<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <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=1265746128571"
                     
      &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="0.012"
                     href="http://www.medpagetoday.com/Cardiology/MyocardialInfarction/tb/18319?impressionId=1265746128571"
                     
      &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_446"
                     title="Proteins Linked to Stress-Induced ACS (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Cardiology/AcuteCoronarySyndrome/tb/18373?impressionId=1265746128571"
                     
      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_439"
                     title="Heart Often Affected in Churg-Strauss (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Rheumatology/GeneralRheumatology/tb/18353?impressionId=1265746128571"
                     
      &lt;p&gt;Cardiac involvement is common in patients with Churg-Strauss syndrome, even when their vasculitis is in clinical remission, a Dutch study found.&lt;/p&gt;
&lt;p&gt;Cardiac MRI detected abnormalities in 62% of patients with this rare, systemic disorder but in only 3% of matched controls (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001), according to Robert M. Dennert, MD, of Maastricht University in the Netherlands, and colleagues.&lt;/p&gt;
&lt;p&gt;Yet only 26% of the patients had clinical symptoms suggesting cardiac involvement, the researchers reported in February&apos;s &lt;em&gt;Arthritis &amp;amp; Rheumatism.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;Cardiac involvement is an important predictor of poor outcome in Churg-Strauss syndrome, with approximately half of the associated mortality being heart-related. Myocardial damage typically results from eosinophilic infiltration and granuloma formation.&lt;/p&gt;
&lt;p&gt;However, the cardiac manifestations are often subclinical. They remain undiagnosed, and the exact incidence is unclear.&lt;/p&gt;
&lt;p&gt;So Dennert and colleagues enrolled 32 patients with confirmed Churg-Strauss syndrome who were in complete clinical remission, performing detailed imaging assessments to determine the frequency and extent of heart involvement.&lt;/p&gt;
&lt;p&gt;About two-thirds were men. The mean age was 61 years, and disease duration was slightly over six years.&lt;/p&gt;
&lt;p&gt;A total of 41% had antineutrophil cytoplasmic antibodies (ANCA), and most were on maintenance steroids or immunosuppressants.&lt;/p&gt;
&lt;p&gt;On EKG, major abnormalities (atrial fibrillation and conduction disturbances) were detected in only 13% of patients. Minor abnormalities such as T wave abnormalities were seen in 50% of patients and in one control subject.&lt;/p&gt;
&lt;p&gt;Echocardiography identified abnormalities in 50% of patients and in 3% of controls (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001). These included wall motion and valvular abnormalities, pericardial effusion, and pulmonary hypertension.&lt;/p&gt;
&lt;p&gt;In the 62% of patients whose MRIs revealed abnormalities, findings included fibrosis, inflammation, wall motion and valvular abnormalities, pericardial effusion, and obliterated right ventricle.&lt;/p&gt;
&lt;p&gt;Previous reports had suggested that ANCA positivity in Churg-Strauss syndrome was more often associated with renal disease and peripheral neuropathy, while ANCA negativity was associated with fever and heart involvement.&lt;/p&gt;
&lt;p&gt;In this cohort, 74% of ANCA-negative patients had cardiac involvement, and in 64%, these were wall motion disturbances.&lt;/p&gt;
&lt;p&gt;In comparison, only 23% of ANCA-positive patients had heart involvement.&lt;/p&gt;
&lt;p&gt;Defects were identified with echocardiography or MRI in 88% of patients who had clinical symptoms, and in all who had major EKG abnormalities.&lt;/p&gt;
&lt;p&gt;But in the absence of symptoms and even with a normal EKG, abnormalities could still be detected on echocardiography or MRI in almost 40% of patients, according to the investigators.&lt;/p&gt;
&lt;p&gt;&quot;We therefore recommend that the evaluation for cardiac involvement in patients with [Churg-Strauss syndrome] should include not only detailed history of cardiac symptoms and EKG, but also imaging with echocardiography or cardiac MRI,&quot; they stated.&lt;/p&gt;
&lt;p&gt;The high prevalence of heart abnormalities could not be attributed to concomitant heart disease such as coronary artery disease or hypertension, because the prevalence of these diseases among patients was comparable to that in controls.&lt;/p&gt;
&lt;p&gt;Churg-Strauss syndrome typically develops in three phases, beginning with asthma, followed by peripheral and tissue eosinophilia accompanied by pulmonary infiltrates, and finally the systemic small-vessel vasculitis.&lt;/p&gt;
&lt;p&gt;During this late phase the vasculitic lesions in the coronary vessels and myocardium can lead to myocardial infarction, heart failure, and cardiac tamponade.&lt;/p&gt;
&lt;p&gt;Studies have shown that long-term treatment with immunosuppressive drugs can improve survival and resolve the cardiac abnormalities, so early diagnosis is needed.&lt;/p&gt;
&lt;p&gt;The authors acknowledged that their study was cross-sectional, and that a longitudinal study could have provided more detailed data.&lt;/p&gt;
&lt;p&gt;Nonetheless, the study revealed a high incidence of cardiac involvement, which was often unrecognized, and they concluded that a multidisciplinary approach to management therefore should include a cardiologist.&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 funded by the Netherlands Heart Foundation and the Dutch Organization for Scientific Research.&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=1265746128571"
                     
      &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>
</recommendedContent>