<?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="0.014"
                     href="http://www.medpagetoday.com/Cardiology/AcuteCoronarySyndrome/tb/18373?impressionId=1265731073075"
                     
      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_411"
                     title="Older Women with Gout at Risk of MI (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/Cardiology/MyocardialInfarction/tb/18319?impressionId=1265731073075"
                     
      &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="0.01"
                     href="http://www.medpagetoday.com/Cardiology/PCI/tb/18226?impressionId=1265731073075"
                     
      &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_231"
                     title="FDA Adds Cardio Warnings to Weight-Loss Drug"
                     score="-0"
                     href="http://www.medpagetoday.com/ProductAlert/DevicesandVaccines/tb/18088?impressionId=1265731073075"
                     
      &lt;p&gt;WASHINGTON  --  The FDA said the weight-loss drug sibutramine (Meridia) should not be taken by patients with history of cardiovascular disease following a review of additional data showing an increased risk of heart attack and stroke among that population.&lt;/p&gt;
&lt;p&gt;The agency said the manufacturer, Abbott, has agreed to add the contraindication to its labeling, which will be expanded to include patients with a history of the following: &lt;ul&gt; &lt;li&gt;Coronary artery disease (i.e., heart attack, angina)&lt;/li&gt; &lt;li&gt;Stroke or transient ischemic attack&lt;/li&gt; &lt;li&gt;Heart arrhythmia&lt;/li&gt; &lt;li&gt;Congestive heart failure&lt;/li&gt; &lt;li&gt;Peripheral arterial disease&lt;/li&gt; &lt;li&gt;Uncontrolled hypertension (&amp;gt;145/90 mmHg)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;The initial review of sibutramine began in November 2009 when the FDA received preliminary data from the SCOUT study suggesting patients using the drug had a higher risk for cardiovascular events. (See &lt;a href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/17147&quot; mce_href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/17147&quot; target=&quot;_blank&quot;&gt;Early Data Link Diet Drug to MI, Stroke, and Cardiac Death&lt;/a&gt;)&lt;/p&gt;
&lt;p&gt;Prior to review, the product label included a warning for patients with cardiovascular disease.&lt;/p&gt;
&lt;p&gt;Healthcare professionals should monitor patients for increase in blood pressure and heart rate and should discontinue therapy if either increase is observed, an FDA statement said.&lt;/p&gt;
&lt;p&gt;Patients should also discontinue use of sibutramine if they do not lose 5% of their baseline body weight within the first three to six months of treatment, as the drug may not be effective and puts the patient at unnecessary risk, the release said.&lt;/p&gt;
&lt;p&gt;The FDA said its review of SCOUT study data, as well as other information related to the drug&apos;s risks and benefits, is ongoing and will be followed by an open public advisory committee meeting to determine if it requires additional regulatory action.&lt;/p&gt;

    </recommendedItem>
    <recommendedItem id="20100101_19_224"
                     title="Prehospital ECG Speeds STEMI Care (CME/CE)"
                     score="-0.001"
                     href="http://www.medpagetoday.com/Cardiology/MyocardialInfarction/tb/18052?impressionId=1265731073075"
                     
      Transmitting ECG results from the field to the emergency department dramatically improved door-to-balloon time for patients with ST-elevation myocardial infarction (STEMI), researchers found.&lt;br&gt;
&lt;br&gt;The strategy cut a half hour from the process, from 90.5 minutes to 60.2 minutes (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001), well within the recommended 90-minute window, according to Shukri David, MD, of Providence Hospital and Medical Center in Southfield, Mich., and colleagues.&lt;br&gt;
&lt;br&gt;Nearly all patients who had a prehospital ECG (97.4%) had a door-to-balloon time of less than 90 minutes, compared with only 61.5% of those who had an ECG upon arrival at the hospital (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001), the researchers reported in the January issue of &lt;em&gt;Catheterization and Cardiovascular Interventions&lt;/em&gt;.&lt;br&gt;

&lt;br&gt;&quot;It&apos;s very important that patients who are suffering a myocardial infarction get to a cath lab so that we can establish blood flow to the injured myocardium,&quot; David said in an interview. &quot;That will save lives.&quot;&lt;/p&gt;

&lt;p&gt;Guidelines from both the American College of Cardiology and the American Heart Association have called for patients with STEMI to have blocked vessels opened within 90 minutes of arriving at the hospital, citing ECG conducted by emergency medical services personnel as one way to meet this goal.&lt;/p&gt;
&lt;p&gt;Previous studies, including a pilot study by David&apos;s group, have supported this approach.&lt;/p&gt;
&lt;p&gt;To validate the use of prehospital ECG, David and his colleagues conducted a prospective, observational study at three hospitals in Michigan over a 55-month period.&lt;/p&gt;
&lt;p&gt;When possible, EMS personnel obtained a 12-lead ECG during the initial assessment of patients with chest pain. The findings were transmitted to the emergency department via cellular link.&lt;/p&gt;
&lt;p&gt;Once STEMI was confirmed, the physician in the emergency department activated the cardiac catheterization team as the patient was en route to the hospital. This allowed the patient to head directly to the cath lab.&lt;/p&gt;
&lt;p&gt;Patients with STEMI who did not have prehospital ECGs but were treated at the same hospitals served as the controls.&lt;/p&gt;
&lt;p&gt;Although both groups of patients were generally similar, blacks were much less likely to get a prehospital ECG than whites  --  15.7% versus 31% (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001)  --  primarily because ambulances in Detroit only received ECG capabilities at the end of the study, according to the researchers.&lt;/p&gt;
&lt;p&gt;Prehospital ECG reduced door-to-balloon time, but did not have a significant effect on either length of hospital stay or inhospital mortality. David and his colleagues said they likely didn&apos;t observe a mortality benefit because of the relatively low number of total deaths (2% in controls versus 0% in the intervention group).&lt;/p&gt;
&lt;p&gt;In the control group, the time of presentation with STEMI affected the door-to-balloon time. Patients treated during working hours had a shorter time to reperfusion than those treated during off-hours (75 versus 98 minutes, &lt;em&gt;P&lt;/em&gt;=0.04).&lt;/p&gt;
&lt;p&gt;However, with the use of prehospital ECG, there was a significant reduction in door-to-balloon time regardless of the time of presentation.&lt;/p&gt;
&lt;p&gt;&quot;The use of the prehospital ECG is a way of overcoming the obstacle of delay in cardiac catheterization laboratory activation during off-hours,&quot; the researchers wrote.&lt;/p&gt;

&lt;p&gt;&quot;We were able to take the disadvantage out of having a patient show up on off-hours, or weekends, or holidays,&quot; David said.&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 authors did not report any conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
</recommendedContent>