<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_3191"
                     title="ESC: It&apos;s Not Butter and It&apos;s Not Better (CME/CE)"
                     score="0.013"
                     href="http://www.medpagetoday.com/MeetingCoverage/ESCCongress/tb/21921?impressionId=1283457945605"
                     
      STOCKHOLM  --  Adding margarine enriched with omega-3 fatty acids as a dietary intervention did not prevent second heart attacks in older men and women at risk for worsening heart disease, researchers said here.&lt;br&gt;
&lt;br&gt;The study results are doubly disappointing since the margarine intervention did initially reduce events, but by 30 months the evidence of that benefit had disappeared, said Daan Kromhout, MPH, PhD, of Wageningen University in the Netherlands.&lt;br&gt;
&lt;br&gt;After more than 40 months, consumption of the omega-3 fatty acid fortified margarines &quot;had no effect on the rate of major cardiovascular events,&quot; he reported at a Hot Line session today at the European Society of Cardiology meeting. The findings were simultaneously published online by the &lt;em&gt;New England Journal of Medicine.&lt;/em&gt;&lt;/p&gt;
&lt;p&gt;The ALPHA-OMEGA trial randomized 4,837 MI survivors, 60 to 80 years old, to margarine supplemented with a combination of eicosapentaenoic acid and docosahexaenoic acid (EPA and DHA), or with 2 grams of the plant-derived fatty acid alpha-linolenic acid (ALA), or a third supplemented with all three versus a placebo margarine.&lt;/p&gt;
&lt;p&gt;The primary endpoint was the combined rate of fatal and non-fatal cardiovascular events and cardiac interventions.&lt;/p&gt;
&lt;p&gt;Neither EPA-DHA nor ALA reduced this endpoint, the researchers reported (hazard ratio with EPA-DHA, 1.01; 95% confidence interval 0.87 to 1.17, &lt;em&gt;P &lt;/em&gt;=0.93).&lt;/p&gt;
&lt;p&gt;A prespecified subgroup analysis in women found that use of the ALA-fortified margarine reduced the rate of cardiovascular events compared with placebo or with the EPA-DHA margarine, but the difference failed to reach statistical significance (HR 0.73, 95% CI 0.51 to 1.03, &lt;em&gt;P&lt;/em&gt;=0.07).&lt;/p&gt;
&lt;p&gt;Alfred Bove, MD, of Temple University in Philadelphia, said the findings surprised him &quot;because most of the data on omega-3 fatty acids come from epidemiologic studies and those were positive.&quot;&lt;/p&gt;
&lt;p&gt;He likened the situation to hormone therapy, which had been widely recommended to reduce cardiovascular risk in postmenopausal women based on data from epidemiologic studies.&lt;/p&gt;
&lt;p&gt;That hypothesis was initially questioned when a randomized controlled trial (Estrogen/Progestin Replacement Study [HERS]) linked hormones to increased risk of events. The HERS finding was confirmed in the landmark Women&apos;s Health Initiative trial in which ischemic events were more common among women randomized to estrogen/progestin.&lt;/p&gt;
&lt;p&gt;R. Scott Wright, MD, of the Mayo Clinic in Rochester, Minn., told &lt;em&gt;MedPage Today&lt;/em&gt; that the trial design was faulty, in that margarine was a bad choice of vehicle for omega-3 fatty acids.&lt;/p&gt;
&lt;p&gt;&quot;It needs to be combined with another food  --  bread,&quot; he said. &quot;So this not a good option for Americans because it would mean eating more bread, which is likely to lead to weight gain and bread is high in sodium, so blood pressure would be a factor.&quot;&lt;/p&gt;
&lt;p&gt;Wright noted that the ALPHA-OMEGA study did not include information on weight or blood pressure, so he considered the findings at best incomplete.&lt;/p&gt;
&lt;p&gt;All of the patients received &quot;state-of-the-art antihypertensive, antithrombotic, and lipid-modifying therapy,&quot; according to Kromhout and colleagues, in addition to margarine, and it may have been that optimal therapy that limited the potential for an omega-3 benefit.&lt;/p&gt;
&lt;p&gt;Statin therapy, along with other improvements in cardiovascular care, means &quot;a beneficial effect of low doses of EPA-DHA is difficult to prove,&quot; the authors wrote.&lt;/p&gt;
&lt;p&gt;Wright said he wasn&apos;t persuaded by that explanation since, even after optimal therapy, there is about a 30% residual risk. &quot;There is plenty of room to show a benefit,&quot; he declared.&lt;/p&gt;
&lt;p&gt;Most of the patients in ALPHA-OMEGA were men (78%) and 24% were obese, but they differed from the typical high-risk American in at least one way: at baseline they consumed about three times more fish than does the typical American, a median of 15 grams a day.&lt;/p&gt;
&lt;p&gt;According to a report from the Environmental Protection Agency, average fish consumption in the U.S. works out to 4.58 &amp;#177; 0.42 grams a day.&lt;/p&gt;
&lt;p&gt;The authors conducted a post hoc exploratory analysis in patients with diabetes, finding significant reductions in events among patients in the EPA-DHA group. But the authors noted that &quot;[the] results with respect to patients with diabetes are only hypothesis-generating and do not permit definitive conclusions to be drawn.&quot;&lt;/p&gt;
&lt;p&gt;Bove, a former president of the American College of Cardiology, added that the results from the subset analysis in diabetics was reassuring, since patients with diabetes and elevated triglycerides are the patients that &quot;we have believed would be most likely to benefit&quot; from omega-3 fatty acids.&lt;/p&gt;
&lt;p&gt;The margarines used in the trial were supplied by Unilever, an international maker of food and consumer goods, and included the well-known &quot;I Can&apos;t Believe It&apos;s Not Butter,&quot; which contains 420 mg of ALA per serving.&lt;/p&gt;

&lt;p&gt;In a statement released after the ALPHA-OMEGA trial findings were presented, Unilever said the &quot;study outcome for EPA and DHA is surprising considering the weight of evidence published to date. This could be the result of methodological issues such as the relatively low daily dosage compared with previous studies or the fact that in this study serious cardiovascular events were much lower than in studies performed in the past. This is probably due to extensive drug treatment that is nowadays applied. The finding needs further study, but given the totality of evidence does not immediately impact the current advice on fish and fish oil consumption for prevention of cardiovascular disease.&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 trial was supported by the Netherlands Heart Foundation, the National Institutes of Health, and Unilever.&lt;/p&gt;&lt;p&gt;Kromhout reported that his institution received grant support form Unilever to cover distribution of the trial margarines to patients. His institution also received a grant from the Product Board for Margarine Fats and Oils to support research on polyunsaturated fats and cardiovascular diseases done by a PhD student.&lt;/p&gt;&lt;p&gt;Bove said he had no financial conflicts.&lt;/p&gt;&lt;p&gt;Wright said he consults for Roche and Genentech and conducts trial work for 3M/Littman.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3174"
                     title="Diabetes, Insulin Resistance Linked to Alzheimer&apos;s (CME/CE)"
                     score="0.011"
                     href="http://www.medpagetoday.com/Neurology/AlzheimersDisease/tb/21902?impressionId=1283457945605"
                     
      Insulin resistance and type 2 diabetes may contribute to the development of one type of brain plaque linked to Alzheimer&apos;s disease, according to an autopsy study.&lt;br&gt;
&lt;br&gt;An analysis of autopsy samples from 135 Japanese men and women found that high insulin and glucose levels appeared to accelerate the formation of neuritic plaques, especially among those carrying a high-risk gene for Alzheimer&apos;s, Kensuke Sasaki, MD, PhD, of Kyushu University in Fukuoka City, Japan, and colleagues, reported.&lt;p&gt;&lt;/p&gt;
&lt;p&gt;The association of neuritic plaques with higher levels of two-hour post-load plasma glucose, fasting insulin, and insulin resistance measured in the decade before death was found to be independent of other risk factors like age, blood pressure, smoking, and cerebrovascular disease, Sasaki and co-authors wrote in the Aug. 25 issue of &lt;em&gt;Neurology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Thus, &quot;adequate control of diabetes might contribute to a strategy for the prevention of Alzheimer&apos;s disease,&quot; they concluded.&lt;/p&gt;
&lt;p&gt;Although these findings strengthen evidence for a causal link with dementia, an accompanying editorial by Jos&amp;#233; A. Luchsinger, MD, MPH, of Columbia University Medical Center and School of Public Health in New York City, cautioned that alternative explanations must be considered.&lt;/p&gt;
&lt;p&gt;For example, Luchsinger noted, the relatively small sample size selected from a much larger pool of participants who did not have an autopsy may have led to selection bias or to chance findings.&lt;/p&gt;
&lt;p&gt;Reverse causality was also a possibility since brain pathology and metabolic changes may precede dementia diagnosis by decades and diabetes and insulin resistance could result from or correlate with Alzheimer&apos;s, he added.&lt;/p&gt;
&lt;p&gt;On the assumption that the association may be causal, though, several randomized trials are already testing insulin sensitizers in older adults or those with mild cognitive impairment to see if the strategy has an effect on cognition.&lt;/p&gt;
&lt;p&gt;&quot;This is urgent considering that over half the U.S. population in the age group most at risk for cognitive impairment has prediabetes or type 2 diabetes, preceded or accompanied by insulin resistance and hyperinsulinemia,&quot; Luchsinger concluded in the editorial.&lt;/p&gt;
&lt;p&gt;The researchers analyzed autopsy results from 74 men and 64 women (average age 67) who died between 1998 and 2003 after participating in the long-term prospective Hisayama Study, which looked at cerebro-cardiovascular diseases among almost 3,400 residents of the Japanese town. During this period 290 Hisayama residents died and 214 were autopsied (73.8%).&lt;/p&gt;
&lt;p&gt;A total of 2,520 participants had received oral glucose tolerance tests in 1988 and were free of signs of dementia at that time. During the ensuing decades, 15.6% developed Alzheimer&apos;s-type dementia.&lt;/p&gt;
&lt;p&gt;However, among the 135 participants autopsied, 65% actually had neuritic plaques characteristic of Alzheimer&apos;s disease.&lt;/p&gt;
&lt;p&gt;Presence of these plaques was associated with significantly higher levels of the following after adjustment for age, sex, and a full set of potential confounders: &lt;ul&gt; &lt;li&gt;Two-hour post-load plasma glucose in a 75-g oral glucose tolerance test (odds ratio 1.71, &lt;em&gt;P&lt;/em&gt;=0.03) &lt;/li&gt; &lt;li&gt;Fasting insulin (OR 2.03, &lt;em&gt;P&lt;/em&gt;=0.02)&lt;/li&gt; &lt;li&gt;Insulin resistance measured by the homeostasis model of assessment (HOMA-IR, OR 2.11, &lt;em&gt;P&lt;/em&gt;=0.01)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;These endocrine factors also appeared to combine with genetic risk to accelerate formation of neuritic&lt;strong&gt; &lt;/strong&gt;plaques.&lt;/p&gt;
&lt;p&gt;Those with low glucose levels on the glucose tolerance test who didn&apos;t carry the &lt;em&gt;apolipoprotein E-4 &lt;/em&gt;gene&lt;em&gt; (APOE-4)&lt;/em&gt; allele associated with Alzheimer&apos;s disease were least likely to show neuritic plaques in their brain on autopsy whereas hyperglycemia alone was associated with 1.5-fold risk and the &lt;em&gt;APOE&lt;/em&gt; carriers had 19.7-fold risk.&lt;/p&gt;
&lt;p&gt;The greatest likelihood of neuritic plaques was seen in those with both hyperglycemia and the &lt;em&gt;APOE&lt;/em&gt; allele (38.0-fold compared with neither).&lt;/p&gt;
&lt;p&gt;The pattern was similar for fasting insulin and insulin resistance, although the interactions with the &lt;em&gt;APOE&lt;/em&gt; genotype weren&apos;t statistically significant.&lt;/p&gt;
&lt;p&gt;Neurofibrillary tangles  --  another type of brain pathology seen with Alzheimer&apos;s disease considered to be due to beta-amyloid plaque deposition  --  correlated neither with any insulin or glucose measures nor with the presence of neuritic plaques.&lt;/p&gt;
&lt;p&gt;&quot;The diabetes-related factors may act upstream of the cascade, and might trigger the Alzheimer&apos;s disease pathogenesis,&quot; Sasaki&apos;s group suggested in the paper.&lt;/p&gt;
&lt;p&gt;The authors cited several limitations to their study: First, the crude, semiquantitative evaluations of neuritic plaques could have affected the statistical analyses, and &quot;the medical history of diabetes, such as disease duration, glucose control, and complications, were not considered in this study,&quot; they wrote.&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 a grants from the Ministry of Health, Labour and Welfare of Japan and the Ministry of Education, Culture, Sports, Science and Technology of Japan.&lt;/p&gt;&lt;p&gt;Matsuzaki reported having no conflicts of interest to disclose.&lt;/p&gt;&lt;p&gt;Co-authors reported having received research support from the Ministry of Health, Labor and Welfare of Japan; having served on scientific advisory boards for Eli Lilly, GlaxoSmithKline, Pfizer, Mitsubishi Tanabe Pharma, Ono Pharmaceutical, Astellas Pharma, Asahi Kasei, Shionogi, and Otsuka Pharmaceutical; having served on the editorial boards of multiple journals; having received speaker honoraria from Eli Lilly, GlaxoSmithKline, Pfizer, Asahi Kasei, Janssen, Tsumura, Ajinomoto, Mitsubishi Tanabe Pharma, Meiji Techno, Kyowa Hakko Kirin Pharma, Dainippon Sumitomo Pharma, Organon International (Schering-Plough), Otsuka Pharmaceutical, and Astellas Pharma; and having received research support from Eli Lilly, GlaxoSmithKline, Pfizer, Asahi Kasei, Janssen, Tsumura, Ajinomoto, Mitsubishi Tanabe Pharma, Meiji Techno, Kyowa Hakko Kirin Pharma, Dainippon Sumitomo Pharma, Organon International (Schering-Plough), Otsuka Pharmaceutical, and the Ministry of Education, Culture, Sports, Science and Technology of Japan.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3147"
                     title="One TZD No Safer than Another (CME/CE)"
                     score="0.01"
                     href="http://www.medpagetoday.com/Cardiology/Diabetes/tb/21877?impressionId=1283457945605"
                     
      &lt;p&gt;The diabetes drug pioglitazone (Actos) carries cardiac risk similar to that found for embattled sister compound rosiglitazone (Avandia), according to an analysis of an administrative claims database.&lt;/p&gt;
&lt;p&gt;The composite rate of acute myocardial infarction, acute heart failure, and death from any cause was 4.14% with pioglitazone compared with 4.16% with rosiglitazone when propensity score-matched patients were followed from the time they started the drug.&lt;/p&gt;
&lt;p&gt;The difference was not significant (hazard ratio 1.03, 95% confidence interval 0.91 to 1.15, &lt;em&gt;P&lt;/em&gt;=0.666), Debra Wertz, PharmD, of the healthcare database and analysis firm HealthCore in Wilmington, Del., and colleagues reported in the September issue of &lt;em&gt; Circulation: Cardiovascular Quality and Outcomes&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;These results counter prior observational findings, most notably an FDA analysis of &lt;a href=&quot;http://www.medpagetoday.com/MeetingCoverage/ADA/20933&quot; mce_href=&quot;http://www.medpagetoday.com/MeetingCoverage/ADA/20933&quot; target=&quot;_blank&quot;&gt;Medicare claims data&lt;/a&gt; released just prior to the recent FDA advisory committee panel on rosiglitazone.&lt;/p&gt;
&lt;p&gt;The Medicare data showed a number needed to harm of just 60 over one year and a hazard ratio of 1.18 (95% CI 1.12 to 1.23) for the composite of stroke, heart failure, MI, and death with use of rosiglitazone rather than pioglitazone.&lt;/p&gt;
&lt;p&gt;A &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/Diabetes/18625&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/Diabetes/18625&quot; target=&quot;_blank&quot;&gt;Senate Finance Committee report&lt;/a&gt; issued earlier in the year also uncovered a 2008 FDA analysis of all available studies comparing the two thiazolidinediones (TZDs) that had turned up &quot;strong evidence&quot; for greater MI and heart failure risk with rosiglitazone than pioglitazone.&lt;/p&gt;
&lt;p&gt;When the FDA panelists considered hundreds of pages of data that represent the cumulative evidence on rosiglitazone&apos;s potential cardiovascular risk for the &lt;a href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/21161&quot; mce_href=&quot;http://www.medpagetoday.com/ProductAlert/Prescriptions/21161&quot; target=&quot;_blank&quot;&gt;advisory panel meeting&lt;/a&gt; in July, they concluded in an 18-6 vote that rosiglitazone is riskier than non-TZD diabetes drugs and pioglitazone.&lt;/p&gt;
&lt;p&gt;The conflicting results from Wertz&apos;s group may not actually be that contrary, explained Frederick A. Masoudi, MD, MSPH, of the University of Colorado Denver, in an editorial accompanying the paper.&lt;/p&gt;
&lt;p&gt;Although length of follow-up is an unlikely explanation for the difference in findings between the Medicare and Wertz analyses, the time frame may have contributed, Masoudi suggested.&lt;/p&gt;
&lt;p&gt;Wertz&apos;s group used HealthCore&apos;s databases on managed care health plan members to identify 36,628 adults who started TZD therapy between 2001 and 2005  --  before the controversy over rosiglitazone&apos;s cardiovascular safety ignited.&lt;/p&gt;
&lt;p&gt;The Medicare analysis included 227,571 older adults initiating therapy between 2006 and 2009, which encompassed the period after release of the initial meta-analysis indicating safety was a concern.&lt;/p&gt;
&lt;p&gt;&quot;It is conceivable that after the publication of the meta-analysis, only those physicians who were unaware of the safety concerns (and thus potentially less aware of other important developments in medicine) would continue prescribing rosiglitazone, thus confounding the [Medicare] findings,&quot; Masoudi wrote in the editorial.&lt;/p&gt;

&lt;p&gt;Aside from population composition, means of outcome collection may have played a role as well, commented endocrinologist David Nathan, MD, of Massachusetts General Hospital in Boston, who has also been involved in rosiglitazone safety research.&lt;/p&gt;

&lt;p&gt;But perhaps the best explanation is that Wertz&apos;s study was simply underpowered, Masoudi pointed out.&lt;/p&gt;
&lt;p&gt;The confidence intervals overlapped substantially, both including the possibility of a 12% to 15% increased risk with rosiglitazone compared with pioglitazone.&lt;/p&gt;
&lt;p&gt;A subanalysis of the Wertz data in only those 65 and older again indicated no significant difference between composite event rates (13.88% rosiglitazone versus 13.94% pioglitazone) but hazard ratio confidence intervals that also overlapped (HR 0.97, 95% CI 0.83 to 1.12).&lt;/p&gt;
&lt;p&gt;&quot;Certainly, an increase in relative risk of 10% to 20% in a relatively high-risk population should be considered clinically significant,&quot; Masoudi wrote in the editorial. &quot;A risk of this magnitude seems even more important in light of the availability of numerous therapeutic alternatives to rosiglitazone.&quot;&lt;/p&gt;
&lt;p&gt;Wertz&apos; group cautioned that their study included a commercially insured, relatively young population that may have been less susceptible to cardiovascular event risk, which may have contributed to finding too few risks to document increased risk, and that it excluded those with prior insulin use and did not assess glucose and other laboratory values.&lt;/p&gt;
&lt;p&gt;But &quot;another explanation for absence of elevated risk is that both rosiglitazone and pioglitazone confer an additional cardiovascular risk and that this would result in lack of difference between drugs when they were compared with one another,&quot; the researchers wrote.&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 WellPoint.&lt;/p&gt;&lt;p&gt;Wertz and several co-authors reported being employees of HealthCore, a fully owned subsidiary of WellPoint, at the time this study was conducted.&lt;/p&gt;&lt;p&gt;One co-author is now an independent consultant in Pharmacoepidemiology, another is now an employee of Mu Sigma.&lt;/p&gt;&lt;p&gt;Masoudi reported having no conflicts of interest to declare.&lt;/p&gt;&lt;p&gt;Nathan reported having no financial conflicts of interest to disclose&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3180"
                     title="ESC: ECG Not Much Help for Screening Athletes&apos; Hearts (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/MeetingCoverage/ESCCongress/tb/21911?impressionId=1283457945605"
                     
      STOCKHOLM  --  While hypertrophic cardiomyopathy is the most common cause of sudden death in competitive soccer players, when pro players were screened for the problem with electrocardiography (ECG), the positive results all turned out to be false positives, according to a small study.&lt;br&gt;
&lt;br&gt;The study of 30 pro soccer players who underwent 12-lead ECG screening showed that nearly 60% displayed abnormalities suggestive of cardiac hypertrophy  --  but none were confirmed with MRI scans, according to Jose Angel Cabrera, MD, of Hospital Quiron in Madrid, Spain, and colleagues.&lt;br&gt;
&lt;br&gt;In an abstract scheduled for presentation here at the European Society of Cardiology (ESC) annual meeting, the researchers indicated that recommendations for routine ECG-based screening of athletes &quot;should be reevaluated.&quot;&lt;p&gt;&lt;/p&gt;
&lt;p&gt;Some earlier studies, particularly from Italy, had indicated that 12-lead ECG screening &lt;a href=&quot;http://www.medpagetoday.com/MeetingCoverage/ESCCongress/10738&quot; mce_href=&quot;http://www.medpagetoday.com/MeetingCoverage/ESCCongress/10738&quot; target=&quot;_blank&quot;&gt;could identify athletes&lt;/a&gt; with hypertrophic cardiomyopathy, putting them at risk for sudden cardiac death. Making such screening routine in Italy was said to &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/Arrhythmias/4230&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/Arrhythmias/4230&quot; target=&quot;_blank&quot;&gt;reduce cardiac arrests&lt;/a&gt; among athletes by 90%.&lt;/p&gt;
&lt;p&gt;However, the new Spanish study suggests that instituting such screening may also involve a great deal of waste  --  since positive findings typically result in expensive follow-up evaluations.&lt;/p&gt;
&lt;p&gt;Cabrera and colleagues reported on their experience with 30 professional soccer players, mean age 31 (SD 4), who underwent 12-lead ECG screening conducted and interpreted according to proposed ESC guidelines.&lt;/p&gt;
&lt;p&gt;The participants also underwent MRI cardiac scans and genotyping for mutations in nine genes known to be associated with various types of heart disease.&lt;/p&gt;
&lt;p&gt;ECG results in 17 of the players showed abnormalities that, under the guidelines, were indicative of cardiac hypertrophy warranting follow-up.&lt;/p&gt;
&lt;p&gt;But the MRI results in all 17 showed normal left ventricular wall thickness and no signs of systolic anterior mitral valve motion or left ventricular outflow obstruction.&lt;/p&gt;
&lt;p&gt;On the other hand, the evaluations failed to identify minor pericardial effusion in two players and persistent ductus arteriosus in another.&lt;/p&gt;
&lt;p&gt;None of the participants had risk-associated genotype findings.&lt;/p&gt;
&lt;p&gt;Alfred Bove, MD, of Temple University in Philadelphia and past president of the American College of Cardiology, told &lt;em&gt;MedPage Today&lt;/em&gt; in an interview that the findings are plausible but at the same time pose a conundrum for clinical practice.&lt;/p&gt;
&lt;p&gt;&quot;It&apos;s a tough call,&quot; he said. &quot;How do you find these kids [with serious cardiac abnormalities]? It&apos;s very small numbers, one in 100,000 or something like that. How many do you screen with expensive tests to find the one kid  --  it becomes a big issue.&quot;&lt;/p&gt;
&lt;p&gt;He noted that ECG screening is relatively cheap and easy to perform, and there is nothing else available for mass use that would not cost substantially more.&lt;/p&gt;
&lt;p&gt;But Bove agreed that relying on ECG causes problems, particularly in the U.S. where rates of actual cardiac abnormalities are much lower than in northern Italy, where the research underlying the current recommendations was conducted.&lt;/p&gt;
&lt;p&gt;&quot;The Italians have convinced the world that everybody should have an electrocardiogram,&quot; he quipped.&lt;/p&gt;
&lt;p&gt;Bove, who said he sometimes helps evaluate young athletes with suspected heart problems, indicated that, as a result, it&apos;s common to see one athlete &quot;with a very bizarre-looking electrocardiogram  --  perfectly normal kid, playing excellent sports, no history of anything ... and everybody gets all upset.&quot;&lt;/p&gt;
&lt;p&gt;He said these athletes can get &quot;million-dollar workups&quot; that, most times, show nothing abnormal other than the &quot;weird&quot; ECG.&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;No external funding for the study was reported.&lt;/p&gt;&lt;p&gt;Cabrera had no conflict of interest disclosures.&lt;/p&gt;&lt;p&gt;Bove said he had no relationships with commercial entities relevant to the research.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_3177"
                     title="ESC: Switching Statins Often Leads to Wrong Doses (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/MeetingCoverage/ESCCongress/tb/21906?impressionId=1283457945605"
                     
      &lt;p&gt;STOCKHOLM  --  A third of patients on lipid-lowering therapy received inadequate doses of generic simvastatin after being switched from atorvastatin (Lipitor), an analysis of a large pharmacy database showed.&lt;/p&gt;
&lt;p&gt;On the basis of atorvastatin&apos;s 2:1 potency ratio versus simvastatin, fewer than half of patients received equipotent doses after the switch. The switching occurred after a government-mandated change in rules for using branded statins in the Netherlands.&lt;/p&gt;
&lt;p&gt;Statistical models suggested inadequate dosing would lead to a 5.6% increase in LDL cholesterol, possibly increasing the risk of cardiovascular events, according to a study that will be reported here at the European Society of Cardiology meeting next week.&lt;/p&gt;
&lt;p&gt;&quot;The predicted net effect of this would be at least a 5% to 6% increase in low-density lipoprotein cholesterol, which translates to a 3% average increase in the risk of heart disease and stroke,&quot; Danny Liew, MD, of the University of Melbourne in Australia, said in a statement.&lt;/p&gt;
&lt;p&gt;&quot;Our study highlights the need for health policymakers to be conscious of the potential adverse and unintended consequences of policy changes and for clinicians to be aware of dose equivalences among statins,&quot; Liew added in an e-mail to &lt;em&gt;MedPage Today&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;Patients on higher doses of atorvastatin were more likely to be switched to less than equipotent doses of simvastatin, he said.&lt;/p&gt;
&lt;p&gt;The findings came from an analysis of a nationwide pharmacy database and included 39,031 patients switched from atorvastatin to simvastatin during the first quarter of 2009. The switches occurred after the Dutch government began requiring physicians to justify prescriptions for branded statins.&lt;/p&gt;
&lt;p&gt;Liew and colleagues conducted the analysis after prescription data suggested that switching often resulted in simvastatin doses that did not have potency equivalent to that of atorvastatin. They determined relative potency on the basis of a published meta-analysis of randomized clinical trials comparing the two drugs (&lt;em&gt;Clin Ther&lt;/em&gt; 2007; 29: 242-252).&lt;/p&gt;
&lt;p&gt;Their analysis showed that 33.7% of patients received less than equipotent doses of simvastatin after switching from atorvastatin, 19.1% received more potent doses of simvastatin, and 47.2% received equipotent doses. The weighted-average initial doses were 19.6 mg for atorvastatin and 32.9 mg of simvastatin.&lt;/p&gt;
&lt;p&gt;Among the subgroup of patients switched to less potent doses of simvastatin, the initial dose averaged 28.9 mg for atorvastatin and 27.8 mg for simvastatin.&lt;/p&gt;
&lt;p&gt;&quot;Patients on higher doses of initial atorvastatin were more likely to switch to less potent doses of simvastatin,&quot; Liew commented. &quot;It may be that clinicians may be reluctant to prescribe high doses of simvastatin.&quot;&lt;/p&gt;
&lt;p&gt;A recent meta-regression study showed that every 25 mg/dL (0.65 mmol/L) reduction in LDL lowers the risk of any CVD event by 14%, a coronary event by 16%, stroke by 10%, and cardiovascular death by 11% (&lt;em&gt;Curr Ther&lt;/em&gt; 2009; 31: 236-244). Given that inadequate simvastatin dosing was modeled to lead to a 5.6% increase in LDL, the investigators estimated that inadequate dosing of simvastatin would increase cardiovascular risk by 3%.&lt;/p&gt;
&lt;p&gt;The magnitude of the increase in risk varied by baseline LDL value and the type of CVD event assessed. The estimated added risk ranged from a 1.7% increase in stroke for patients with a baseline LDL of 2.0 mmol/L to a 5.5% increase in coronary events among patients with a baseline LDL of 4.0 mmol/L.&lt;/p&gt;
&lt;p&gt;A U.S. cardiologist echoed Liew&apos;s cautionary statements regarding the possible risks associated with switching to an inadequate statin dose.&lt;/p&gt;
&lt;p&gt;&quot;The consequences of switching from Lipitor to simvastatin on LDL cholesterol on any CVD event, coronary event, stroke, and CVD death in the Dutch population are noteworthy and of concern,&quot; said Robert Eckel, MD, of the University of Colorado. &quot;Despite the cost-saving benefits of such a change, the increased risk demands better guidance on how to prescribe equipotent doses.&quot;&lt;/p&gt;
&lt;p&gt;Eckel is a spokesperson for the American Heart Association and was not involved in the study.&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;Liew and Eckel reported no relevant disclosures. Liew&apos;s co-investigators included employees of Pfizer.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
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