<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_446"
                     title="Proteins Linked to Stress-Induced ACS (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/Cardiology/AcuteCoronarySyndrome/tb/18373?impressionId=1265771744478"
                     
      The heart-pounding excitement of Sunday&apos;s Super Bowl football game might have sent some fans to hospital with acute coronary syndrome.&lt;br&gt;
&lt;br&gt;But researchers in Germany say it may be possible to distinguish these cases from people whose coronary syndrome wasn&apos;t stress-related.&lt;br&gt;
&lt;br&gt;Two proteins known as endothelin-1 (ET-1) and &lt;span&gt;monocyte&lt;/span&gt; chemoattractant protein-1 (MCP-1) appear to be highly sensitive and specific markers of excitement-induced acute coronary syndromes, according to Ute Wilbert-Lampen, MD, and colleagues at Ludwig-Maximilians-Universit&amp;#228;t in Munich.&lt;/p&gt;
&lt;p&gt;In a cohort study, the two compounds were markedly elevated in people whose coronary syndromes were associated with excitement and stress over World Cup soccer games, the researchers reported in the Feb. 16 issue of the &lt;em&gt;Journal of the American College of Cardiology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;And the protein levels were significantly higher than in either healthy controls or a group of matched patients whose coronary syndrome was not associated with the soccer matches, the researchers said.&lt;/p&gt;
&lt;p&gt;Wilbert-Lampen and colleagues reported in 2008 that they had found 2.7-fold spike in the incidence of acute cardiovascular events in association with the 2006 World Cup soccer matches. (See &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/Atherosclerosis/8171&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/Atherosclerosis/8171&quot; target=&quot;_blank&quot;&gt;Cardiovascular Events Spike During Critical World Cup Soccer Matches&lt;/a&gt;)&lt;/p&gt;
&lt;p&gt;Although excitement and stress caused the events, exactly how remained unclear, they reported in the journal.&lt;/p&gt;
&lt;p&gt;To help clarify the issue, they looked at 58 representative patients from the earlier analysis for whom blood samples were available. They were compared with the same number of healthy controls and 58 reference patients with acute coronary syndromes&lt;strong&gt; &lt;/strong&gt;who reported no emotional involvement with the World Cup.&lt;/p&gt;
&lt;p&gt;In addition to ET-1 and MCP-1, blood samples were tested for a range of substances, including soluble CD40L (sCD40L), soluble vascular cell adhesion molecule-1 (sVCAM-1), tumor necrosis factor-&amp;#945; (TNF-&amp;#945;), high-sensitivity C-reactive protein (hsCRP), and regulated on activation, normal T-cell expressed and secreted (RANTES).&lt;/p&gt;
&lt;p&gt;The researchers found: &lt;ul&gt; &lt;li&gt;The study group had average ET-1 levels of 4.0 picograms per milliliter, compared with 2.0 for the reference patients and 1.1 for the health controls. Both between-group differences were significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001.&lt;/li&gt; &lt;li&gt;A similar pattern was seen for MCP1 and TNF-&amp;#945;.&lt;/li&gt; &lt;li&gt;The other markers  --  sVCAM-1, hsCRP, and RANTES -- yielded less clear results.&lt;/li&gt; &lt;li&gt;In both groups of patients, ET-1 was significantly correlated (at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) with sCD40L and with MCP-1, but other markers were correlated with one or the other or neither.&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;In a receiver operating curve analysis, ET-1 and MCP-1 were found to have diagnostic potential, the researchers said, with the areas under the curve being 0.99 and 0.98, respectively.&lt;/p&gt;
&lt;p&gt;In such an analysis, an area under the curve of 1.0 would mean the proposed diagnostic tool would be completely accurate, without either false positives or false negatives.&lt;/p&gt;
&lt;p&gt;Using a cutoff of 3.1 picograms per milliliter, ET-1 had a sensitivity of 100% and a specificity of 96.6%, the researchers said, while a cutoff of 396 picograms per milliliter for MCP-1 resulted in 93.1% sensitivity and 93.1% specificity.&lt;/p&gt;
&lt;p&gt;One implication of the findings, the researchers said, is that it may be valuable to begin developing prophylactic and therapeutic drugs targeting ET-1.&lt;/p&gt;
&lt;p&gt;They noted that because of the design of the original study, a range of information was not available, including data on troponin or stress-hormone levels, cardiovascular risk factors, infarct size, or clinical outcome.&lt;/p&gt;
&lt;p&gt;Despite those gaps, the study has &quot;some exciting features,&quot; according to Karina Davidson, PhD, of Columbia University College of Physicians and Surgeons in New York City.&lt;/p&gt;
&lt;p&gt;Among other things, she wrote in an accompanying editorial, the study provides &quot;evidence for the importance&quot; of ET-1 in stress-induced ischemic syndromes.&lt;/p&gt;
&lt;p&gt;It may now be possible, she argued, to identify what other factors come into play and eventually to determine who is at risk for such events.&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 Else Kr&amp;#246;ner-Fresenius Stiftung. The researchers did not report potential conflicts.&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=1265771744478"
                     
      &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_411"
                     title="Older Women with Gout at Risk of MI (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Cardiology/MyocardialInfarction/tb/18319?impressionId=1265771744478"
                     
      &lt;p&gt;Elderly women with gout are at increased risk of acute myocardial infarction (MI), even more so than men with this painful arthritis, a population-based study found.&lt;/p&gt;
&lt;p&gt;After adjusting for age, comorbidities such as hypertension and diabetes, and prescription drug use, the relative risk of MI among women ages 65 and older was 1.39 (95% CI 1.20 to 1.61), according to Mary A. De Vera of the Arthritis Research Centre of Canada in Vancouver, and colleagues.&lt;/p&gt;
&lt;p&gt;In comparison, the multivariate relative risk among men was 1.11 (95% CI 0.99 to 1.23, &lt;em&gt;P&lt;/em&gt;=0.003 for interaction), the researchers reported online in the &lt;em&gt;Annals of the Rheumatic Diseases&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Men with gout are known to be at higher risk for coronary heart disease and acute MI, but corresponding data for women were sparse.&lt;/p&gt;
&lt;p&gt;So De Vera and colleagues conducted a cohort study using the British Columbia Linked Health Database, comparing the incidence rates of MI between 9,642 patients with gout and 48,210 matched controls with no history of ischemic heart disease.&lt;/p&gt;
&lt;p&gt;A total of 3,890 of the cases were women, as were 19,450 of the controls.&lt;/p&gt;
&lt;p&gt;The gout incidence rate in women ages 65 to 85 years was 2.5 per 1,000 person-years, and 2.9 per 1,000 person-years in those ages 85 and higher.&lt;/p&gt;
&lt;p&gt;The rates in men of the corresponding ages were 5.7 and 6.5 per 1,000 person-years.&lt;/p&gt;
&lt;p&gt;Hospital records indicated that the incidence rates of acute MI among women and men were 6.7 and 10.7 per 1,000 person-years, respectively.&lt;/p&gt;
&lt;p&gt;During a median of seven years&apos; follow-up there were 3,268 incident cases of MI, including 996 in women.&lt;/p&gt;
&lt;p&gt;In unadjusted analysis, the relative risk of acute MI among women with gout was 1.67 (95% CI 1.45 to 1.93), while that for men with gout was 1.19 (95% CI 1.07 to 1.32).&lt;/p&gt;
&lt;p&gt;Multivariate analysis determined that the relative risk for nonfatal MI in women was 1.41 (95% CI 1.19 to 1.67), while that in men was 1.11 (95% CI 0.98 to 1.25, &lt;em&gt;P&lt;/em&gt;=0.005 for interaction).&lt;/p&gt;
&lt;p&gt;The gender difference did not show up in fatal events, however. The relative risk for fatal MI was 1.33 in women (95% CI 0.99 to 1.78) and 1.10 in men (95% CI 0.88 to 1.38, &lt;em&gt;P&lt;/em&gt;=0.30 for interaction).&lt;/p&gt;
&lt;p&gt;Overall, there was a 39% increased risk for MI among women with gout, an association that was independent of age, comorbidities, and use of prescription drugs including nonsteroidal anti-inflammatories, diuretics, statins, anticoagulants, and aspirin.&lt;/p&gt;
&lt;p&gt;The association was significantly stronger than for men, according to the researchers.&lt;/p&gt;
&lt;p&gt;These gender differences may relate to serum uric acid levels and metabolism. Levels in men are about 1 mg/dL higher, although levels do rise in women at menopause.&lt;/p&gt;
&lt;p&gt;&quot;Thus, the relative physiological impact of having gout or a certain level of hyperuricemia may be stronger among women than men,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;Possible mechanisms for the contribution of hyperuricemia to cardiovascular disease include vascular smooth muscle cell proliferation and inflammation, as well as platelet adhesiveness and aggregation.&lt;/p&gt;
&lt;p&gt;&quot;Inflammation associated with gout may also have a role in potential mechanisms, including promotion of atherogenesis and thrombogenesis, similar to other inflammatory arthritides associated with cardiovascular disease,&quot; the investigators noted.&lt;/p&gt;
&lt;p&gt;A strength of the study was its population-based design, which makes its findings generalizable. Limitations include the potential for misclassification of diagnosis because of the use of diagnostic codes, and the inability to adjust for lifestyle factors such as smoking.&lt;/p&gt;
&lt;p&gt;Nonetheless, according to the investigators, &quot;These findings provide support for the aggressive management of cardiovascular risk factors for male and female patients with gout.&quot;&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 partly funded by the National Institute of Health.&lt;/p&gt;&lt;p&gt;The authors have received support from the Canadian Arthritis Network/The Arthritis Society, and one disclosed receiving research funding and honoraria from TAP Pharmaceuticals and Savient.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_348"
                     title="No Rebound Seen After Antiplatelet Withdrawal (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Cardiology/PCI/tb/18226?impressionId=1265771744478"
                     
      &lt;p&gt;No evidence of a platelet aggregation rebound occurs with abrupt discontinuation of clopidogrel (Plavix) in patients undergoing percutaneous coronary intervention (PCI), investigators in a randomized clinical trial concluded.&lt;/p&gt;
&lt;p&gt;Values for adenosine diphosphate (ADP)-induced platelet aggregation did not differ significantly between patients whose clopidogrel therapy was withdrawn abruptly and those in whom clopidogrel was tapered before discontinuation, they wrote in an article in the Feb. 9 issue of the &lt;em&gt;Journal of the American College of Cardiology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;The findings also showed that tapering of clopidogrel does not lead to lower platelet aggregation values after clopidogrel withdrawal, according to Dirk Sibbing, MD, of Technical University Munich in Germany, and colleagues&lt;em&gt;&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;The time course of platelet aggregation values  --  regardless of the device, the agonist, or the agonist concentration used  --  after clopidogrel cessation provides no evidence for the existence of a rebound phenomenon of platelets after discontinuing clopidogrel,&quot; they wrote in conclusion.&lt;/p&gt;
&lt;p&gt;For patients undergoing PCI, dual antiplatelet therapy with aspirin and clopidogrel has become the mainstay for prevention of thrombotic events. Lifelong aspirin therapy is recommended for patients after PCI, but clinical guidelines recommend discontinuation of clopidogrel after six or 12 months. The standard practice is to withdraw clopidogrel abruptly, the authors noted.&lt;/p&gt;
&lt;p&gt;Recent studies have shown a clustering of thrombotic events in the first few weeks after discontinuation of long-term clopidogrel therapy. The observations have led to the hypothesis of a rebound phenomenon of platelet aggregation. However, the hypothesis had not been examined specifically within the context of clopidogrel withdrawal.&lt;/p&gt;
&lt;p&gt;&quot;Because different studies have demonstrated that insufficient suppression of platelet reactivity to ADP is associated with an increased risk of thrombotic events after coronary stent placement, the observed clustering of adverse events reported in clinical studies might be related to an intermittent status of platelet hyperreactivity or so-called platelet rebound with very high ADP-induced platelet aggregation levels,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;A tapering of clopidogrel treatment over a certain period of time before stopping the intake of the drug completely might provide a beneficial treatment strategy to attenuate this supposed rebound phenomenon of platelets.&quot;&lt;/p&gt;
&lt;p&gt;Sibbing and colleagues designed a randomized clinical trial to determine whether a rebound phenomenon exists after discontinuation of clopidogrel and whether the rebound can be attenuated by a clopidogrel-tapering regimen.&lt;/p&gt;
&lt;p&gt;The investigators enrolled 69 patients receiving clopidogrel in association with PCI procedures. In all cases, discontinuation of clopidogrel was planned.&lt;/p&gt;
&lt;p&gt;The patients were randomized to two strategies of discontinuation: tapering of the clopidogrel dose over four weeks, followed by discontinuation; or treatment for four weeks, as planned, followed by abrupt discontinuation.&lt;/p&gt;
&lt;p&gt;Investigators assessed platelet aggregation at enrollment and during weeks two through eight after randomization. Aggregation was assessed simultaneously by light transmission aggregometry (LTA) and multiple electrode aggregometry (MEA).&lt;/p&gt;
&lt;p&gt;The primary endpoint was the highest rate of ADP-induced platelet aggregation by LTA in weeks five through eight after clopidogrel withdrawal.&lt;/p&gt;
&lt;p&gt;Platelet aggregation by LTA peaked at 73% in the group that had clopidogrel abruptly withdrawn and at 69.3% in the tapering group, resulting in a nonsignificant difference (&lt;em&gt;P&lt;/em&gt;=0.21). The between-group values did not differ across the range of ADP concentrations used (1.25 to 20 &amp;#181;mol/L).&lt;/p&gt;
&lt;p&gt;Results by MEA were similar: The peak aggregation value associated with abrupt withdrawal was 925 AU x min compared with 890 AU x min with clopidogrel tapering (&lt;em&gt;P&lt;/em&gt;=0.55).&lt;/p&gt;
&lt;p&gt;Studies with different agonists of platelet aggregation also yielded similar results in the two patient groups.&lt;/p&gt;
&lt;p&gt;Despite finding no difference between the two strategies for clopidogrel withdrawal, the authors did not rule out the possibility of a beneficial effect of tapering clopidogrel.&lt;/p&gt;
&lt;p&gt;&quot;It could be hypothesized that, apart from the maximal values of platelet aggregation observed, a more gradual increase of platelet aggregation values achieved by a clopidogrel-tapering regimen is beneficial for the reduction of thrombotic events,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;&quot;In fact, we observed a relatively rapid increase of platelet aggregation values in the [abrupt withdrawal] group of patients in our study. Whether this rapid increase might be disadvantageous in case of stopping clopidogrel treatment remains uncertain.&quot;&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 Cordis, Medtronic, and Dynabyte.&lt;/p&gt;&lt;p&gt;Sibbing disclosed relationships with Dynabyte and Eli Lilly.&lt;/p&gt;&lt;p&gt;Co-author Adnan Kastrati disclosed relationships with Eli Lilly, sanofi-aventis, and Bristol-Myers Squibb.&lt;/p&gt;&lt;p&gt;Co-author Nicolas von Beckerath disclosed relationships with Eli Lilly and sanofi-aventis.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_358"
                     title="Poststroke Antidepressant Boosts Mental Agility (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Cardiology/Strokes/tb/18240?impressionId=1265771744478"
                     
      &lt;p&gt;Antidepressants in the first months after a stroke may aid cognitive recovery for patients without depression, according to a randomized trial analysis.&lt;/p&gt;
&lt;p&gt;Global cognitive function scores improved significantly more with escitalopram (Lexapro) than with problem-solving therapy or placebo (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01), according to Ricardo E. Jorge, MD, of the University of Iowa in Iowa City, and colleagues.&lt;/p&gt;
&lt;p&gt;Memory scores rose significantly higher with the antidepressant as well (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01), with both effects independent of those on depression, they reported in the February &lt;em&gt;Archives of General Psychiatry&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;Adjunctive restorative therapies administered during the first few months after stroke, the period with the greatest degree of spontaneous recovery, reduce the number of stroke patients with significant disability,&quot; the researchers concluded.&lt;/p&gt;
&lt;p&gt;The &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/Strokes/9621&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/Strokes/9621&quot; target=&quot;_blank&quot;&gt;primary analysis&lt;/a&gt; of the trial, reported in the &lt;em&gt;Journal of the American Medical Association on&lt;/em&gt; May 28, 2008, showed that prophylactic escitalopram treatment would prevent poststroke depression in one patient for every 7.2 treated &lt;em&gt;(P&lt;/em&gt;&amp;lt;0.001 compared with placebo). That article ultimately raised a controversy over an undisclosed conflict of interest.&lt;/p&gt;
&lt;p&gt;Escitalopram is a selective serotonin reuptake inhibitor (SSRI). Since serotonin plays a role in neuroplastic changes in the developing brain as well as in depression, Jorge&apos;s group analyzed whether there might be such an effect after a stroke.&lt;/p&gt;
&lt;p&gt;The study randomized patients to double-blind treatment with escitalopram (10 mg/d under age 65 or 5 mg/day age 65 and older) or placebo or unblinded problem-solving therapy (12 sessions of going through steps to arrive at a course of action for a patient-selected problem).&lt;/p&gt;
&lt;p&gt;The intent-to-treat analysis included 129 patients treated starting within the first three months after their mild to moderate severity stroke and who did not meet criteria for major or minor depression.&lt;/p&gt;
&lt;p&gt;Overall, global cognitive functioning was significantly changed between groups as measured on the Repeatable Battery for the Assessment of Neuropsychological Status (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01).&lt;/p&gt;
&lt;p&gt;After controlling for change in depression score and type of stroke, escitalopram was associated with the best cognitive recovery, an adjusted mean change of 9.9 points compared with 1.9 for problem-solving therapy (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01) and 4.0 for placebo (&lt;em&gt;P&lt;/em&gt;=0.02).&lt;/p&gt;
&lt;p&gt;Similarly, for delayed memory scores on the same test battery, escitalopram came out on top (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.01).&lt;/p&gt;
&lt;p&gt;After adjustment for depression score change and stroke mechanism, the antidepressant was associated with an 11.2 point improvement in delayed memory, compared with a change of -0.7 with problem-solving therapy (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) and 3.9 with placebo (&lt;em&gt;P&lt;/em&gt;=0.02).&lt;/p&gt;
&lt;p&gt;On test of immediate memory, escitalopram again yielded the best recovery.&lt;/p&gt;
&lt;p&gt;The researchers found mean improvement of 13.4 points with the antidepressant compared with 2.0 with problem-solving therapy (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) and 7.2 with placebo (&lt;em&gt;P&lt;/em&gt;=0.04), after adjustment for time between stroke and treatment, depression score change, and stroke type.&lt;/p&gt;
&lt;p&gt;These mental benefits appeared to have an impact on functional status as well.&lt;/p&gt;
&lt;p&gt;Cognitive domain scores on the Functional Independence Measure were better for escitalopram-treated patients than those who didn&apos;t get the drug (&lt;em&gt;P&lt;/em&gt;=0.05), as were memory domain scores on the same measure (&lt;em&gt;P&lt;/em&gt;=0.03).&lt;/p&gt;
&lt;p&gt;At baseline, the global cognitive functioning and delayed and immediate memory scores were nonsignificantly lower in the antidepressant group than in the other two groups, which could have biased the results.&lt;/p&gt;
&lt;p&gt;However, the treatment effects appeared to be real, Jorge explained in an interview.&lt;/p&gt;
&lt;p&gt;In an unpublished regression analysis, the baseline scores were not a significant covariate. &quot;If [the results were] related only to the difference in baseline, this would be significant but it wasn&apos;t,&quot; he told &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Moreover, with an initially lower score it might have been expected that the escitalopram-treated group would have had a lower score at the end of the study than the other groups, added co-author Robert G. Robinson, MD, also of the University of Iowa.&lt;/p&gt;
&lt;p&gt;But that wasn&apos;t the case, he said in an interview. With regard to delayed memory, for example, &quot;the escitalopram-treated group went from the most impaired to the best performing.&quot;&lt;/p&gt;
&lt;p&gt;The researchers didn&apos;t compare end scores for the escitalopram, problem solving therapy, and placebo groups, but they were: &lt;ul&gt; &lt;li&gt;For global cognitive functioning 89.8, 89.1, and 91.0 points, respectively&lt;/li&gt; &lt;li&gt;For delayed memory, 96.6, 89.1, and 94.2, respectively&lt;/li&gt; &lt;li&gt;For immediate memory, 95.1, 94.9, and 98.5, respectively&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The treatment showed no effect on other individual cognitive measurements, including those for attention, language, and IQ. Nor were there significant differences in changes in occupational or living conditions.&lt;/p&gt;
&lt;p&gt;Although SSRIs such as escitalopram have been associated with hospitalization for GI bleeding and falls in prior studies, these complications did not occur in Jorge&apos;s study.&lt;/p&gt;
&lt;p&gt;&quot;Long-term administration of SSRIs appears to be an effective and safe treatment option to improve cognitive outcomes among patients with cerebrovascular disease,&quot; they concluded in the &lt;em&gt;Archives&lt;/em&gt; paper.&lt;/p&gt;
&lt;p&gt;The researchers cautioned that the study was limited by lack of CT or MRI scans and the younger age of escitalopram-treated patients, compared with other groups. That may have been a source of bias, although age did not appear to be a significant factor in the trial results.&lt;/p&gt;
&lt;p&gt;In this analysis, the researchers emphasized that the trial was not financially supported in any way by any drug company  --  a declaration hinting at the controversy that brewed last year over failure of one of the authors of the original &lt;em&gt;JAMA&lt;/em&gt; article to &lt;a href=&quot;http://www.medpagetoday.com/PublicHealthPolicy/HealthPolicy/13391&quot; mce_href=&quot;http://www.medpagetoday.com/PublicHealthPolicy/HealthPolicy/13391&quot; target=&quot;_blank&quot;&gt;properly disclose ties&lt;/a&gt; to Forest Pharmaceuticals, which makes escitalopram.&lt;/p&gt;
&lt;p&gt;Another scientist who discovered that omission published the information in a competing journal, inducing &lt;em&gt;JAMA&lt;/em&gt; to issue a gag rule on reporting of undisclosed conflicts of interest. That policy encourages those who discover such conflicts to report them to &lt;em&gt;JAMA&apos;s&lt;/em&gt; editors but prohibits them from disclosing the conflicts publicly pending an investigation by the journal.&lt;/p&gt;
&lt;p&gt;In the current analysis, the disclosure statement indicated that co-author Robertson, had received honoraria and speakers&apos; bureau fees from Forest, with the caveat that &quot;none of the design, analysis, or expenses (including the cost of medications) of this study were supported by monies, materials, or any intellectual input from Forest Laboratories.&quot;&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 solely by a grant from the National Institute of Mental Health.&lt;/p&gt;&lt;p&gt;Jorge reported having received travel awards to participate in national meetings from the former Hamilton Pharmaceutical Company and Avanir Pharmaceutical Company.&lt;/p&gt;&lt;p&gt;Co-authors reported financial conflicts of interest with Merck, NMT Medical, Eli Lilly, Centocor, Sanofi-Bristol-Meyers-Squibb, Boerhringer-Ingelheim, Schering-Plough, AstraZeneca, and GlaxoSmithKline, the former Hamilton Pharmaceutical Company, Avanir Pharmaceutical Company, Lubeck, Forest Laboratories, and Pfizer.&lt;/p&gt;&lt;p&gt;No pharmaceutical company donated medications for or had any financial interest in the study.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
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