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However , late loss ( 0.04 0.5 mm vs. 0.14 0.5 mm , p = 0.14 ) and binary restenosis rate ( 4.7 % vs. 9.5 % , p = 0.22 ) were very low and similar in both groups .
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Clinical follow-up ( median 365 days ) was obtained in all ( 100 % ) patients .
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Occurrences of the combined clinical outcome measure ( cardiac death , myocardial infarction , and target vessel revascularization ; 6 % vs. 8 % ; hazard ratio [ HR ] : 0.76 ; 95 % CI : 0.26 to 2.18 , p = 0.6 ) and the need for target vessel revascularization ( 2 % vs. 6 % ; HR : 0.32 : 95 % CI : 0.07 to 1.59 , p = 0.17 ) were similar in the 2 groups .
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In patients with BMS-ISR , both DEB and EES provided excellent clinical results with a very low rate of clinical and angiographic recurrences .
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However , compared with DEB , EES provide superior late angiographic findings .
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( Restenosis Intra-stent of Bare Metal Stents : Paclitaxel-eluting Balloon vs. Everolimus-eluting Stent [ RIBS V ] ; NCT01239953 ) .
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Irregularity measures have been suggested as risk indicators in patients with atrial fibrillation ( AF ) ; however , it is not known to what extent they are affected by commonly used rate-control drugs .
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We aimed at evaluating the effect of metoprolol , carvedilol , diltiazem , and verapamil on the variability and irregularity of the ventricular response in patients with permanent AF .
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Sixty patients with permanent AF were part of an investigator-blind cross-over study , comparing 4 rate-control drugs ( diltiazem , verapamil , metoprolol , and carvedilol ) .
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We analyzed five 20-minute segments per patient : baseline and the 4 drug regimens .
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On every segment , heart rate ( HR ) variability and irregularity of RR series were computed .
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The variability was assessed as standard deviation , pNN20 , pNN50 , pNN80 , and rMSSD .
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The irregularity was assessed by regularity index , approximate ( ApEn ) , and sample entropy .
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A significantly lower HR was obtained with all drugs , the HR was lowest using the calcium channel blockers .
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All drugs increased the variability of ventricular response in respect to baseline ( as an example , rMSSD : baseline 171 47 milliseconds , carvedilol 229 58 milliseconds ; P < 0.05 vs. baseline , metoprolol 226 66 milliseconds ; P < 0.05 vs. baseline , verapamil 228 84 ; P < 0.05 vs. baseline , diltiazem 256 87 milliseconds ; P < 0.05 vs. baseline and all other drugs ) .
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Only - blockers significantly increased the irregularity of the RR series ( as an example , ApEn : baseline 1.86 0.13 , carvedilol 1.92 0.09 ; P < 0.05 vs. baseline , metoprolol 1.93 0.08 ; P < 0.05 vs. baseline , verapamil 1.86 0.22 ns , diltiazem 1.88 0.16 ns ) .
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Modification of AV node conduction by rate-control drugs increase RR variability , while only - blockers affect irregularity .
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Among patients with quiescent ulcerative colitis ( UC ) , lower fecal concentrations of calprotectin are associated with lower rates of relapse .
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We performed an open-label , randomized controlled trial to investigate whether increasing doses of mesalamine reduce concentrations of fecal calprotectin ( FC ) in patients with quiescent UC .
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We screened 119 patients with UC in remission on the basis of Simple Clinical Colitis Activity Index scores , FC > 50 g/g , and intake of no more than 3 g/day mesalamine .
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Participants taking mesalamine formulations other than multimatrix mesalamine were switched to multimatrix mesalamine ( 2.4 g/day ) for 6 weeks ; 52 participants were then randomly assigned ( 1:1 ) to a group that continued its current dose of mesalamine ( controls , n = 26 ) or a group that increased its dose by 2.4 g/day for 6 weeks ( n = 26 ) .
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The primary outcome was continued remission with FC < 50 g/g .
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Secondary outcomes were continued remission with FC < 100 g/g or < 200 g/g ( among patients with pre-randomization values above these levels ) .
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The primary outcome was achieved by 3.8 % of controls and 26.9 % of the dose escalation group ( P = .0496 ) .
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More patients in the dose escalation group reduced FC to below 100 g/g ( P = .04 ) and 200 g/g ( P = .005 ) .
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Among the patients who were still in remission after the randomization phase , clinical relapse occurred sooner in patients with FC > 200 g/g compared with those with FC < 200 g/g ( P = .01 ) .
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Among patients with quiescent UC and increased levels of FC , increasing the dose of mesalamine by 2.4 g/day reduced fecal concentrations of calprotectin to those associated with lower rates of relapse .
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Clinicaltrials.gov number : NCT00652145 .
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Despite standard statin therapy , a majority of patients retain a high `` residual risk '' of cardiovascular events .
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The aim of this study was to evaluate the effects of ezetimibe plus atorvastatin versus atorvastatin monotherapy on the lipid profile and coronary atherosclerosis in Japanese patients who underwent percutaneous coronary intervention ( PCI ) .
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This trial was a prospective , randomized , controlled , multicenter study .
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Eligible patients who underwent PCI were randomly assigned to atorvastatin alone or atorvastatin plus ezetimibe ( 10 mg ) daily .
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Atorvastatin was uptitrated with a treatment goal of low-density lipoprotein cholesterol ( LDL-C ) < 70 mg/dl .
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Serial volumetric intravascular ultrasound was performed at baseline and again at 9 to 12 months to quantify the coronary plaque response in 202 patients .
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The combination of atorvastatin/ezetimibe resulted in lower levels of LDL-C than atorvastatin monotherapy ( 63.2 16.3 mg/dl vs. 73.3 20.3 mg/dl ; p < 0.001 ) .
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For the absolute change in percent atheroma volume ( PAV ) , themean difference between the 2 groups ( -1.538 % ; 95 % confidence interval [ CI ] : -3.079 % to 0.003 % ) did not exceedthe pre-defined noninferiority margin of 3 % , but the absolute change in PAV did show superiority for the dual lipid-lowering strategy ( -1.4 % ; 95 % CI : -3.4 % to -0.1 % vs. -0.3 % ; 95 % CI : -1.9 % to 0.9 % with atorvastatin alone ; p = 0.001 ) .
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For PAV , a significantly greater percentage of patients who received atorvastatin/ezetimibe showed coronary plaque regression ( 78 % vs. 58 % ; p = 0.004 ) .
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Both strategies had acceptable side effect profiles , with a low incidence oflaboratory abnormalities and cardiovascular events .
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Compared with standard statin monotherapy , the combination of statin plus ezetimibe showed greater coronary plaque regression , which might be attributed to cholesterol absorption inhibition-induced aggressive lipid lowering .
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( Plaque Regression With Cholesterol Absorption Inhibitor or Synthesis Inhibitor Evaluated by Intravascular Ultrasound [ PRECISE-IVUS ] ; NCT01043380 ) .
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