) score. The estimate of duration includes a series of questions about the duration of specific symptoms that might be a sign of AD, medical records review, and informant interview.
The study authors explain, “Since a cognitively intact individual should obtain the maximum MMSE score of 30, the preprogression rate is given by the formula: (30 − baseline MMSE)/estimated duration of symptoms in years.”
Those with an MMSE score decrease of less than 2 points per year were classified as slow progressors. Intermediate progressors were defined as having a 2- to 4-point decrease per year and rapid progression as a 5 point or greater decrease per year in MMSE score.
Dr. Doody told Medscape Neurology, “The procedures for obtaining and using the information are not yet in common use, but they could be. With further refinement, physicians could use this work to tell patients whether they fall into a slow, intermediate, or rapidly progressing category with respect to the intrinsic progression of their AD. They might decide upon follow-up intervals and how aggressive to be with medications based upon the progression rate. Once started on therapy, it might be possible to alter the intrinsic rate, but this requires further study.”
The researchers examined outcomes for patients annually for up to 15 years using the MMSE, the Alzheimer’s Disease Assessment Scale–Cognitive Subscale (ADAScog), the Verbal Series Attention Test, the Clinical Dementia Rating Scale Sum of Boxes, and the Lawton and Brody Activities of Daily Living Scale, which combines the Physical Self-Maintenance Scale and the Instrumental Activities of Daily Living Scale.
Slow Progressors Also Live Longer
The investigators found that patients in the slow and intermediate groups maintained better performance on tests of cognitive function, global function, and complex activities of daily living than the rapid progressors. For example, slow progressors gained 0.6 fewer points per year on the ADAScog and intermediate progressors 0.8 fewer points per year than rapid progressors.
At study entry, the slow progressors also had a longer estimated duration of symptoms than intermediate or fast progressors, as well as higher IQ and education.
Slow progressors also lived longer. Median survival was 4.7 years for slow, 4.1 years for intermediate, and 2.5 years for rapid progressors, adjusted for age, sex, education, and baseline severity (hazard ratio, 0.62 for slow vs fast progressors).
“Our results suggest that prognostications based upon initial progression rate are most reliable for slow and fast progressors but that long duration reliability of an intermediate progression rate may depend upon the patient’s age and life expectancy at diagnosis,” the study authors conclude. “It would be safe to say that an intermediate progressor may remain so for several years, but that, if the patient lives for a long time after diagnosis, the rate may increase sufficiently to affect both abilities and survival.”
Next Question: Can Drugs Alter Progression Rate?
Whether these “apparently intrinsic” progression rates can be modified by antidementia drug treatment is a key unanswered question that must be answered before the progression rate tool can be adopted for clinical use, the study authors say.
For now, Dr. Doody said, “Physicians could tell patients that people do not progress naturally at the same rate and that their individualized progression characteristics should be taken into account in planning their treatment and in monitoring their response to therapy. They could also say that the proposed rate requires some procedures that are not yet in everyday use (a standardized estimate of duration) and that they will decide over time whether or not to incorporate these procedures into what they do based upon continued studies of its utility.”
This study also has implications for AD clinical trial design. “Currently, parallel group studies count on randomization to yield comparable placebo and treatment groups,” the study authors write. “Preprogression rates are not assessed, yet imbalances across the treatment groups in this important variable could obscure or create treatment differences. Future clinical trials may benefit from gathering systematic data regarding individual symptom onset in order to perform a formal estimate of duration and to calculate preprogression rates.”
Not Ready for Routine Use
Cognitive neurologist Alireza Atri, MD, PhD, agreed that this might be useful. Dr. Atri, who recently analyzed long-term effectiveness of combination therapy in AD (Alzheimer Dis Assoc Disord. 2008;11:209-221), is director of the Memory Disorders & Special Dementia Units at the Veterans’ Affairs Geriatric Research Education and Clinical Center in Bedford, Massachusetts, and assistant in neurology at Massachusetts General Hospital/Harvard Medical School in Boston.
Asked by Medscape Neurology to comment on this study, Dr. Atri said, “I think this is an important study with several exceptional strengths, including utilization of a large, well-characterized longitudinal clinical cohort with useful measure and endpoints and analysis using sophisticated methods guided by good clinical and scientific knowledge from a leader in the field who has an uncommon perspective and expertise, working at the interface of clinical care and clinical trials and utilizing quantitative methodology to address important questions with great practical implications that, thus far, have been mostly neglected, overlooked, and/or underappreciated.”
Dr. Atri noted that although this model for predicting risk and prognosis in AD is not yet ready for routine use, it “provides a very good enhancement/upgrade from previous work and prognostication models, including some of Dr. Doody’s own work, that integrate patient demographics and clinical characteristics and measures, including test scores, type and duration of symptoms, and physical exam findings, at a first clinical visit to a neurologist/physician in order to better predict the highly variable individual course we see in patients with Alzheimer’s disease.”
Dr. Atri said that the study raises questions that need to be addressed further, including the effect of antidementia medications, vitamins and dietary supplements, vascular risk factors, behavioral symptoms, physical findings, especially parkinsonism and extrapyramidal signs, and genetic susceptibility factors, such as APOE-e4 status.
“We are a ways away still, but we desperately need to be wiser and more efficient in our approaches to gathering and using clinical data,” Dr. Atri said. “I agree that clinical trials should heed Dr. Doody’s findings and incorporate more data and approaches like this to minimize risk of imbalances between or within treatment groups that can easily obscure signals of efficacy in Alzheimer’s disease trials.”
The study was supported by the National Institutes of Health and by the Alzheimer’s Association. Dr. Doody receives support from the Cain Foundation and from the Cynthia and George Mitchell Foundation. Dr. Atri has disclosed no relevant financial relationships.
Alzheimer Res Ther. Published online February 23, 2009.
March 5, 2010 (San Francisco, California) — Vigorous physical activity is associated with a modestly lower risk of cardiovascular disease when compared with activities of moderate intensity, a new study shows [1]. The researchers found that the total volume of activity may be associated with the greatest reduction in risk, however, and that increased physical activity, even vigorous activity, did not appear to have any detrimental effects.
“If two people are expending a thousand calories per week, does it matter if they do that by running or by walking?” said lead investigator Dr Andrea Chomistek (Harvard Medical School, Boston, MA) in explaining the rationale of the study to heartwire. “We found that there might be some benefit to doing it with vigorous activity such as running, but it doesn’t appear to be a very strong benefit. As long as you’re burning a certain amount of calories per week, between 600 or 1000 calories per week, it’s okay if you do that by walking. You don’t necessarily have to go out and run a marathon.”
Presenting the results of the study here this week at EPI|PNAM 2010, the Cardiovascular Disease Epidemiology and Prevention and Nutrition, Physical Activity, and Metabolism 2010 Conference, Chomistek said that approximately 2.5 hours per week of moderate to vigorous physical activity has been shown to lower the risk of cardiovascular disease, but the dose-response curve is not well defined.
There is limited evidence, for example, to support the beneficial effects of large amounts of vigorous activity, and some researchers have even observed cardiovascular injury, as evidenced by elevated troponin levels, among marathon runners and endurance athletes, she noted.
Health Professionals Follow-Up Study
In this analysis of 43 647 individuals participating in the HealthProfessionals Follow-Up Study, the researchers, with senior investigator Dr Eric Rimm (Harvard Medical School), wanted to determine whether vigorous activity, independent of the amount of time spent exercising, was associated with a lower risk of cardiovascular disease compared with moderate exercise, and if it was, whether more was better.
In the study, baseline physical activity levels were first collected in 1986 and assessed every two years thereafter until 2004. To control for the time spent exercising, researchers calculated the average intensity of weekly exercise, and this was based on the time spent exercising and the number of metabolic-equivalent-task (MET)-hours expended per week. The primary end point of the study, total cardiovascular disease, included fatal coronary heart disease, nonfatal MI, and fatal and nonfatal stroke.
Among individuals who exercised the same number of MET-hours per week, vigorous activity was associated with a trend toward lower risk of cardiovascular disease compared with individuals who performed moderate activity. For example, for those who expended six to 15 MET-hours per week, there was a modestly lower risk of cardiovascular disease among those who performed vigorous activity, such as bicycling or running, compared with those walked briskly or lifted weights.
Risk Ratios (95% CI) of Cardiovascular Disease Associated With Exercise Intensity and MET-Hours Per Week
MET-hours/week
Low moderate (average intensity 3–4.4 METs)
High moderate (average intensity 4.5– 5.9 METs)
Low vigorous (average intensity 6–7.4 METs)
High vigorous (average intensity >7.5 METs)
The researchers point out that the total volume of physical activity at all intensity levels appeared to be associated with the largest reduction in risk, and that there doesn’t appear to be any harm in the amount of exercise done weekly.
“There has been some concern among individuals, such as those who run triathlons and marathons, that doing long amounts of endurance activity could actually damage the heart,” said Chomistek. “We’ve seen elevations in troponin levels in these athletes, so we wanted to see whether there was a point at which maybe too much running isn’t good. We found that wasn’t really true. You can really do as much as you want. It’s still effective.”
The researchers did report that the lowest risk of cardiovascular disease was observed in men performing 6 to 7.9 hours of vigorous activity per week, and the risk of cardiovascular disease was slightly higher, but not statistically so, in those who performed more exercise.
Nadir of Cardiovascular Risk
Commenting on the results of the study for heartwire, Dr William Krauss (Duke University Medical Center, Durham, NC), who was not involved in the analysis, noted the Harvard Alumni Health Study, led by the late Dr Ralph Paffenbarger (Stanford University School of Medicine, CA), suggested there might be a nadir of cardiovascular risk among runners who ran 20 miles per week, but an increased risk among those who ran 50 to 60 miles per week. Krauss noted that this increased risk was not statistically significant, and other studies have not shown an inverse risk with more time spent exercising.
“This is still an open question,” said Krauss. “Six hours of vigorous activity per week is lot. When you’re starting to get to eight or 10 hours per week, that’s training for marathons and other endurance events. I wouldn’t suspect there would be an adverse cardiovascular effect, but more adverse noncardiac effects, such as injuries, that would lead to long-term inactivity. But this study is reassuring in that there is no adverse effect on the cardiovascular system.”
Asked about the current guidelines, Chomistek told heartwire that the focus remains on getting individuals active.
“There are still so many people in the population who don’t do anything,” she said. “If we tell these patients that they have to go out and run a marathon, they’re probably not going to do it. We can still have the guidelines for those people, but for people who are already active, we can tell them to keep increasing their activity, because you’re going to get greater benefit. So even if you’re doing the two-and-a-half hours a week that you’re supposed to do, there is still greater benefit if you do more than that.”
Senate Passes H.R. 4213; Therapy Cap Exceptions and Medicare Physician Fee Schedule Fix Included
This afternoon, the US Senate passed H.R. 4213, the Tax Extenders Act of 2009 by a vote of 62-36. This legislation includes APTA’s three priorities of extending the therapy cap exception process until December 31, 2010, freezing payments at the 2009 level under the Medicare Physician Fee Schedule preventing the 21.2% reduction until September 30, 2010 and re-instating the Geographical Practice Cost Indices (GPCI) floor at 1.0 for the remainder of 2010.
Next Steps. The bill now has to be passed by the House of Representatives and signed by President Obama before becoming law.
January 29, 2010 — A ghostly “suicide” drug wafts into immune cells in joints, making the cells self-destruct and reducing rheumatoid arthritis in mice.
The drug, technically a BH3 mimetic dubbed TAT-BH3, is a man-made molecule. One part of the molecule lets it drift through cell walls. The other part mimics a chemical signal missing in the macrophage immune cells that build up inside joints afflicted by rheumatoid arthritis (RA).
Because they are missing this signal, macrophages in RA joints don’t die off as they are supposed to do. They live on, destroying bone and inflaming the joint, says Harris Perlman, PhD, associate professor of medicine at Chicago’s Northwestern University Feinberg School of Medicine.
“In RA, there is this persistent inflammation that never shuts down. Part of the reason is these macrophages are missing a protein they need to die off,” Perlman tells WebMD. “So this drug says OK, let’s replace this protein. Let’s bring back the death pathway.”
Perhaps because normal cells aren’t clinging to life like the zombie macrophages involved in RA, the drug doesn’t kill normal macrophages. The drug was not toxic to mice.
But in mice with RA, injections of TAT-BH3 cut bone erosion by as much as 39% and thinned the too-thick lining of the joint by up to 34%.
Perlman says that by hitting it’s Bim-protein target, TAT-BH3 has therapeutic effects that go beyond just killing macrophages.
“This drug does far more than cause cell death,” he says. “We think this Bim protein has multiple functions and may be a great target for disease.”
Perlman’s team and others are making their molecule more appropriate for human treatment. One approach they are trying is to use tiny nanoparticles to speed the BH3 mimetic through cell walls. Much work remains before their drug prototype is ready for human studies.
Other BH3 mimetics, with targets different from the so-called Bim protein that is the focus of the Perlman study, are being developed as cancer treatments. Some already are showing promising results in clinical trials.
The Perlman study appears in the February issue of Arthritis & Rheumatism.
SOURCES:
Perlman, H. Arthritis & Rheumatism, February 2010; published online Jan. 28, 2010.
Harris Perlman, PhD, associate professor of medicine, Northwestern University Feinberg School of Medicine, Chicago.
January 29, 2010 - Elevated levels of inflammatory proteins called cytokines and related factors in the blood may be an early warning sign of impending rheumatoid arthritis (RA), according to a new study.
Researchers have found that levels of certain cytokines and related factors in the blood increase significantly prior to the development of rheumatoid arthritis, long before symptoms emerge. They say the finding paves the way for developing a blood test for early diagnosis of the mysterious disease.
“Our findings present an opportunity for better predicting the risk of developing RA and possibly preventing disease progression,” says researcher Solbritt Rantapää-Dahlqvist, MD, of University Hospital in Umea, Sweden, in a news release.
Rheumatoid arthritis is a painful, progressive condition that can be difficult to diagnose in the early stages because it often begins with only subtle symptoms, such as achy joints or early morning stiffness. Other conditions, such as lupus, osteoarthritis, and fibromyalgia may also mimic the early symptoms of rheumatoid arthritis, which makes a definitive diagnosis difficult.
But studies have shown that early diagnosis and treatment of rheumatoid arthritis can help sufferers live a more active life and potentially avoid the type of joint damage that leads to disability.
Early Signs of RA
The cause of rheumatoid arthritis is not understood, but various components of the immune system and synovial tissue, which lubricates the joints, are thought to be involved.
Cytokines are pro-inflammatory proteins that are often found in the synovial tissue after rheumatoid arthritis has developed.
In the study, published in Arthritis & Rheumatism, researchers examined whether particular cytokines and related factors are elevated prior to the emergence of rheumatoid arthritis symptoms.
They analyzed blood samples from 86 people in Sweden without symptoms of rheumatoid arthritis at the time of donation who later developed RA and compared them with samples from 256 healthy individuals.
The results showed levels of several cytokines and related factors were elevated up to years before diagnosis with rheumatoid arthritis.
Researchers say the findings support the idea that the immune system was already stimulated and rheumatoid arthritis was developing. If further studies confirm these results, a blood test to screen for these elevated cytokines may help diagnose RA before symptoms emerge.
NEW YORK (Reuters Health) Jan 29 - A simple management program, featuring a brief educational session and monthly follow-up calls, can reduce hospitalizations and emergency room visits for chronic obstructive pulmonary disease (COPD), new research shows.
As reported in the January 14th online issue of the American Journal of Respiratory and Critical Care Medicine, the management program yielded a 1-year mean cumulative frequency of COPD-related hospitalizations and emergency room visits of 0.48 per patient. This rate is much lower than the 0.82 per patient seen with usual care (p < 0.001), representing a 41% reduced risk.
“In 2000, COPD was responsible for 726,000 hospital admissions and 1.5 million emergency department visits in the United States,” lead author Dr. Kathryn L. Rice, from the University of Minnesota, Minneapolis, and colleagues note. “COPD exacerbations are associated with impaired respiratory health status and more rapid disease progression.”
The team points out that disease management programs have been successful in chronic conditions such as heart failure and diabetes. “However,” they add, “compelling evidence that disease management improves COPD care is lacking.”
In a multicenter randomized trial, the researchers aimed to determine whether a disease management program, with an emphasis on early recognition and self-treatment of COPD flare-ups, could benefit patients with severe COPD. The 1-year study, which was conducted at 5 Veterans Affairs medical centers, included 743 patients who, in the previous year, had a hospital admission or emergency department visit for COPD, chronic home oxygen use, or received systemic corticosteroids for their disease.
Patients randomized to the disease management program received a 1 to 1.5 hour educational session by a respiratory therapist case manager. Topics discussed included general information about COPD, how to use an inhaler properly, a review of COPD medications, smoking cessation, influenza and pneumococcal vaccine recommendations, the importance of regular exercise, and instructions in hand hygiene.
Subjects in the program also received an individualized action plan, which included refillable prescriptions for prednisone and an oral antibiotic, case manager contact information, and a telephone number for a 24-hour Veterans Affairs helpline. Lastly, case managers made monthly telephone calls to check up on each patient.
By contrast, subjects in the usual care comparison group received only a one-page handout discussing the principles of COPD care and listing the telephone number for the helpline.
As noted, the disease management program was associated with a marked reduction in COPD-related hospital admissions and emergency room visits - but the intervention had significant positive effects on several non-COPD-related outcomes as well. For instance, per 100 patient-years, the intervention decreased the hospitalizations for cardiac or non-COPD pulmonary conditions by 49% (to 8.7, from 17.0 with usual care), all-cause hospitalizations by 28% (to 56.8, from 79.3 with usual care), and all-cause emergency room visits by 27% (to 67.0, from 91.2 with usual care).
“Although a formal cost benefit analysis has not been done, this intervention shows potential for reducing healthcare costs in addition to improving quality,” Dr. Rice’s team concludes. Still, additional studies in other settings are needed to confirm these findings, they point out.
