***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Abstract Background Acute pulmonary embolism may be ruled out by combining nonhigh clinical probability and a normal D‐dimer level . Both antiplatelet drugs and HMG‐CoA reductase inhibitors ( statins ) have been associated with effects on thrombus formation , potentially influencing D‐dimer levels in this setting , leading to a higher rate of false‐negative tests . Therefore , we determined whether D‐dimer levels in patients with suspected pulmonary embolism are affected by concomitant use of antiplatelet drugs and /or statins and evaluated whether the effect of antiplatelet drugs or statins might affect diagnostic accuracy . Material s and methods We performed a posthoc analysis in the YEARS diagnostic study , comparing age‐ and sex‐adjusted D‐dimer levels among users of antiplatelet drugs , statins and nonusers . We then reclassified patients within the YEARS algorithm by developing a model in which we adjusted D‐dimer cut‐offs for statin use and evaluated diagnostic accuracy . Results We included 156 statins users , 147 antiplatelet drugs users and 726 nonusers of either drugs , all with suspected pulmonary embolism . Use of antiplatelet drugs did not have a significant effect , whereas statin use was associated with 15 % decrease in D‐dimer levels ( 95 % CI , −28 % to −0.6 % ) . An algorithm with lower D‐dimer thresholds in statin users yielded lower specificity ( 0.42 compared to 0.33 ) with no difference in false‐negative tests . Conclusions We conclude that use of statins but not of antiplatelet agents is associated with a modest decrease in D‐dimer levels . Adjusting D‐dimer cut‐offs for statin use did , however , not result in a safer diagnostic strategy in our cohort Abstract Background : Treatment with HMG-CoA reductase inhibitors ( statins ) reduces the morbidity and mortality of coronary artery disease ( CAD ) . In addition to their lipid-lowering actions , pleiotropic effects of statins have been demonstrated . Objective : The aim of the present study was to assess if atorvastatin therapy has an impact on haemostasis , fibrinolysis and inflammation in normocholesterolaemic patients with CAD . Methods : Fifty-four patients with CAD who had received atorvastatin treatment for at least 8 weeks ( mean dosage 30 mg/day ) and 54 patients with CAD who had not received atorvastatin therapy were selected from a larger prospect i ve , r and omized , double-blind study for inclusion in this post hoc analysis . Patients were matched by their total cholesterol levels . All patients were normocholesterolaemic . Results : In the atorvastatin-treated patients significantly lower plasma levels of thrombin-antithrombin complexes ( p<0.05 ) , plasminogen activator inhibitor-1 activity ( PAI-1 ) [ p<0.05 ] , soluble vascular cell adhesion molecule-1 ( p<0.05 ) , soluble platelet selectin ( p < 0.05 ) and high-sensitivity C-reactive protein ( p < 0.05 ) were measured compared with patients not on atorvastatin therapy . Additionally , a strong trend towards lower soluble intercellular adhesion molecule-1 plasma levels was detected in patients treated with atorvastatin . No differences were found in tissue-type plasminogen activator antigen , plasmin-plasmin inhibitor complexes , fibrinogen , D-dimer and activated factor XII values . Conclusion : Atorvastatin appears to have an effect on coagulation activation , fibrinolysis and inflammation in patients with CAD . Reduction in PAI-1 and reduced thrombin formation may have an impact on cardiovascular morbidity and mortality in patients with CAD OBJECTIVE Type 2 diabetes is associated with increased plasma concentrations of coagulation and inflammation markers . Different studies have shown that treatment with hydroxymethylglutaryl-CoA reductase inhibitors ( statins ) is associated with antithrombotic and anti-inflammatory effects in addition to a cholesterol-lowering effect . Our objective was to evaluate the effect of pravastatin ( 40 mg/day ) on coagulation and inflammation markers in type 2 diabetic patients . RESEARCH DESIGN AND METHODS This was an open , r and omized , crossover study design ed with an 8-week intervention period . The study group was comprised of 50 patients with type 2 diabetes ( median HbA(1c ) 7.1 % ) and serum total cholesterol of 5 - 10 mmol/l . We evaluated plasma levels of fibrinogen , F1 + 2 , D-dimer , soluble tissue factor ( sTF ) , von Willebr and Factor antigen ( vWFag ) , and C-reactive protein ( CRP ) in blood sample s drawn after fasting on day 1 and after 8 and 16 weeks . RESULTS Significant reductions of total cholesterol ( -22 % ; P < 0.001 ) , LDL cholesterol ( -32 % ; P < 0.001 ) , and triglycerides ( -10 % ; P < 0.05 ) were achieved after 8 weeks of treatment with pravastatin . In addition , significant reductions of plasma levels of F1 + 2 ( -4.4 % ; P < 0.05 ) , vWFag ( -5.3 % ; P < 0.05 ) , and sTF ( -3.4 % ; P < 0.05 ) were observed after treatment with pravastatin . Furthermore , plasma levels of CRP were also significantly reduced ( -13 % ; P < 0.05 ) . Levels of fibrinogen and D-dimer did not decrease after treatment with pravastatin . CONCLUSIONS The results indicated that pravastatin reduces levels of coagulation and inflammation markers in type 2 diabetic patients . These antithrombotic and anti-inflammatory effects of treatment with statins could play a role in reducing cardiovascular complications in type 2 diabetic patients Background — Statins exert an antithrombotic effect in patients at risk of or with acute thrombosis , but no study has investigated whether this effect is immediate and whether there is an underline mechanism . Methods and Results — Patients with hypercholesterolemia were r and omly allocated to a Mediterranean diet with low cholesterol intake ( < 300 mg/d ; n=15 ) or atorvastatin ( 40 mg/d ; n=15 ) . Oxidative stress , as assessed by serum Nox2 and urinary isoprostanes , and platelet activation , as assessed by platelet recruitment , platelet isoprostanes , and thromboxane A2 , platelet Nox2 , Rac1 , p47phox , protein kinase C , vasodilator-stimulated phosphoprotein , nitric oxide , and phospholipase A2 , were determined at baseline and after 2 , 24 , and 72 hours and 7 days of follow-up . An in vitro study was also performed to see whether atorvastatin affects platelet oxidative stress and activation . The atorvastatin-assigned group showed a significant and progressive reduction of urinary isoprostanes and serum Nox2 , along with inhibition of platelet recruitment , platelet isoprostanes , Nox2 , Rac1 , p47phox , and protein kinase C , starting 2 hours after administration . Platelet phospholipase A2 and thromboxane A2 significantly decreased and vasodilator-stimulated phosphoprotein and nitric oxide increased after 24 hours . Low-density lipoprotein cholesterol decreased significantly after 72 hours and further declined after 7 days . No changes were observed in the Mediterranean diet group . In vitro experiments demonstrated that atorvastatin dose-dependently inhibited platelet Nox2 and phospholipase A2 activation , along with inhibition of platelet recruitment , platelet isoprostanes , and thromboxane A2 , and increased vasodilator-stimulated phosphoprotein and nitric oxide . Conclusions — The study provides the first evidence that atorvastatin acutely and simultaneously decreases oxidative stress and platelet activation by directly inhibiting platelet Nox2 and ultimately platelet isoprostanes and thromboxane A2 . These findings provide a rationale for the use of statins to prevent or modulate coronary thrombosis . Clinical Trial Registration — URL : http://www . clinical trials.gov . Unique identifier : NCT01322711 This study assessed hemostatic effects of an HMC-CoA reductase inhibitor , atorvastatin , on different parameters in 32 hypercholesterolemic patients of both sexes . In the patients and in 25 control subjects , plasma levels of tissue-type plasminogen activator , plasminogen activator inhibitor ( PAI-1 ) , D-dimer , prothrombin fragment 1 + 2 ( F1 + 2 ) , total cholesterol , triglycerides and fibrinogen had been measured . All these parameters were evaluated in patients after 6 and 12 months of treatment with atorvastatin at a dosage of 20 mg/day . This treatment significantly lowered the total cholesterol level in all patients . Moreover , after 6 months of atorvastatin treatment , PAI-1 and F1 + 2 , which were both increased at baseline , were significantly reduced . This reduction continued after 12 months . The present results show that a reduction of hemostatic abnormalities , which exist in hypercholesterolemia , may be another important effect of the atorvastatin therapy The study was aim ed to investigate the effect of two different statins on the levels of haemostatic variables reflecting procoagulant and fibrinolytic activity in patients with coronary heart disease ( CHD ) , with the hypothesis that statins might beneficially modify these levels . Fifty-eight patients were r and omized to treatment with atorvastatin ( n=28 ) or simvastatin  ( n=30 ) for 1 year . The starting dose in both groups was 20 mg/day . Fasting blood sample s were collected before and after 12-month treatment for determinations of fibrinogen , prothrombin fragment 1 + 2 ( F1 + 2 ) , plasma D-dimer , soluble tissue factor , tissue plasminogen activator ( tPA ) antigen , tPA activity , plasminogen activator inhibitor type-1 activity ( PAI-1 activity ) and serum D-dimer as a global test of fibrinolytic activity . In the total population , improved fibrinolytic activity was observed after 1 year with increased levels of serum D-dimer ( P=.001 ) and tPA activity ( P=.024 ) and a reduction in tPA antigen ( P=.048 ) . No statistically significant changes were observed in any of the measured coagulation variables . Separately examined , an improved fibrinolytic profile was seen in the atorvastatin group with a significant increase in serum D-dimer ( P=.005 ) , a borderline increase in tPA activity ( P=.083 ) and a borderline reduction in tPA antigen ( P=.069 ) . Within the simvastatin group , a reduction in prothrombin F1 + 2 was observed ( P=.038 ) . The differences in changes between the groups were statistically significant only for global fibrinolysis ( serum D-dimer , P=.046 ) . In conclusion , an improved fibrinolytic profile was observed after statin treatment , most pronounced with atorvastatin . The results indicate that the drugs promote a profibrinolytic profile , and may in part explain the benefit of statin treatment rendered in the prevention of CHD OBJECTIVES The study sought to determine the effects of lipid-lowering with pravastatin on the systemic fibrinolytic profile and on thrombus formation under dynamic flow conditions . BACKGROUND Lowering cholesterol ( C ) decreases clinical events in coronary artery disease ( CAD ) patients , but an analysis of the effects of lipid-lowering on the entire hemostatic and thrombotic profile has not been conducted . METHODS We prospect ively studied 93 stable patients with untreated low-density lipoprotein cholesterol ( LDL-C ) > 145 mg/dl . The CAD patients received pravastatin , and non-CAD patients were r and omized to pravastatin versus placebo ( double-blind ) . Thrombus formation upon an injured vascular surface was assessed in a sub study of 40 patients with a previously vali date d ex vivo perfusion chamber system . Systemic hemostatic markers and thrombus formation were evaluated at baseline , three and six months . RESULTS Placebo produced no changes in either the lipid profile , any of the hemostatic markers , or the ex vivo thrombus formation . Both pravastatin groups ( CAD and non-CAD ) showed decreased LDL-C by 30 % within 6 weeks ( 188 to 126 mg/dl , p < 0.001 vs. baseline ) , and decreased plasminogen activator inhibitor-1 at 3- and 6-month follow-up compared to baseline ( 15 % to 18 % decrease at 3 months and 21 % to 23 % at 6 months ) . For the tissue plasminogen activator antigen , CAD and non-CAD groups showed significant decreases at 6 months compared to baseline ( 10 % and 13 % , respectively ) . No significant changes were observed with treatment in d-dimer , fibrinopeptide A , prothrombin fragment F1.2 , factor VIIa , von Willebr and factor , or C-reactive protein . Fibrinogen levels were significantly increased at 6 months compared to baseline , though still below the upper normal limit . In the perfusion chamber sub study , there was a decrease in thrombus area in 
    Output:
    
This meta- analysis suggests an association between use of statins and reduction of D-dimer levels , independent of treatment duration and type of statin used .