<?xml version="1.0" encoding="utf-8"?>
<recommendedContent xmlns="http://api.mspoke.com">
    <recommendedItem id="20100101_19_458"
                     title="Calcium Scoring Misses 20% of CAD Cases (CME/CE)"
                     score="0.012"
                     href="http://www.medpagetoday.com/Cardiology/AcuteCoronarySyndrome/tb/18387?impressionId=1265777130227"
                     
      &lt;p&gt;Contrary to guidelines, the absence of coronary artery calcium doesn&apos;t rule out coronary artery disease in symptomatic patients, researchers found in a new study.&lt;/p&gt;
&lt;p&gt;In a multicenter clinical trial, 19% of patients with a coronary calcium score of 0 had stenosis of at least 50% in one or more coronary artery segments, according to Carlos E. Rochitte, MD, of the University of S&amp;#227;o Paulo, Brazil, and colleagues.&lt;/p&gt;
&lt;p&gt;Likewise, 20% of vessels seen to be totally occluded on revascularization had no calcium on scans, they 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;&quot;The absence of coronary calcification should not be used as a gatekeeper and should not prevent a symptomatic patient from undergoing angiography,&quot; the researchers wrote.&lt;/p&gt;
&lt;p&gt;Currently, American Heart Association/American College of Cardiology guidelines suggest that excluding measurable coronary calcium could serve as an effective filter for sending patients on to invasive testing or admitting them.&lt;/p&gt;
&lt;p&gt;One systematic review of 18 studies had indicated that a zero calcium score had a negative predictive value of 93% for stenosis and a positive predictive value of 68% in symptomatic patients.&lt;/p&gt;
&lt;p&gt;However, in Rochitte&apos;s trial  --  CORE64 (Coronary Evaluation Using Multi-Detector Spiral Computed Tomography Angiography Using 64 Detectors)  --  the negative predictive value of a coronary calcium score of 0 was 68%, while the positive predictive value was 81%.&lt;/p&gt;
&lt;p&gt;Overall sensitivity to predict the absence of significant (at least 50%) stenosis was 45%, while specificity was 91%.&lt;/p&gt;
&lt;p&gt;&quot;This apparent lack of predictive value of a calcium scan should be enough to give a clinician pause,&quot; Rita F. Redberg, MD, of the University of California San Francisco, wrote in an accompanying editorial.&lt;/p&gt;
&lt;p&gt;Whatever the reason for the discrepancy, neither the trial nor the review provided any information on how coronary calcium scans add incrementally to traditional predictors of coronary artery disease, such as clinical assessment and stress testing, she said. Nor would she rule out their use entirely for patients with chest pain.&lt;/p&gt;
&lt;p&gt;&quot;Given the significant &lt;a href=&quot;http://www.medpagetoday.com/Cardiology/AcuteCoronarySyndrome/12732&quot; mce_href=&quot;http://www.medpagetoday.com/Cardiology/AcuteCoronarySyndrome/12732&quot; target=&quot;_blank&quot;&gt;radiation risks&lt;/a&gt; of coronary artery calcium scans, however, clinicians must use extreme caution when ordering such scans,&quot; Redberg cautioned.&lt;/p&gt;
&lt;p&gt;The prospective &lt;a href=&quot;http://www.medpagetoday.com/Radiology/DiagnosticRadiology/11927&quot; mce_href=&quot;http://www.medpagetoday.com/Radiology/DiagnosticRadiology/11927&quot; target=&quot;_blank&quot;&gt;CORE64 study&lt;/a&gt; was originally designed to compare diagnostic performance of CT and invasive angiography in symptomatic patients with suspected coronary artery disease. But it also included a coronary calcium scan up to 30 days prior to conventional angiography.&lt;/p&gt;
&lt;p&gt;Of the 291 patients included in the calcium score analysis (73% male, mean age 59.3), 56% had at least 50% coronary stenosis by conventional angiography and 45% had at least 70% stenosis.&lt;/p&gt;
&lt;p&gt;Calcium score only weakly correlated with the highest degree of coronary stenosis found in a patient. Its ability to predict presence of significant lesions was &quot;moderate&quot; (area under the receiver-operating characteristic curve 0.77, &lt;em&gt;P&lt;/em&gt;&amp;lt;0.001).&lt;/p&gt;
&lt;p&gt;A non-zero score was associated with 8.1-fold likelihood of having at least 50% coronary stenosis (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001) after adjusting for age, sex, hypertension, dyslipidemia, family history of premature heart disease, diabetes, race, and hospitalization.&lt;/p&gt;
&lt;p&gt;Among the 100 patients who went on to revascularization within 30 days of angiography, 13% had a coronary calcium score of 0, 25% had a score of 1 to 10, and 44% had a score over 10 (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.001 for trend).&lt;/p&gt;
&lt;p&gt;The fact that significant coronary artery disease occurred in the absence of calcification in almost 20% of patients should not be surprising, since coronary calcification is thought to occur late in the atherosclerotic process, while obstruction can occur earlier, Redberg asserted.&lt;/p&gt;
&lt;p&gt;The researchers also cautioned that the results would not apply to asymptomatic patients with intermediate risk for events, a group in which a score of 0 has been consistently shown to indicate low risk.&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 grants from Toshiba Medical Systems, the Doris Duke Charitable Foundation, the National Heart, Lung, and Blood Institute, the National Institute on Aging, and the Donald W. Reynolds Foundation.&lt;/p&gt;&lt;p&gt;Rochitte reported no conflicts of interest. Co-authors reported financial relationships with Toshiba Medical Systems, Bayer, Schering, GE Healthcare, Bracco, Bristol-Myers Squibb, sanofi-aventis, and Vital Images.&lt;/p&gt;&lt;p&gt;Redberg provided no information on conflicts of interest.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_373"
                     title="Protein in Urine Presages More Severe Problems (CME/CE)"
                     score="0.009"
                     href="http://www.medpagetoday.com/Nephrology/ESRD/tb/18265?impressionId=1265777130227"
                     
      &lt;p&gt;The three-year risk of death, heart attack, and kidney failure was markedly increased in patients with baseline proteinuria, regardless of their estimated glomerular filtration rate (eGFR), researchers said.&lt;/p&gt;
&lt;p&gt;In a population-based study of nearly 1 million people, mortality was approximately doubled with heavy proteinuria among individuals stratified according to their eGFR, reported Brenda R. Hemmelgarn, MD, PhD, of the University of Calgary in Canada, and colleagues.&lt;/p&gt;
&lt;p&gt;Rates of myocardial infarction were increased by about 50% with heavy proteinuria, and end-stage renal disease and doubled levels of serum creatinine were as much as 30 times more common, the researchers reported in the Feb. 3 issue of the &lt;em&gt;Journal of the American Medical Association&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;Prognosis associated with a given level of eGFR varies substantially based on the presence and severity of proteinuria,&quot; Hemmelgarn and colleagues concluded.&lt;/p&gt;
&lt;p&gt;&quot;In fact, patients with heavy proteinuria but without overtly abnormal eGFR appeared to have worse clinical outcomes than those with moderately reduced eGFR but without proteinuria.&quot;&lt;/p&gt;
&lt;p&gt;They added that the findings were important because current recommendations for managing chronic kidney disease rely on eGFR for staging purposes without consideration of proteinuria.&lt;/p&gt;
&lt;p&gt;&quot;Future revisions of the classification system for chronic kidney disease should incorporate information from proteinuria,&quot; the researchers urged.&lt;/p&gt;
&lt;p&gt;The results emerged from a laboratory registry covering some 921,000 adults in the province of Alberta who had had measurements of eGFR, serum creatinine, and urinary protein from 2002 to 2007.&lt;/p&gt;
&lt;p&gt;Proteinuria was measured with a urine dipstick or the albumin-creatinine ratio. Dipstick readings of at least 2 points were considered heavy proteinuria. Readings showing at least trace protein but less than 2 points were classed as mild; negative readings were considered normal.&lt;/p&gt;
&lt;p&gt;The stratifications of albumun-creatinine ratio were greater than 300 mg/g, 30 to 300 mg/g, and less than 30 mg/g for heavy, mild, and normal, respectively.&lt;/p&gt;
&lt;p&gt;Other registry data for the province provided outcomes in these individuals, with median follow-up of 35 months.&lt;/p&gt;
&lt;p&gt;Among individuals with eGFR rates of at least 60 mL/min/1.73 m&lt;sup&gt;2&lt;/sup&gt;, death rates were 7.2 per 1,000 for those with dipstick-measured heavy proteinuria (95% CI 6.6 to 7.8) and 5.8 per 1,000 for mild proteinuria (95% CI 5.5 to 6.0) compared with 2.7 per 1,000 for those with normal urine protein (95% CI 2.6 to 2.8).&lt;/p&gt;
&lt;p&gt;At the other end of the eGFR spectrum  --  those with levels of 15 to 29.9 mL/min/1.73 m&lt;sup&gt;2&lt;/sup&gt;  --  proteinuria remained an independent predictor of death: Mortality rates were 10.4 per 1,000 with heavy proteinuria (95% CI 9.3 to 11.6) and 9.1 per 1,000 with mild proteinuria (95% CI 8.2 to 10.0) versus 6.7 per 1,000 with normal urine protein (95% CI 6.2 to 7.3).&lt;/p&gt;
&lt;p&gt;These death rates reflected adjustments for a host of potential confounding factors and comorbidities, including age, sex, diabetes, hypertension, liver disease, and cardiovascular conditions.&lt;/p&gt;
&lt;p&gt;Proteinuria also predicted myocardial infarction in patients stratified by eGFR, but not as strongly. In the group with eGFR above 60 mL/min/1.73 m&lt;sup&gt;2&lt;/sup&gt;, rates of MI were 1.6 per 1,000 (95% CI 1.3 to 2.0) and 0.9 (95% CI 0.9 to 1.0) for heavy and normal urinary protein, respectively, as measured by dipstick.&lt;/p&gt;
&lt;p&gt;MI rates were also increased with proteinuria in participants with eGFR below 30 mL/min/1.73 m&lt;sup&gt;2&lt;/sup&gt;, the researchers reported.&lt;/p&gt;
&lt;p&gt;End-stage renal disease was enormously more common with dipstick-measured heavy proteinuria, independent of baseline eGFR.&lt;/p&gt;
&lt;p&gt;Individuals with eGFR above 60 mL/min/1.73 m&lt;sup&gt;2&lt;/sup&gt; were diagnosed with the condition at a rate of 1.0 per 1,000 (95% CI 0.7 to 1.4) if they had heavy proteinuria, compared with 0.03 per 1,000 (95% CI 0.02 to 0.09) among those with normal urine protein.&lt;/p&gt;
&lt;p&gt;A five-fold difference in rates of end-stage renal disease was still apparent among those with eGFR below 30 mL/min/1.73 m&lt;sup&gt;2&lt;/sup&gt;: 65.9 (95% CI 52.3 to 82.9) versus 12.7 per 1,000 (95% CI 9.3 to 17.3) for heavy versus normal protein, respectively.&lt;/p&gt;
&lt;p&gt;These results were confirmed when cross-checked against the more accurate albumin-creatinine ratio, Hemmelgarn and colleagues indicated.&lt;/p&gt;
&lt;p&gt;Each 10-fold increase in albumin-creatinine ratio was associated with the following relative rates of the major study outcomes, after adjusting for eGFR:&lt;ul&gt; &lt;li&gt;Death: 1.22 (95% CI 1.21 to 1.24)&lt;/li&gt; &lt;li&gt;MI: 1.18 (95% CI 1.14 to 1.21)&lt;/li&gt; &lt;li&gt;Doubling of serum creatinine: 1.76 (95% CI 1.70 to 1.82)&lt;/li&gt; &lt;li&gt;End-stage renal disease: 1.92 (95% CI 1.81 to 2.04)&lt;/li&gt; &lt;/ul&gt;&lt;/p&gt;
&lt;p&gt;Hemmelgarn and colleagues noted several limitations to the study including the fact that the sample was restricted to outpatients undergoing laboratory evaluations for kidney function and urinary protein, and the data were based on single measurements. Missing were data on alcohol, tobacco, and antihypertensive drug use, which might have affected the findings.&lt;/p&gt;
&lt;p&gt;The researchers also indicated that the follow-up period may have been too short to fully evaluate risks of progression to kidney failure.&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;Support for the study came from the Alberta Heritage Foundation for Medical Research, the Canadian Institutes of Health Research, Alberta Health and Wellness, and internal funds.&lt;/p&gt;&lt;p&gt;No potential conflicts of interest were reported.&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="0.008"
                     href="http://www.medpagetoday.com/Cardiology/PCI/tb/18226?impressionId=1265777130227"
                     
      &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_325"
                     title="MRI Reveals Risk for Kidney Failure in Diabetic Patients (CME/CE)"
                     score="0.005"
                     href="http://www.medpagetoday.com/Nephrology/Diabetes/tb/18195?impressionId=1265777130227"
                     
      So-called silent strokes, visible on cerebral MRI scans, predict kidney failure in patients with type 2 diabetes, Japanese researchers said.&lt;br&gt;
&lt;br&gt;After an average follow-up of 7.5 years, diabetic patients with evidence of small cerebral infarctions at baseline later suffered death or kidney failure at more than twice the rate seen in patients who had not had silent strokes, reported Takashi Uzu, MD, of Shiga University of Medical Sciences in Shiga, Japan, and colleagues.&lt;br&gt;
&lt;br&gt;Silent strokes are a consequence of cerebral microvascular disease and thus may logically accompany the development of similar abnormalities in renal blood vessels, ultimately leading to kidney failure, the researchers explained online in the &lt;em&gt;Journal of the American Society of Nephrology&lt;/em&gt;.&lt;/p&gt;
&lt;p&gt;&quot;It is important to identify individuals who are at risk of progression of diabetic renal disease,&quot; Uzu and colleagues wrote.&lt;/p&gt;
&lt;p&gt;The current standard prognostic test is the albumin-creatinine ratio, but it is not entirely adequate for the purpose, they suggested: &quot;Recent clinical studies have shown that renal insufficiency can occur in the absence of microalbuminuria in patients with type 2 diabetes.&quot;&lt;/p&gt;
&lt;p&gt;But they acknowledged that brain MRI scans would be too expensive and inconvenient for routine prognostic testing.&lt;/p&gt;
&lt;p&gt;&quot;New strategies are needed to determine the presence of renal and/or extrarenal microvascular diseases,&quot; Uzu and colleagues wrote.&lt;/p&gt;
&lt;p&gt;Their study involved 608 patients with type 2 diabetes who had no clinical signs of cerebrovascular or cardiovascular disease or overt nephropathy. Their mean age at baseline was about 60 and the average glycated hemoglobin level was about 8.6%.&lt;/p&gt;
&lt;p&gt;Participants underwent cerebral MRI scans at baseline, with 177 showing evidence of silent cerebral infarctions, defined as focal lesions of at least 3 mm in diameter with low signal intensity on T1-weighted images and high intensity with T2 weighting. Dilated perivascular spaces were distinguished from infarcts with proton density scans. Patients with positive findings who had a history of stroke or transient ischemic attack were excluded.&lt;/p&gt;
&lt;p&gt;Those with silent infarctions at baseline differed significantly from other participants according to several parameters. Not surprisingly, patients with cerebral infarcts on average were somewhat older (63 versus 57), had had diabetes for a longer period of time (9.8 years versus 7.6), had higher blood pressure (146.8 mm Hg systolic versus 136.5 ), and were more likely to have a history of smoking (58% versus 46%). All differences were significant at &lt;em&gt;P&lt;/em&gt;&amp;lt;0.01.&lt;/p&gt;
&lt;p&gt;On the other hand, baseline fasting plasma glucose and glycated hemoglobin levels were both significantly lower in the patients who&apos;d had silent infarctions: mean 163 mg/dL versus 176 for glucose and 8.3% versus 8.7% for HbA1c (&lt;em&gt;P&lt;/em&gt;&amp;#8804;0.01 for both).&lt;/p&gt;
&lt;p&gt;Patients were followed for up to 10 years, with a mean of 7.5. The primary outcome was end-stage renal disease or death, and Uzu and colleagues chose a secondary outcome combining dialysis with doubling of serum creatinine.&lt;/p&gt;
&lt;p&gt;Kaplan-Meier curves for the patients with and without silent infarctions at baseline indicated that the primary outcome occurred at equal rates through the first four years of follow-up, but then the curves diverged abruptly.&lt;/p&gt;
&lt;p&gt;At year eight, approximately 6% of the noninfarcted group had experienced the primary outcome, compared with 21% of those who&apos;d had silent strokes (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001), according to Uzu and colleagues.&lt;/p&gt;
&lt;p&gt;Curves for the secondary outcome began diverging by year three. At year eight, about 6% of the noninfarct participants had gone to dialysis or had serum creatinine levels double, whereas these endpoints occurred in nearly 30% of the infarct group (&lt;em&gt;P&lt;/em&gt;&amp;lt;0.0001).&lt;/p&gt;
&lt;p&gt;Overall, the hazard ratio associated with baseline silent cerebral infarctions for the primary outcome during follow-up was 2.44 (95% CI 1.36 to 4.38).&lt;/p&gt;
&lt;p&gt;The hazard ratio for death alone was somewhat smaller (1.61, 95% CI 0.71 to 3.62), indicating that most of the risk measured by the primary outcome was actually in end-stage renal disease.&lt;/p&gt;
&lt;p&gt;For the secondary outcome, the hazard ratio was 4.79 (95% CI 2.72 to 8.46).&lt;/p&gt;
&lt;p&gt;All the hazard ratios reflected adjustments for age, sex, duration of diabetes, body mass index, smoking status, HbA1c, blood pressure, serum lipids, and standard lab indices of kidney function at baseline.&lt;/p&gt;
&lt;p&gt;Estimated glomerular filtration rate (eGFR) during follow-up also decreased faster in patients with silent strokes. After five years, mean eGFR had fallen by 8 ml/min/m&lt;sup&gt;2&lt;/sup&gt; in the patients without silent infarcts at baseline compared with 10.5 ml/min/m&lt;sup&gt;2&lt;/sup&gt; in those with cerebral microvascular disease.&lt;/p&gt;
&lt;p&gt;The researchers noted that the study was conducted at two clinical sites, which used somewhat different MRI procedures. But they also indicated that the prevalence of silent infarctions did not differ between the sites.&lt;/p&gt;
&lt;p&gt;Other limitations included use of an older creatinine assay, inclusion of larger silent infarcts which could reflect macrovascular disease, and more patients in the cerebral infarct group who were taking renin-angiotensin system blocking drugs, which have renal impairment as an adverse effect.&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;External funding for the study was not reported.&lt;/p&gt;&lt;p&gt;No potential conflicts of interest were reported.&lt;/p&gt;&lt;/div&gt;&lt;div style=&quot;clear:both;&quot;&gt;&lt;/div&gt;
    </recommendedItem>
    <recommendedItem id="20100101_19_278"
                     title="FDA Okays First Percutaneous Heart Valve"
                     score="0.001"
                     href="http://www.medpagetoday.com/ProductAlert/DevicesandVaccines/tb/18135?impressionId=1265777130227"
                     
      &lt;p&gt;WASHINGTON  --  The FDA has approved the Melody Transcatheter Pulmonary Valve and Ensemble Delivery System, the first heart valve designed for implantation through a catheter in a leg vein.&lt;/p&gt;
&lt;p&gt;The device gives congenital heart defect patients with poorly functioning pulmonary valve conduits new treatment options without requiring open heart surgery.&lt;/p&gt;
&lt;p&gt;The valve does not cure the condition and may wear to the point of needing replacement over time, but a tissue valve in the device maintains proper blood flow-direction, which allows the valve to function longer than usual, an FDA statement said.&lt;/p&gt;
&lt;p&gt;Approval was based on clinical studies of 99 U.S. patients and 68 European patients.&lt;/p&gt;
&lt;p&gt;Participants showed improved heart function, and a majority noted improvements in clinical symptoms, the statement said.&lt;/p&gt;
&lt;p&gt;The limited durability of the device was similar to other existing treatments in the trial, with 21% of U.S. patients experiencing a stent fracture, the release said.&lt;/p&gt;
&lt;p&gt;Device manufacturer Medtronic must complete two postapproval studies to test long-term risks and benefits, including one study with 150 participants from the original clinical trials and more than 100 additional patients, who will each undergo a five-year evaluation.&lt;/p&gt;
&lt;p&gt;An additional condition of the device&apos;s approval is a review of healthcare professional specialization required for device implantation. The manufacturer must also maintain a database of valve recipients.&lt;/p&gt;
&lt;p&gt;The transcatheter valve was approved under the Humanitarian Device Exception (HDE) program, which supports device development for conditions affecting fewer than 4,000 people and allows approval for limited use with reasonable assurances that the device health benefit outweighs risk of injury or illness.&lt;/p&gt;
&lt;p&gt;Products with HDE approval can only be used at medical institutions under an institutional review board and cannot be sold for more than the cost of research, development, fabrication, and distribution.&lt;/p&gt;

    </recommendedItem>
</recommendedContent>