<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_455"
                     title="Low Vitamin D Linked to Hip OA (CME/CE)"
                     score="0.014"
                     href="http://www.medpagetoday.com/Rheumatology/Arthritis/tb/18379?impressionId=1265741112417"
                     
      &lt;p&gt;Elderly men with low serum levels of vitamin D are at increased risk for developing hip osteoarthritis, a prospective cohort study found.&lt;/p&gt;
&lt;p&gt;Men whose levels of 25-hydroxyvitamin (OH)D were between 15.1 to 30 ng/mL had twice the likelihood of prevalent radiographic hip osteoarthritis than those whose levels were normal (OR 2.19, 95% CI 1.21 to 3.97), according to R. Krishna Chaganti, MD, of the University of California at San Francisco, and colleagues.&lt;/p&gt;
&lt;p&gt;Conversely, after adjusting for age, season at blood draw, and clinic site, higher vitamin D levels were associated with a lower prevalence of hip osteoarthritis (OR 1.39 per 1 SD decrease in 25(OH)D level, 95% CI 1.11 to 1.74), the researchers reported in the February issue of &lt;em&gt;Arthritis &amp;amp; Rheumatism&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Because the role vitamin D may play in the pathogenesis and progression of osteoarthritis is unclear, Chaganti and colleagues analyzed data from the Osteoporotic Fractures in Men Study, which enrolled a large cohort of elderly men between 2000 and 2002 from six centers across the U.S.&lt;/p&gt;
&lt;p&gt;A total of 1,104 men whose mean age was 77.2 years had baseline measurements of serum vitamin D, and about 4.5 years later pelvic radiographs were obtained.&lt;/p&gt;
&lt;p&gt;Radiographs were scored to reflect joint space narrowing, osteophyte formation, cysts, subchondral sclerosis, and femoral head deformity.&lt;/p&gt;
&lt;p&gt;Vitamin D levels were categorized as deficiency (&amp;#8804;15 ng/mL), insufficiency (15.1 to 30 ng/mL), and sufficiency (&amp;gt;30 ng/mL).&lt;/p&gt;
&lt;p&gt;Mean vitamin D level was 23.38 ng/mL in men who had radiographic hip osteoarthritis, compared with 26.04 ng/mL in men without radiographic abnormalities (&lt;em&gt;P&lt;/em&gt;=0.0002).&lt;/p&gt;
&lt;p&gt;Men with hip osteoarthritis had a higher prevalence of both vitamin D insufficiency (77% versus 65%, &lt;em&gt;P&lt;/em&gt;=0.002) and deficiency (10.2% versus 7.5%, &lt;em&gt;P&lt;/em&gt;=0.012).&lt;/p&gt;
&lt;p&gt;Moreover, they had slower six-meter walking speed (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001) and reported more hip pain (&lt;em&gt;P&lt;/em&gt;=0.0001).&lt;/p&gt;
&lt;p&gt;Men who were vitamin D deficient also tended to have an increased likelihood of hip osteoarthritis (OR 1.99, 95% CI 0.83 to 4.74), but after adjustment in multivariate models, statistical significance was lost with this level of the vitamin.&lt;/p&gt;
&lt;p&gt;&quot;The association of low 25(OH)D levels with prevalent radiographic hip [osteoarthritis] underscores the potentially important role of vitamin D in the pathogenesis of [osteoarthritis]. Vitamin D metabolites have been found to be associated with the regulation of the Wnt pathway, products of which play important roles in the development and maintenance of bone and cartilage,&quot; the investigators explained.&lt;/p&gt;
&lt;p&gt;Furthermore, in vitro studies have suggested that serum levels of 25-hydroxyvitamin D&lt;sub&gt;3&lt;/sub&gt; can affect the ratio of RANKL to osteoprotegerin and thereby influence bone deterioration and repair.&lt;/p&gt;
&lt;p&gt;Previous investigations have yielded conflicting results. One study found that low levels of vitamin D were not associated with worsening of knee osteoarthritis, as reflected in loss of articular cartilage on MRI.&lt;/p&gt;
&lt;p&gt;Another study, however, linked knee osteoarthritis with low vitamin D levels, particularly in patients who also had decreased bone mineral density in the lumbar spine.&lt;/p&gt;
&lt;p&gt;&quot;Vitamin D influences the mineralization of bone matrix, and low serum levels of vitamin D may result in poorly mineralized bone that might alter forces across the joint and reduce joint deterioration,&quot; the authors suggested.&lt;/p&gt;
&lt;p&gt;On the other hand, low levels may interfere with chondrocyte metabolism and thereby increase degeneration.&lt;/p&gt;
&lt;p&gt;Further studies will be needed to more fully clarify the effects of the vitamin on the development and progression of osteoarthritis, the investigators cautioned.&lt;/p&gt;
&lt;p&gt;Strengths of the study include the large cohort of participants, careful classification of radiographic osteoarthritis, and reliance on the gold standard of vitamin D measurement, the 25(OH)D level.&lt;/p&gt;
&lt;p&gt;Limitations include the cross-sectional design, precluding the inference of causality, and the gap in time between measurement of serum vitamin D and radiography.&lt;/p&gt;
&lt;p&gt;The authors concluded that therapeutic interventions to increase vitamin D serum levels in the elderly &quot;are warranted,&quot; with the goal of improving skeletal health in this vulnerable age group.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, the National Institute on Aging, the National Center for Research Resources, and the NIH Roadmap for Medical Research.&lt;/p&gt;&lt;p&gt;The lead author was supported by a grant from the American College of Rheumatology Research and Education Foundation.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_443"
                     title="Evidence-Based Treatment Improves Older Stroke Victims&apos; Chances (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/Cardiology/Strokes/tb/18360?impressionId=1265741112417"
                     
      &lt;p&gt;Older stroke patients remain at higher risk for adverse outcomes than younger ones, but the gap has narrowed with wider implementation of evidence-based guidelines, researchers say.&lt;/p&gt;
&lt;p&gt;More than 10% of stroke patients over 80 died in the hospital, compared with 3% of those under age 50, Gregg C. Fonarow, MD, of the University of California Los Angeles, and colleagues reported online in &lt;em&gt;Circulation&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;But overall use of guideline-recommended therapies improved substantially in older patients from 2003 to 2009, particularly for patients over 90, they said.&lt;/p&gt;
&lt;p&gt;During that time, several hospitals and stroke centers have adopted &quot;Get with the Guidelines,&quot; an intervention to apply evidence-based guidelines to care. Adopters have seen &quot;substantial improvements ... in performance measures for ischemic stroke patients, including pharmacological and nonpharmacological management in each age group,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;Before launching the initiative in 2003, studies generally showed lower use of guideline-recommended therapy and worse outcomes in older stroke patients.&lt;/p&gt;
&lt;p&gt;To assess changes since initiative started, the researchers analyzed more than 502,036 ischemic stroke admissions to 1,256 hospitals participating in the guidelines program between 2003 and 2009. Mean patient age was 71, and 52.5% were women.&lt;/p&gt;
&lt;p&gt;They found that performance on most evidence-based measures was lower in older patients  --  those ages 80 and up  --  compared with younger patients.&lt;/p&gt;
&lt;p&gt;The largest differences were seen in the proportion of eligible patients who received intravenous tissue plasminogen activator (tPA) treatments (51.1% for older patients versus 61.6% for those under 50, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;Providers were also less likely to treat older stroke patients with lipid-lowering therapies than younger patients (54.2% versus 71.7%, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;The smallest differences involved antithrombotic therapy within 48 hours of admission and at discharge.&lt;/p&gt;
&lt;p&gt;In terms of outcomes, older patients had a significantly higher inhospital mortality rate (10.3% versus 3%), and they were less likely to be discharged home. Rather, they were more likely to be discharged to a skilled nursing facility (42.1% versus 5.3%, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) or hospice (12% versus 0.5%, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;With each 10-year age increase, patients with ischemic stroke were 31% less likely to be discharged home and 27% more likely to die in the hospital.&lt;/p&gt;
&lt;p&gt;But the researchers said that, generally, the use of guideline-recommended therapies improved substantially in older patients from 2003 to 2009.&lt;/p&gt;
&lt;p&gt;In those ages 90 and older, use of intravenous tPA increased threefold, from 20.4% in 2003 to 62.4% in 2009. And use of lipid lowering therapy increased from 15.6% in 2003 to 71.7%.&lt;/p&gt;
&lt;p&gt;The researchers wrote that by 2009, &quot;many of the age-related differences in care had narrowed or were eliminated.&quot;&lt;/p&gt;
&lt;p&gt;They cautioned, however, that there could be residual confounding by unmeasured factors. For example, physicians may be uncertain about risks versus benefits in treating older patients who are under-represented in RCTs.&lt;/p&gt;
&lt;p&gt;The authors noted that their study was limited by its reliance on the accuracy and completeness of medical records.&lt;/p&gt;
&lt;p&gt;Also, they noted, the &quot;Get with the Guidelines&quot; program tends to attract larger teaching hospitals, which already have a &quot;strong interest in stroke care and quality improvement,&quot; and thus the findings may not be generalizable.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The &quot;Get with the Guidelines&quot; program is supported by the American Heart Association and the American Stroke Association, as well as grants from Pfizer and the Merck-Schering Plough Partnership.&lt;/p&gt;&lt;p&gt;Fonarow reported relationships with Pfizer, Merck/Schering Plough, BMS/Sanofi.&lt;/p&gt;&lt;p&gt;Co-authors reported relationships with Boehringer Ingelheim, Ferrer, CoAxia, Talecris, Concentric Medical, and Cygnis.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_364"
                     title="ADT for Prostate Cancer Raises Heart Risks"
                     score="0.011"
                     href="http://www.medpagetoday.com/Urology/ProstateCancer/tb/18250?impressionId=1265741112417"
                     
      &lt;p&gt;Androgen deprivation therapy (ADT) for prostate cancer can exacerbate cardiac risk factors and may increase the risk of heart attack and cardiac death, according to an advisory supported by four medical organizations.&lt;/p&gt;
&lt;p&gt;However, the groups did not offer specific guidelines for clinicians on when to employ ADT therapy or avoid it.&lt;/p&gt;
&lt;p&gt;Clinical trials have shown that ADT increases body weight, decreases lean mass and increases fat mass, reduces insulin sensitivity, and triggers or worsens dyslipidemia.&lt;/p&gt;
&lt;p&gt;Several studies have demonstrated a significant increase in cardiovascular death in prostate cancer patients treated with hormonal therapy or bilateral orchiectomy, although some studies have shown no association between ADT and increased cardiovascular risk, according to a report that will appear in the Feb. 16 issue of &lt;em&gt;Circulation: Journal of the American Heart Association&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Some evidence also suggests ADT may predispose men to metabolic syndrome.&lt;/p&gt;
&lt;p&gt;&quot;Based on current data, it was appropriate to conclude that there may be a relationship between ADT therapy in patients with prostate cancer and future cardiovascular risk,&quot; Glenn N. Levine, MD, of Baylor College of Medicine in Houston and chair of the advisory writing committee, said in a statement.&lt;/p&gt;
&lt;p&gt;The writing committee comprised representatives of the American Heart Association, American Urological Association, and American Cancer Society. Additionally, the American Society for Radiation Oncology endorsed the advisory.&lt;/p&gt;
&lt;p&gt;The authors&apos; review of literature showed that ADT increased cardiovascular risk in 1% to 6% of various studies&apos; patient populations. With that in mind, &quot;the decision about whether to initiate ADT should be based on weighing the benefits of therapy with this potential modest risk,&quot; Levine said.&lt;/p&gt;
&lt;p&gt;The decision to initiate ADT should remain with the physician who has responsibility for treating a patient with prostate cancer, the authors wrote. That includes patients with known cardiac disease.&lt;/p&gt;
&lt;p&gt;&quot;It is the consensus of the writing group that there is no clear indication for patients for whom ADT is believed to be beneficial to be referred to internists, endocrinologists, or cardiologists for evaluation before initiation of ADT,&quot; the authors said.&lt;/p&gt;
&lt;p&gt;&quot;The decision as to whether or not to initiate ADT in patients with cardiac disease, in whom the benefits of therapy would be weighed against any possible risks, is most appropriately made by the physician treating the patient for prostate cancer.&quot;&lt;/p&gt;
&lt;p&gt;However, the potential adverse metabolic effects warrant periodic evaluation by a patient&apos;s primary care physician, they added.&lt;/p&gt;
&lt;p&gt;Noting a lack of clinical guidance for follow-up of patients treated with ADT, the advisory authors concluded that at least an annual assessment of blood glucose and lipids seems reasonable. They also called for prospective assessment of cardiovascular risk factors before and after ADT is begun in future clinical trials.&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20100101_19_346"
                     title="Daytime Sleepiness More Common in Young (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/PrimaryCare/SleepDisorders/tb/18221?impressionId=1265741112417"
                     
      &lt;p&gt;Compared with 20-somethings and seniors, middle-age adults are less likely to suffer daytime sleepiness when they don&apos;t get a good night&apos;s sleep, according to a small study.&lt;/p&gt;
&lt;p&gt;When three groups of healthy adults  --  young (20 to 30 years old), middle-age (40 to 55) and older (66 to 83)  --  were studied over four nights, slow wave sleep decreased and the number of nocturnal awakenings progressively increased with age, wrote Derk-Jan Dijk, PhD, of the Surrey Sleep Center at the University of Surrey in Guildford, England, and colleagues in the Feb. 1 issue of &lt;em&gt;Sleep.&lt;/em&gt;&lt;/p&gt;

&lt;p&gt;As the likelihood for eight hours of uninterrupted deep sleep decreased with age, there was no increase in the likelihood of daytime sleepiness, which led Dijk and colleagues to conclude that as people age there may be a change in the &quot;sleep (duration and depth) required to maintain alertness.&quot;&lt;/p&gt;
&lt;p&gt;Based on that observation, the authors wrote that it could be argued that &quot;an eight-hour episode rich in [slow wave sleep] is insufficient for young adults but that an eight-hour sleep episode with less [slow wave sleep] is sufficient for older adults.&quot;&lt;/p&gt;
&lt;p&gt;As a result, middle-age and older adults are less likely to build up &quot;sleep debt&quot; during the daylight hours, so they manage with less time in deep sleep at night, less homeostatic sleep pressure.&lt;/p&gt;
&lt;p&gt;The authors hypothesized that this apparent need for less sleep may be a factor in age-related insomnia.&lt;/p&gt;
&lt;p&gt;If older adults are unaware of the need for less sleep, &quot;their self-selected time in bed, which provides an input to the sleep homeostat, may become maladaptive and lead to reduced sleep consolidation and associated complaints.&quot;&lt;/p&gt;
&lt;p&gt;Dijk and colleagues recruited 44 young adults, 35 middle-age adults, and 31 older adults for their study. All were healthy at baseline and all were initially assessed for an eight-hour nocturnal sleep episode.&lt;/p&gt;
&lt;p&gt;They were then randomized to two nights of either selective short wave sleep interruption by acoustic stimuli or sleep without disruption, followed by one night of recovery sleep.&lt;/p&gt;
&lt;p&gt;Two standardized measurement tools, the Multiple Sleep Latency Test (MSLT) and the Karolinska Sleepiness Scale (KSS), were used to assess objective and subjective sleep propensity.&lt;/p&gt;
&lt;p&gt;&quot;Total sleep time per eight hour time in bed decreased significantly and progressively across the age groups such that older adults slept approximately 20 minutes less than middle-aged, who slept 23 minutes less than young adults,&quot; they wrote.&lt;/p&gt;
&lt;p&gt;The reduction in total sleep time &quot;was primarily related to an increase in the number of awakenings and the duration of wakefulness after sleep onset, rather than an increase in latency to sleep onset.&quot;&lt;/p&gt;
&lt;p&gt;As a result, sleep efficiency decreased significantly from 92.1% for the youngest group, to 82% for the older group (effect of age, &lt;em&gt;P&amp;lt;&lt;/em&gt;0.0001).&lt;/p&gt;
&lt;p&gt;The subjective sleep propensity tests revealed that &quot;young people were significantly sleepier than the middle-age people, who were the least sleepy of the three groups.&quot; Daytime sleepiness for the oldest group &quot;fell in between the other two groups [and] was not significantly different from either.&quot;&lt;/p&gt;
&lt;p&gt;All three groups, regardless of age, demonstrated increased daytime sleepiness following a night of experimental disruption of slow wave sleep, but when the participants had an uninterrupted eight hours of deep sleep, it was only the youngest group that was drowsy during the daytime hours.&lt;/p&gt;
&lt;p&gt;The authors noted that although there was less daytime sleepiness among middle-age and older adults in this study, sleep propensity was not measured during the evening hours, so it was possible that the age-related difference might diminish at twilight.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was sponsored by H. Lundbeck A/S.&lt;/p&gt;&lt;p&gt;Dijk reported receiving research support from the Air Force Office of Scientific Research, the Biotechnology and Biological Sciences Research Council, GlaxoSmithKline, H. Lundbeck A/S, Merck, Pfizer, Philips Lighting, sanofi-aventis, and Takeda.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_323"
                     title="Peptide Predicts Heart Failure in Older Patients (CME/CE)"
                     score="0.007"
                     href="http://www.medpagetoday.com/Cardiology/CHF/tb/18193?impressionId=1265741112417"
                     
      &lt;p&gt;Serial measurement of a natriuretic peptide predicted the risk of heart failure and cardiovascular death in older patients who were initially free of heart failure, data from a longitudinal cohort study showed.&lt;/p&gt;
&lt;p&gt;An increase of more than 25% in levels of N-terminal pro-B type natriuretic peptide (NT-proBNP) doubled the risk of heart failure and cardiovascular death. In contrast, a more than 25% decrease in NT-proBNP was associated with a greater than 40% reduction in the risk of both end points.&lt;/p&gt;
&lt;p&gt;&quot;NT-proBNP levels frequently change over time, and these fluctuations reflect dynamic changes in cardiovascular risk,&quot; Christopher R. deFilippi, MD, of the University of Maryland in Baltimore, and co-authors concluded in an article in the Feb. 2 issue of the &lt;em&gt;Journal of the American College of Cardiology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;This change in [NT-proBNP] level reflects a significant change in patient risk independent of cardiovascular risk factors, ejection fraction, or medication use,&quot; they added. &quot;Ultimately, NT-proBNP levels may guide further diagnostic testing or potential preventive measures to reduce the risk of developing heart failure or dying of cardiovascular disease.&quot;&lt;/p&gt;
&lt;p&gt;About 80% of cardiovascular deaths occur in older adults. Assessing cardiovascular risk in older patients is challenging because traditional cardiovascular risk factors are less predictive in older versus middle-age populations, the authors wrote.&lt;/p&gt;
&lt;p&gt;Subclinical cardiovascular disease is common among older adults and increases the risk of cardiovascular events, including heart failure. Repeated measures of traditional markers of cardiovascular disease in patients with subclinical disease are associated with increased risk compared with patients who remain free of identifiable disease, the authors continued.&lt;/p&gt;
&lt;p&gt;Levels of BNP and NT-proBNP are associated with long-term cardiovascular outcomes in the general population. However, the peptides&apos; ability to provide additional prognostic information beyond that of traditional risk factors remained controversial.&lt;/p&gt;
&lt;p&gt;To examine the prognostic value of NT-proBNP in an older population, deFilippi and colleagues analyzed data on 3,000 participants in the Cardiovascular Health Study. The authors hypothesized that NT-proBNP levels in an ambulatory population of older patients would independently predict new-onset heart failure and cardiovascular death.&lt;/p&gt;
&lt;p&gt;&quot;Furthermore, we anticipated that serial measurements of NT-proBNP, as a possible surrogate for change in subclinical disease status, identify a dynamic change in long-term risk of incident heart failure and cardiovascular mortality,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;Stored serum samples obtained at enrollment and two to three years later were used to measure NT-proBNP levels. Median follow-up for the cohort was 11.9 years.&lt;/p&gt;
&lt;p&gt;After separating the study group into quintiles of NT-proBNP levels, investigators found that patients with the highest baseline levels of the peptide (&amp;gt;267.7 pg/mL) had a threefold greater risk of new-onset heart failure (HR 3.05, 95% CI 2.46 to 3.78) and cardiovascular death (HR 3.02, 95% CI 2.36 to 3.86) compared with patients in the lowest NT-proBNP quintile (&amp;lt;47.5 pg/mL).&lt;/p&gt;
&lt;p&gt;The researchers identified 190 pg/mL as the NT-proBNP threshold for increased risk. Among study participants with baseline levels less than 190 pg/mL, an increase greater than 25% to a level above 190 pg/mL had a twofold increased risk of heart failure (HR 2.13, 95% CI 1.68 to 2.71) and cardiovascular death (HR 1.91, 95% CI 1.43 to 2.53) compared with participants whose NT-proBNP levels remained below 190 pg/mL.&lt;/p&gt;
&lt;p&gt;Among study participants with elevated baseline NT-proBNP levels, an increase greater than 25% also doubled the risk of heart failure (HR 2.06, 95% CI 1.56 to 2.72) and cardiovascular disease (HR 1.88, 95% CI 1.37 to 2.57).&lt;/p&gt;
&lt;p&gt;A decrease greater than 25% from baseline significantly reduced the risk of heart failure (HR 0.58, 95% CI 0.36 to 0.93) and cardiovascular death (HR 0.57, 95% CI 0.32 to 1.01) compared with participants whose baseline levels remained elevated.&lt;/p&gt;
&lt;p&gt;The investigators noted limitations of the study including the fact that a quarter of the participants did not have a follow-up blood sample and those who did were younger and had fewer cardiac risk factors.&lt;/p&gt;
&lt;p&gt;In addition, the length of follow-up could not account for differences in treatment over time, and the accuracy of NT-proBNP levels in samples as much as 20 years old cannot be assured.&lt;/p&gt;
&lt;p&gt;The study is noteworthy for highlighting the concept of dynamic risk assessment based on serial measurement of NT-proBNP, Richard W. Troughton, MB ChB, PhD, Matthew G. Daly, MB ChB, and Christopher M. Frampton, PhD, of the University of Otago in Christchurch, New Zealand, wrote in an editorial.&lt;/p&gt;
&lt;p&gt;&quot;The findings confirm a modest improvement in risk stratification by including a single measurement of NT-proBNP levels,&quot; they wrote &quot;The investigators take this a step further by showing that serial NT-proBNP measurement at a later time provides a further modest improvement in risk stratification.&quot;&lt;/p&gt;
&lt;p&gt;&quot;Whether the improvement in risk stratification achieved by performing serial NT-proBNP testing crosses a threshold of definite clinical value needs further evaluation, with particular consideration of the cost-effectiveness of such a strategy,&quot; they added.&lt;/p&gt;
&lt;div style=&quot;float:left;border-style:solid;border-width:1px;border-color:#8dabbc;font-family:arial;font-size:12px;background-color:#DBE9F2;padding:5px;&quot;&gt;&lt;p&gt;The study was supported by the National Institutes of Health, University of Pittsburgh, and Roche Diagnostics.&lt;/p&gt;&lt;p&gt;DeFilippi disclosed relationships with Siemens, Roche Diagnostics, BG Medicine, and Critical Diagnostics. Co-author Robert H. Christenson disclosed relationships with Roche Diagnostics, Siemens Healthcare Diagnostics, and Response Biomedical. Co-author Stephen L. Seliger disclosed a relationship with Roche.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>