human
***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: Background —We investigated whether serum concentration of carboxy-terminal propeptide of procollagen type I ( PIP ) , a marker of collagen type I synthesis , can be used to assess the ability of antihypertensive treatment to regress myocardial fibrosis in hypertensive patients . Methods and Results —The study was performed in 37 patients with essential hypertension and hypertensive heart disease . After r and omization , 21 patients were assigned to losartan and 16 patients to amlodipine treatment . At baseline and after 12 months , right septal endomyocardial biopsies were performed to quantify collagen volume fraction ( CVF ) on picrosirius red – stained sections with an automated image- analysis system . Serum PIP was measured by specific radioimmunoassay . Nineteen patients in the losartan group and 11 in the amlodipine group finished the study . Time-course changes in blood pressure during treatment were similar in the 2 groups of patients . In losartan-treated patients , CVF decreased from 5.65±2.03 % to 3.96±1.46 % ( P < 0.01 ) and PIP from 127±30 to 99±26 & mgr;g/L ( P < 0.01 ) . Neither CVF or PIP changed significantly in amlodipine-treated patients . CVF was directly correlated with PIP ( r = 0.44 , P < 0.001 ) in all hypertensives before and after treatment . Conclusions —These findings suggest that the ability of antihypertensive treatment to regress fibrosis in hypertensives with biopsy-proven myocardial fibrosis is independent of its antihypertensive efficacy . Our data also suggest that blockade of the angiotensin II type 1 receptor is associated with inhibition of collagen type I synthesis and regression of myocardial fibrosis in hypertensives . Thus , determination of serum PIP may be useful to assess the cardioreparative properties of antihypertensive treatment in hypertensives Epidemiologic studies have shown that hypercholesterolemia is associated with increased left ventricular ( LV ) mass . Free radicals have been shown to be increased in hyperlipidemic patients . This study sought to determine whether pravastatin administration can affect LV mass in patients with untreated total cholesterol ≥240 mg/dl by reducing 8-iso-prostagl and in F2&agr ; concentrations , a reliable marker of oxidant injury . Fifty patients were r and omly assigned to one of two groups , one with ( n = 25 ) and one without ( n = 25 ) treatment with pravastatin ( 10 or 20 mg/d ) . A group of normolipidemic control subjects was used for comparison . Echocardiograms were performed at baseline and after 6 months of therapy . Hyperlipidemic patients showed significant increases in LV mass index at baseline compared with the normolipidemic control group ( 125 ± 8 vs. 107 ± 5 g/m2 , p < 0.0001 ) . Pravastatin treatment significantly reduced plasma total and low-density lipoprotein cholesterol levels , as well as increased high-density lipoprotein cholesterol . After 6 months of therapy with pravastatin , the magnitude of LV mass regression correlated with the magnitude of inhibition of free radical formation assessed by 8-iso-prostagl and in F2&agr ; formation ( r = 0.67 , p = 0.002 ) . Multivariate analysis revealed that regression of LV mass was significantly correlated only with the changes in 8-iso-prostagl and in F2&agr ; ( p < 0.0001 , adjusted R2 = 0.83 ) . These findings demonstrated for the first time that in addition to its primary anti-lipidemia , pravastatin may have an additional effect of reducing LV mass – independent lipid-lowering effects , possibly through attenuation of free radical formation Background — Atrial fibrillation ( AF ) after cardiac surgery is associated with increased risk of complications , length of stay , and cost of care . Observational evidence suggests that patients who have undergone previous statin therapy have a lower incidence of postoperative AF . We tested this observation in a r and omized , controlled trial . Methods and Results — Two hundred patients undergoing elective cardiac surgery with cardiopulmonary bypass , without previous statin treatment or history of AF , were enrolled . Patients were r and omized to atorvastatin ( 40 mg/d , n=101 ) or placebo  ( n=99 ) starting 7 days before operation . The primary end point was incidence of postoperative AF ; secondary end points were length of stay , 30-day major adverse cardiac and cerebrovascular events , and postoperative C-reactive protein ( CRP ) variations . Atorvastatin significantly reduced the incidence of AF versus placebo ( 35 % versus 57 % , P=0.003 ) . Accordingly , length of stay was longer in the placebo versus atorvastatin arm ( 6.9±1.4 versus 6.3±1.2 days , P=0.001 ) . Peak CRP levels were lower in patients without AF ( P=0.01 ) , irrespective of r and omization assignment . Multivariable analysis showed that atorvastatin treatment conferred a 61 % reduction in risk of AF ( odds ratio 0.39 , 95 % confidence interval 0.18 to 0.85 , P=0.017 ) , whereas high postoperative CRP levels were associated with increased risk ( odds ratio 2.0 , 95 % confidence interval 1.2 to 7.0 , P=0.01 ) . The incidence of major adverse cardiac and cerebrovascular events at 30 days was similar in the 2 arms . Conclusions — Treatment with atorvastatin 40 mg/d , initiated 7 days before surgery , significantly reduces the incidence of postoperative AF after elective cardiac surgery with cardiopulmonary bypass and shortens hospital stay . These results may influence practice patterns with regard to adjuvant pharmacological therapy before cardiac surgery BACKGROUND Cholesterol lowering reduces coronary events . One mechanism could be improvement of endothelial function . In line with this hypothesis , this study investigates whether cholesterol reduction can result in rapid improvement of endothelial function  after acute coronary syndromes . METHODS AND RESULTS Patients with acute myocardial infa rct ion or unstable angina and total cholesterol levels at admission > /=5.2 mmol/L or LDL > /=3.4 mmol/L were r and omized to placebo ( n=30 ) or pravastatin 40 mg daily ( n=30 ) for 6 weeks . Brachial ultrasound was used to measure endothelium-dependent flow-mediated dilatation ( FMD ) and response to endothelium-independent nitroglycerin . Changes in the levels of markers of platelet activation , coagulation factors , and plasma endothelin levels were also assessed . Total and LDL cholesterol levels were similar at admission and before r and omization in both groups . With pravastatin , but not with placebo , they decreased by 23 % ( P<0.05 ) and 33 % ( P<0.01 ) , respectively . FMD was unchanged with placebo , 5.43+/-0.74 % ( mean+/-SEM ) to 5.84+/-0.81 % , but increased with pravastatin , 4.93+/-0.81 % to 7.0+/-0.79 % ( P=0.02 ) , representing a 42 % relative increase . Responses to nitroglycerin were similar during the time course of the study in the 2 groups . Markers of platelet activity , coagulation factors , and endothelin levels were not affected by pravastatin . CONCLUSIONS Cholesterol reduction with pravastatin initiated early after acute coronary syndromes rapidly improves endothelial function after 6 weeks of therapy Background —Left ventricular hypertrophy ( LVH ) is a common risk factor for cardiovascular mortality . Causes other than hypertension have not previously been investigated longitudinally . The aim of the present study was to determine hemodynamic , metabolic , and psychosocial predictors at 50 years of age for the prevalence of echocardiographic LVH and geometric subtypes at age 70 by use of a large sample of men from the general population followed up for 20 years . Methods and Results —In 1970 to 1973 , all men born from 1920 to 1924 and residing in Uppsala County , Sweden , were invited to participate in a health survey aim ed at identifying risk factors for cardiovascular disease . At a reinvestigation 20 years later , echocardiographic left ventricular mass index was determined in 475 subjects . A 1-SD increase in body mass index , systolic or diastolic blood pressure , fasting LDL/HDL cholesterol , serum triglycerides , or the serum cholesterol ester proportion of several saturated fatty acids or oleic acid at age 50 significantly increased the odds of having LVH at age 70 by 27 % to 41 % , whereas an increase in linoleic acid proportion was protective . Almost all metabolic predictors were independent of ischemic heart disease , valvular disease , and use of antihypertensive medication at age 70 . Conclusions —Dyslipidemia and indices of a low dietary intake of linoleic acid and high intake of saturated and monounsaturated fats , as well as hypertension and obesity , at age 50 predicted the prevalence of LVH 20 years later in this prospect i ve longitudinal cohort study , thereby suggesting that lipids may be important in the origin of LVH Atrial fibrillation ( AF ) , the most common chronic arrhythmia , increases the risk of stroke and is an independent predictor of mortality . Available pharmacological treatments have limited efficacy . Once initiated , AF tends to self-perpetuate , owing in part to electrophysiological remodeling in the atria ; however , the fundamental mechanisms underlying this process are still unclear . We have recently demonstrated that chronic human AF is associated with increased atrial oxidative stress and peroxynitrite formation ; we have now tested the hypothesis that these events participate in both pacing-induced atrial electrophysiological remodeling and in the occurrence of AF following  cardiac surgery . In chronically instrumented dogs , we found that rapid ( 400 min−1 ) atrial pacing was associated with attenuation of the atrial effective refractory period ( ERP ) . Treatment with ascorbate , an antioxidant and peroxynitrite decomposition catalyst , did not directly modify the ERP , but attenuated the pacing-induced atrial ERP shortening following 24 to 48 hours of pacing . Biochemical studies revealed that pacing was associated with decreased tissue ascorbate levels and increased protein nitration ( a biomarker of peroxynitrite formation ) . Oral ascorbate supplementation attenuated both of these changes . To evaluate the clinical significance of these observations , supplemental ascorbate was given to 43 patients before , and for 5 days following , cardiac bypass graft surgery . Patients receiving ascorbate had a 16.3 % incidence of postoperative AF , compared with 34.9 % in control subjects . In combination , these studies suggest that oxidative stress underlies early atrial electrophysiological remodeling and offer novel insight into the etiology and potential treatment of an enigmatic and difficult to control arrhythmia . The full text of this article is available at http://www.circresaha.org OBJECTIVE It has been recently reported that AF is associated with tissue inflammation . Statins reduce C-reactive protein ( CRP ) levels . However , the effect of statin on atrial fibrillation ( AF ) is unclear . The purpose of the present study was to evaluate the effect of statin on AF in a canine sterile pericarditis model . METHODS Sterile pericarditis was created in 20 dogs r and omly assigned to two groups : a control group ( 10 dogs ) and an atorvastatin treatment group ( 10 dogs ) . Atorvastatin was administered orally ( 2 mg/kg/day ) beginning 1 week before the operation until the end of the study . Before and 2 days after the operation , CRP levels , the duration of induced AF , the atrial effective refractory period ( AERP ) , and intra-atrial conduction time were determined . RESULTS Before the operation , there were no significant differences in any of the parameters between the two groups . On the second postoperative day , the atorvastatin group had a lower CRP level ( 7.6+/-0.5 versus 11.7+/-1.3 mg/dl , P<0.0001 ) , a shorter AF duration ( 177+/-57 versus 534+/-189 s , P<0.0001 ) , a longer AERP ( 138+/-6 versus 130+/-6 ms , P<0.01 ) , and a shorter intra-atrial conduction time ( 46+/-3 versus 51+/-5 ms , P<0.01 ) than the control group . CONCLUSIONS Atorvastatin can prevent maintenance of AF by inhibiting inflammation in the canine sterile pericarditis model . Atorvastatin may thus be a novel therapeutic agent for AF Increased angiotensin II ( Ang II ) sensitivity predisposes to hypertension and plaque instability . Raised low-density lipoprotein cholesterol ( LDL-c ) may increase Ang II sensitivity , but evidence in humans for this effect of LDL-c is limited . In 28 , healthy , nonsmoking subjects , aged 30±8 years , with familial hyper 
    Output:
    
agent
Data from different observational trials have shown that treatment with statins significantly reduces the incidence of new-onset AF in the primary and secondary prevention .
The data are insufficient to recommend the use of statins before EC .
Finally , perioperative statin therapy may represent an important non-antiarrhythmic adjunctive therapeutic strategy for the prevention of postoperative AF
***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: Background —We investigated whether serum concentration of carboxy-terminal propeptide of procollagen type I ( PIP ) , a marker of collagen type I synthesis , can be used to assess the ability of antihypertensive treatment to regress myocardial fibrosis in hypertensive patients . Methods and Results —The study was performed in 37 patients with essential hypertension and hypertensive heart disease . After r and omization , 21 patients were assigned to losartan and 16 patients to amlodipine treatment . At baseline and after 12 months , right septal endomyocardial biopsies were performed to quantify collagen volume fraction ( CVF ) on picrosirius red – stained sections with an automated image- analysis system . Serum PIP was measured by specific radioimmunoassay . Nineteen patients in the losartan group and 11 in the amlodipine group finished the study . Time-course changes in blood pressure during treatment were similar in the 2 groups of patients . In losartan-treated patients , CVF decreased from 5.65±2.03 % to 3.96±1.46 % ( P < 0.01 ) and PIP from 127±30 to 99±26 & mgr;g/L ( P < 0.01 ) . Neither CVF or PIP changed significantly in amlodipine-treated patients . CVF was directly correlated with PIP ( r = 0.44 , P < 0.001 ) in all hypertensives before and after treatment . Conclusions —These findings suggest that the ability of antihypertensive treatment to regress fibrosis in hypertensives with biopsy-proven myocardial fibrosis is independent of its antihypertensive efficacy . Our data also suggest that blockade of the angiotensin II type 1 receptor is associated with inhibition of collagen type I synthesis and regression of myocardial fibrosis in hypertensives . Thus , determination of serum PIP may be useful to assess the cardioreparative properties of antihypertensive treatment in hypertensives Epidemiologic studies have shown that hypercholesterolemia is associated with increased left ventricular ( LV ) mass . Free radicals have been shown to be increased in hyperlipidemic patients . This study sought to determine whether pravastatin administration can affect LV mass in patients with untreated total cholesterol ≥240 mg/dl by reducing 8-iso-prostagl and in F2&agr ; concentrations , a reliable marker of oxidant injury . Fifty patients were r and omly assigned to one of two groups , one with ( n = 25 ) and one without ( n = 25 ) treatment with pravastatin ( 10 or 20 mg/d ) . A group of normolipidemic control subjects was used for comparison . Echocardiograms were performed at baseline and after 6 months of therapy . Hyperlipidemic patients showed significant increases in LV mass index at baseline compared with the normolipidemic control group ( 125 ± 8 vs. 107 ± 5 g/m2 , p < 0.0001 ) . Pravastatin treatment significantly reduced plasma total and low-density lipoprotein cholesterol levels , as well as increased high-density lipoprotein cholesterol . After 6 months of therapy with pravastatin , the magnitude of LV mass regression correlated with the magnitude of inhibition of free radical formation assessed by 8-iso-prostagl and in F2&agr ; formation ( r = 0.67 , p = 0.002 ) . Multivariate analysis revealed that regression of LV mass was significantly correlated only with the changes in 8-iso-prostagl and in F2&agr ; ( p < 0.0001 , adjusted R2 = 0.83 ) . These findings demonstrated for the first time that in addition to its primary anti-lipidemia , pravastatin may have an additional effect of reducing LV mass – independent lipid-lowering effects , possibly through attenuation of free radical formation Background — Atrial fibrillation ( AF ) after cardiac surgery is associated with increased risk of complications , length of stay , and cost of care . Observational evidence suggests that patients who have undergone previous statin therapy have a lower incidence of postoperative AF . We tested this observation in a r and omized , controlled trial . Methods and Results — Two hundred patients undergoing elective cardiac surgery with cardiopulmonary bypass , without previous statin treatment or history of AF , were enrolled . Patients were r and omized to atorvastatin ( 40 mg/d , n=101 ) or placebo  ( n=99 ) starting 7 days before operation . The primary end point was incidence of postoperative AF ; secondary end points were length of stay , 30-day major adverse cardiac and cerebrovascular events , and postoperative C-reactive protein ( CRP ) variations . Atorvastatin significantly reduced the incidence of AF versus placebo ( 35 % versus 57 % , P=0.003 ) . Accordingly , length of stay was longer in the placebo versus atorvastatin arm ( 6.9±1.4 versus 6.3±1.2 days , P=0.001 ) . Peak CRP levels were lower in patients without AF ( P=0.01 ) , irrespective of r and omization assignment . Multivariable analysis showed that atorvastatin treatment conferred a 61 % reduction in risk of AF ( odds ratio 0.39 , 95 % confidence interval 0.18 to 0.85 , P=0.017 ) , whereas high postoperative CRP levels were associated with increased risk ( odds ratio 2.0 , 95 % confidence interval 1.2 to 7.0 , P=0.01 ) . The incidence of major adverse cardiac and cerebrovascular events at 30 days was similar in the 2 arms . Conclusions — Treatment with atorvastatin 40 mg/d , initiated 7 days before surgery , significantly reduces the incidence of postoperative AF after elective cardiac surgery with cardiopulmonary bypass and shortens hospital stay . These results may influence practice patterns with regard to adjuvant pharmacological therapy before cardiac surgery BACKGROUND Cholesterol lowering reduces coronary events . One mechanism could be improvement of endothelial function . In line with this hypothesis , this study investigates whether cholesterol reduction can result in rapid improvement of endothelial function  after acute coronary syndromes . METHODS AND RESULTS Patients with acute myocardial infa rct ion or unstable angina and total cholesterol levels at admission > /=5.2 mmol/L or LDL > /=3.4 mmol/L were r and omized to placebo ( n=30 ) or pravastatin 40 mg daily ( n=30 ) for 6 weeks . Brachial ultrasound was used to measure endothelium-dependent flow-mediated dilatation ( FMD ) and response to endothelium-independent nitroglycerin . Changes in the levels of markers of platelet activation , coagulation factors , and plasma endothelin levels were also assessed . Total and LDL cholesterol levels were similar at admission and before r and omization in both groups . With pravastatin , but not with placebo , they decreased by 23 % ( P<0.05 ) and 33 % ( P<0.01 ) , respectively . FMD was unchanged with placebo , 5.43+/-0.74 % ( mean+/-SEM ) to 5.84+/-0.81 % , but increased with pravastatin , 4.93+/-0.81 % to 7.0+/-0.79 % ( P=0.02 ) , representing a 42 % relative increase . Responses to nitroglycerin were similar during the time course of the study in the 2 groups . Markers of platelet activity , coagulation factors , and endothelin levels were not affected by pravastatin . CONCLUSIONS Cholesterol reduction with pravastatin initiated early after acute coronary syndromes rapidly improves endothelial function after 6 weeks of therapy Background —Left ventricular hypertrophy ( LVH ) is a common risk factor for cardiovascular mortality . Causes other than hypertension have not previously been investigated longitudinally . The aim of the present study was to determine hemodynamic , metabolic , and psychosocial predictors at 50 years of age for the prevalence of echocardiographic LVH and geometric subtypes at age 70 by use of a large sample of men from the general population followed up for 20 years . Methods and Results —In 1970 to 1973 , all men born from 1920 to 1924 and residing in Uppsala County , Sweden , were invited to participate in a health survey aim ed at identifying risk factors for cardiovascular disease . At a reinvestigation 20 years later , echocardiographic left ventricular mass index was determined in 475 subjects . A 1-SD increase in body mass index , systolic or diastolic blood pressure , fasting LDL/HDL cholesterol , serum triglycerides , or the serum cholesterol ester proportion of several saturated fatty acids or oleic acid at age 50 significantly increased the odds of having LVH at age 70 by 27 % to 41 % , whereas an increase in linoleic acid proportion was protective . Almost all metabolic predictors were independent of ischemic heart disease , valvular disease , and use of antihypertensive medication at age 70 . Conclusions —Dyslipidemia and indices of a low dietary intake of linoleic acid and high intake of saturated and monounsaturated fats , as well as hypertension and obesity , at age 50 predicted the prevalence of LVH 20 years later in this prospect i ve longitudinal cohort study , thereby suggesting that lipids may be important in the origin of LVH Atrial fibrillation ( AF ) , the most common chronic arrhythmia , increases the risk of stroke and is an independent predictor of mortality . Available pharmacological treatments have limited efficacy . Once initiated , AF tends to self-perpetuate , owing in part to electrophysiological remodeling in the atria ; however , the fundamental mechanisms underlying this process are still unclear . We have recently demonstrated that chronic human AF is associated with increased atrial oxidative stress and peroxynitrite formation ; we have now tested the hypothesis that these events participate in both pacing-induced atrial electrophysiological remodeling and in the occurrence of AF following  cardiac surgery . In chronically instrumented dogs , we found that rapid ( 400 min−1 ) atrial pacing was associated with attenuation of the atrial effective refractory period ( ERP ) . Treatment with ascorbate , an antioxidant and peroxynitrite decomposition catalyst , did not directly modify the ERP , but attenuated the pacing-induced atrial ERP shortening following 24 to 48 hours of pacing . Biochemical studies revealed that pacing was associated with decreased tissue ascorbate levels and increased protein nitration ( a biomarker of peroxynitrite formation ) . Oral ascorbate supplementation attenuated both of these changes . To evaluate the clinical significance of these observations , supplemental ascorbate was given to 43 patients before , and for 5 days following , cardiac bypass graft surgery . Patients receiving ascorbate had a 16.3 % incidence of postoperative AF , compared with 34.9 % in control subjects . In combination , these studies suggest that oxidative stress underlies early atrial electrophysiological remodeling and offer novel insight into the etiology and potential treatment of an enigmatic and difficult to control arrhythmia . The full text of this article is available at http://www.circresaha.org OBJECTIVE It has been recently reported that AF is associated with tissue inflammation . Statins reduce C-reactive protein ( CRP ) levels . However , the effect of statin on atrial fibrillation ( AF ) is unclear . The purpose of the present study was to evaluate the effect of statin on AF in a canine sterile pericarditis model . METHODS Sterile pericarditis was created in 20 dogs r and omly assigned to two groups : a control group ( 10 dogs ) and an atorvastatin treatment group ( 10 dogs ) . Atorvastatin was administered orally ( 2 mg/kg/day ) beginning 1 week before the operation until the end of the study . Before and 2 days after the operation , CRP levels , the duration of induced AF , the atrial effective refractory period ( AERP ) , and intra-atrial conduction time were determined . RESULTS Before the operation , there were no significant differences in any of the parameters between the two groups . On the second postoperative day , the atorvastatin group had a lower CRP level ( 7.6+/-0.5 versus 11.7+/-1.3 mg/dl , P<0.0001 ) , a shorter AF duration ( 177+/-57 versus 534+/-189 s , P<0.0001 ) , a longer AERP ( 138+/-6 versus 130+/-6 ms , P<0.01 ) , and a shorter intra-atrial conduction time ( 46+/-3 versus 51+/-5 ms , P<0.01 ) than the control group . CONCLUSIONS Atorvastatin can prevent maintenance of AF by inhibiting inflammation in the canine sterile pericarditis model . Atorvastatin may thus be a novel therapeutic agent for AF Increased angiotensin II ( Ang II ) sensitivity predisposes to hypertension and plaque instability . Raised low-density lipoprotein cholesterol ( LDL-c ) may increase Ang II sensitivity , but evidence in humans for this effect of LDL-c is limited . In 28 , healthy , nonsmoking subjects , aged 30±8 years , with familial hyper 
    Output:
    