***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 
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    ***EXAMPLES*** 
    Input: Background : Portal hypertension is one of the most frequent complications of cirrhosis . β-adrenergic blockers , with or without organic nitrates , are currently used as hypotensive agents . Statins such as simvastatin seem to be safe for patients with chronic liver diseases and exert multiple pleiotropic actions . This study aim ed to assess PTH using Doppler ultrasound in patients with cirrhosis before and after simvastatin administration . Methods : This r and omized controlled clinical trial was conducted on 40 patients with cirrhosis who were r and omized into 2 groups : group I included 20 patients with cirrhosis who were administered 20 mg of simvastatin daily for 2 weeks and then 40 mg daily for another 2 weeks , and group II included 20 patients with cirrhosis who did not receive simvastatin  as a control group . All patients underwent full clinical examination , laboratory investigations , and abdominal Doppler ultrasound at baseline and after 30 days to evaluate portal vein diameter , blood flow volume , direction and velocity of portal vein blood flow , hepatic artery resistance and pulsatility indices , splenic artery resistance index , portal hypertension index ( PHI ) , liver vascular index , and modified liver vascular index ( MLVI ) . Results : There was a highly significant decrease in the hepatic artery resistance index in group I , from 0.785 ± 0.088 to 0.717 ± 0.086 ( P < 0.001 ) . There was a significant decrease in the PHI in group I , from 3.915 ± 0.973 m/sec to 3.605 ± 1.168 m/sec ( P = 0.024 ) . Additionally , there was a significant increase in the MLVI in group I from 11.540 ± 3.266 cm/sec to 13.305 ± 3.222 cm/sec , an increase of 15.3 % from baseline ( P = 0.009 ) . No significant adverse effects were detected . Conclusions : Simvastatin is safe and effective in lowering portal hypertension . [ Clinical Trials.gov Identifier : NCT02994485 BACKGROUND In r and omized clinical trials  statins  and  placebo treated patients showed the same degree of coronary artery calcium ( CAC ) progression . We reanalyzed data from two clinical trials to further investigate the time and dose dependent effects of statins on CAC . Additionally , we investigated whether CAC progression was associated with incident cardiovascular events . METHODS AND RESULTS Data were pooled from two clinical trials : St. Francis Heart Study ( SFHS ) ( 419 and 432 patients treated with placebo and 20 mg atorvastatin daily , respectively ) and EBEAT Study ( 164 and 179 patients respectively treated with 10 mg and 80 mg atorvastatin daily ) . CAC scores were assessed at baseline , 2 years and 4 - 6 years in SFHS ; in EBEAT they were measured at baseline and 12 months . After a short-term follow-up ( 12 to 24 months ) placebo and low dose atorvastatin showed a similar CAC increase , although 80 mg/daily atorvastatin increased CAC an additional 12 - 14 % over placebo ( p<0.001 ) . In the long-term , atorvastatin caused a greater progression of CAC compared to placebo ( additional 1.1 % , p=0.04 ) . In SFHS 42 cardiovascular events occurred after the second CT scan . The baseline and progression of CAC were greater in patients with events . However , only baseline CAC and family history of premature cardiovascular disease but not CAC progression were independent predictors of events . CONCLUSIONS Despite a greater CAC increase with high dose and long-term statin therapy , events did not occur more frequently in  statin treated patients . This suggests that CAC growth under treatment with statins represents plaque repair rather than continuing plaque expansion BACKGROUND & AIMS In cirrhosis , an insufficient release of nitric oxide contributes to increased hepatic resistance and portal pressure and enhances the postpr and ial increase in portal pressure . We hypothesized that simvastatin , which enhances Akt-dependent endothelial nitric oxide synthase phosphorylation , may increase hepatic nitric oxide release and decrease hepatic resistance in patients with cirrhosis and portal hypertension . METHODS In protocol 1 , 13 patients had measurements of the hepatic venous pressure gradient , hepatic blood flow , mean arterial pressure , cardiac output , and nitric oxide products before and 30 and 60 minutes after 40 mg of simvastatin . In protocol 2 , 17 patients were r and omized to receive placebo or simvastatin ( 40 mg ) 12 hours and 1 hour before the study . After baseline measurements of the hepatic venous pressure gradient , hepatic blood flow , and nitric oxide products , a st and ard liquid meal was given , and measurements were repeated at 15 , 30 , and 45 minutes . RESULTS In protocol 1 , acute simvastatin did not modify the hepatic venous pressure gradient but increased the hepatic blood flow ( 21 % + /- 13 % at 30 minutes ; P = 0.01 ) and decreased hepatic sinusoidal resistance by 14 % + /- 11 % ( P = 0.04 ) . Nitric oxide product levels significantly increased in hepatic venous blood ( from 31.4 + /- 12.3 nmol . mL(-1 ) to 35.8 + /- 10.7 nmol . mL(-1 ) ; P = 0.04 ) , but not in peripheral blood . Systemic hemodynamics were not modified . In protocol 2 , simvastatin pretreatment significantly attenuated the postpr and ial increase in hepatic venous pressure gradient ( mean peak increase , 10 % + /- 9 % vs. 21 % + /- 6 % in placebo ; P = 0.01 ) . Hepatic blood flow increased similarly in the 2 groups . Hepatic nitric oxide products increased in the simvastatin group but not in the placebo group . CONCLUSIONS Simvastatin administration increases the hepatosplanchnic output of nitric oxide products and decreases hepatic resistance in patients with cirrhosis BACKGROUND & AIMS Simvastatin improves liver generation of nitric oxide and hepatic endothelial dysfunction in patients with cirrhosis , so it could be an effective therapy for portal hypertension . This r and omized controlled trial evaluated the effects of continuous simvastatin administration on the hepatic venous pressure gradient ( HVPG ) and its safety in patients with cirrhosis and portal hypertension . METHODS Fifty-nine patients with cirrhosis and portal hypertension ( HVPG > or = 12 mm Hg ) were r and omized to groups that were given simvastatin 20 mg/day for 1 month ( increased to 40 mg/day at day 15 ) or placebo in a double-blind clinical trial . R and omization was stratified according to whether the patient was being treated with beta-adrenergic blockers . We studied splanchnic and systemic hemodynamics and variables of liver function and safety before and after 1 month of treatment . RESULTS Simvastatin significantly decreased HVPG ( -8.3 % ) without deleterious effects in systemic hemodynamics . HVPG decreases were observed in patients who were receiving beta-adrenergic blockers ( -11.0 % ; P = .033 ) and in those who were not ( -5.9 % ; P = .013 ) . Simvastatin improved hepatic , fractional , and intrinsic clearance of indocyanine green , showing an improvement in effective liver perfusion and function . No significant changes in HVPG and liver function were observed in patients receiving placebo . The number of patients with adverse events did not differ significantly between groups . No patient was withdrawn from the study based on adverse events . CONCLUSIONS Simvastatin decreased HVPG and improved liver perfusion in patients with cirrhosis . These effects were additive with those of beta-adrenergic blockers . The beneficial effects of simvastatin should be confirmed in long-term clinical trials for portal hypertension BACKGROUND Pleiotropic effects of statins decrease intrahepatic resistance and portal hypertension . AIM We evaluated the effects of simvastatin on hepatic venous pressure gradient ( HVPG ) and azygos vein blood flow in cirrhotic patients . METHODS A 3-month prospect i ve , r and omized , triple-blind trial with simvastatin ( 40 mg/day ) vs. placebo was conducted in patients with cirrhotic portal hypertension . HVPG and azygos blood flow , measured by colour Doppler endoscopic ultrasound , were assessed before and after treatment . The primary endpoint was a decrease in the HVPG of at least 20 % from baseline or to ≤12 mmHg after the treatment . RESULTS 34 patients were prospect ively enrolled , and 24 completed the protocol . In the simvastatin group 6/11 patients ( 55 % ) presented a clinical ly relevant decrease in the HVPG ; no decrease was observed in the placebo group ( p=0.036 ) . Patients with medium/large oesophageal varices and previous variceal bleeding had a higher response rate to simvastatin  . HVPG and azygos blood flow values were not correlated . No significant adverse events occurred . CONCLUSION Simvastatin  lowers portal pressure and may even improve liver function . The haemodynamic effect appears to be more evident in patients with severe portal hypertension Background and aim Statins can modulate portal microvascular dynamics in patients with cirrhosis . We present data from a proof-of-concept study aim ed at comparing combination of propranolol and atorvastatin versus propranolol alone in reducing portal pressure in patients with cirrhosis . Patients and methods In this open-label proof-of-concept study , 23 consecutive patients with cirrhosis were r and omized into group A ( incremental dose propranolol , n=12 ) or group B ( atorvastatin 20 mg daily with propranolol in incremental dose , n=11 ) . Hepatic venous pressure gradient ( HVPG ) was estimated at baseline , and after 30 days , clinical outcomes were evaluated after 1 year . Results The two groups were matched with respect to etiology of cirrhosis ; clinical , biochemical , and endoscopic parameters ; child status ; and baseline HVPG . Decreases of wedged hepatic venous pressure , free hepatic venous pressure , and HVPG in group A and group B after 30 days were 4.67±2.57 versus 6.09±3.56 ( P=0.290 ) , 1.83±2.62 versus 1.27±1.67 ( P=0.546 ) , and 2.58±1.88 versus 4.81±2.82 mmHg ( P=0.041 ) , respectively . The proportion of HVPG responders in group A and group B were 50.00 and 90.91 % , respectively . The two groups did not , however , differ significantly in terms of clinical outcomes ( variceal bleed , endoscopic variceal ligation sessions , hepatic encephalopathy , requirement of therapeutic paracentesis , spontaneous bacterial peritonitis , and death ) . Conclusion Decrease of HVPG in patients with cirrhosis treated with atorvastatin and propranolol is significantly more than those treated with only propranolol . Atorvastatin , with its pleiotropic effects , may be useful in portal hypertension in cirrhosis . Larger data sets are required for ratification BACKGROUND & AIMS Concerns related to hepatotoxicity frequently lead to discontinuation or non-initiation of 3-hydroxy-3-methylglutaryl-coenzyme A reductase therapy in patients with cirrhosis despite data supporting statin use . We investigated the independent effects of hyperlipidemia and statin exposure on mortality , hepatic decompensation , and hepatocellular carcinoma development in a large national cohort of patients with cirrhosis . METHODS We performed a retrospective cohort study of patients with newly diagnosed cirrhosis from January 1 , 2008 through June 30 , 2016 in the Veterans Health Administration . Subjects were divided into 2 cohorts : 21,921 patients with prior statin exposure ( existing users ) and 51,023 statin-naïve individuals , of whom 8794 subsequently initiated statin therapy ( new initiators ) and 44,269 did not ( non-initiators ) . Multivariable Cox proportional hazard models with inverse probability weighting were constructed to assess the effects of time-updating lipid profiles and cumulative exposure to statins on survival and hepatic decompensation . Statin-naïve new initiators were propensity matched with non-initiators to simulate a r and omized controlled trial of statin use in cirrhosis . RESULTS In statin-naïve subjects , every 10-mg/dL increase in baseline total cholesterol was associated with a 3.6 % decrease in mortality . In existing users , each year of continued statin exposure was associated with a hazard ratio of 0.920 ( 95 % confidence interval 0.0.897 - 0.943 ) for mortality . After risk 
    Output:
    
Hepatic portal hemodynamic parameters were improved in  statin users for a short-term response .
Statin seemed not to decrease the risk of esophageal variceal bleeding and spontaneous bacterial peritonitis .
However , statin was proved to decrease the risk of hepatic encephalopathy and ascites .
Incidence of drug related adverse events did n’t increase in  statin users .
Dose-dependent effects of statin  on hepatocellular carcinoma development , decompensated cirrhosis events occurrence , and liver cirrhosis progression .
ConclusionS tatin influenced parameters of hepatic portal vessel pressure in short-term treatment .
Prognosis of liver cirrhosis benefited from statin treatment in long term follow-up .
The efficacy and safety of statin in liver cirrhosis treatment is confirmed .