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 Late venous graft thrombosis , leading to recurrent ischemia , is frequently encountered in old , degenerated vein grafts with advanced atherosclerotic plaque formation . Aspirin has been indicated to maintain venous graft patency in the post-operative period . However , there is considerable evidence that aspirin resistance is of concern in patients with venous grafts . MATERIAL AND METHOD Prospect ively enrolled 14 patients ( 11 male , 3 female , Group 1 ) , who were shown to have at least one occluded saphenous vein graft on their late control coronary angiogram after bypass operation , were compared for the presence of aspirin resistance by PFA-100 with age- and sex-matched 14 patients ( 10 male , 4 female , Group 2 ) , who were found patent and well-functioning vein grafts without wall irregularities on late post-operative coronary angiograms ( mean 6.5+/-2.5 years ) , enrolled as a control group . RESULTS Mean CT of collagen/epinephrine cartridge in Group 1 was 197+/-85 s and significantly less than in Group 2 ( 279+/-44 s ; p=0.011 ) . It was found that 50 % of patients in Group 1 were so-called aspirin resistant , whereas in Group 2 , this ratio was 7.1 % ( p=0.033 ) . BMI ( p=0.038 , Beta=-0.322 ) , uric acid level ( p=0.023 , Beta=-0.355 ) , and CT by collagen/epinephrine cartridge ( p=0.008 , Beta=0.431 ) were independently predicting late occlusion of saphenous vein graft . CONCLUSION Aspirin resistance is highly prevalent in patients with occluded venous grafts at a relatively late period OBJECTIVES This study was design ed to determine if aspirin resistance is associated with clinical events . BACKGROUND Aspirin resistance , defined by platelet function testing and presumed clinical unresponsiveness to aspirin , has been previously reported by our group and others . However , little information exists linking the laboratory documentation of aspirin resistance and long-term clinical events . METHODS We prospect ively enrolled 326 stable cardiovascular patients from 1997 to 1999 on aspirin ( 325 mg/day for > or = 7 days ) and no other antiplatelet agents .  We tested for aspirin sensitivity by optical platelet aggregation using adenosine diphosphate ( ADP ) and arachidonic acid ( AA ) . The primary outcome was the composite of death , myocardial infa rct ion ( MI ) , or cerebrovascular accident ( CVA ) . Mean follow-up was 679 + /- 185 days . Aspirin resistance was defined as a mean aggregation of > or = 70 % with 10 microM ADP and > or = 20 % with 0.5 mg/ml AA . RESULTS Of the patients studied , 17 ( 5.2 % ) were aspirin resistant and 309 ( 94.8 % ) were not aspirin resistant . During follow-up , aspirin resistance was associated with an increased risk of death , MI , or CVA compared with patients who were aspirin sensitive ( 24 % vs. 10 % , hazard ratio [ HR ] 3.12 , 95 % confidence interval [ CI ] 1.10 to 8.90 , p = 0.03 ) . Stratified multivariate analyses identified platelet count , age , heart failure , and aspirin resistance to be independently associated with major adverse long-term outcomes ( HR for aspirin resistance 4.14 , 95 % CI 1.42 to 12.06 , p = 0.009 ) . CONCLUSIONS This study demonstrates the natural history of aspirin resistance in a stable population , documenting a greater than threefold increase in the risk of major adverse events associated with aspirin resistance We report the incidence of  aspirin  nonresponsiveness  in a prospect i ve , multicenter registry ( n=422 patients ) to be 23 % using the Ultegra Rapid Platelet Function Assay-ASA , and determined a history of coronary artery disease to be associated with twice the odds of being an  aspirin nonresponder ( odds ratio 2.01 , 95 % confidence interval 1.189 to 3.411 , p=0.009 ) . Further prospect i ve studies are needed to correlate  aspirin nonresponsiveness to adverse clinical events Background and Purpose — Aspirin is used commonly to prevent ischemic strokes and other vascular events . Although aspirin is considered safe and effective , it has limited efficacy with a relative risk reduction of 20 % to 25 % for ischemic stroke . We sought to determine if aspirin as currently used is having its desired antiplatelet effects . Methods — We ascertained patients with cerebrovascular disease who were taking only aspirin as an antiplatelet agent .  Platelet function was evaluated using a platelet function analyzer ( PFA-100 ) . PFA test results were correlated with aspirin dose , formulation , and basic demographic factors . Results — We ascertained 129 patients , of whom 32 % were taking an enteric-coated aspirin preparation and 32 % were taking low-dose ( ≤162 mg/d ) aspirin .  For the entire cohort , 37 % of patients had normal PFA-100 results , indicating normal platelet function . For the patients taking low-dose aspirin , 56 % had normal PFAs compared with 28 % of those taking ≥325 mg/d of aspirin , while 65 % of patients taking enteric-coated aspirin had normal PFAs compared with 25 % taking an uncoated preparation ( P < 0.01 for both comparisons ) . Similar results were obtained if PFA results were analyzed using mean closure times ( low-dose aspirin , 183 sec ; high-dose aspirin , 233 sec ; enteric-coated , 173 sec ; uncoated , 235 sec ; P < 0.01 for comparisons ) . Older patients and women were less likely to have a therapeutic response to aspirin , independent of aspirin dose or formulation . Conclusions — A significant proportion of  patients taking low-dose aspirin or enteric-coated aspirin  have normal platelet function as measured by the PFA-100 test . If these results correlate with clinical events , they have broad implication s in determining how aspirin is used and monitored PURPOSE We sought to investigate the association of aspirin dose and aspirin resistance in stable coronary artery disease patients measured by a point-of-care assay . METHODS We studied 468 consecutive stable coronary artery disease patients in a referral cardiac center who were taking aspirin 80 to 325 mg daily for > or = 4 weeks .  The VerifyNow Aspirin ( Ultegra RPFA-ASA , Accumetrics Inc , San Diego , Calif ) was used to determine aspirin responsiveness . An aspirin reaction unit ( ARU ) > or = 550 indicates the absence of aspirin-induced platelet dysfunction , based on correlation with epinephrine-induced light transmission aggregometry . Demographic and clinical data were collected to analyze the predictors of aspirin resistance . RESULTS  Aspirin resistance was noted in 128 ( 27.4 % ) patients . Univariate predictors of aspirin resistance include elderly ( P = 0.002 ) , women ( P < 0.001 ) , anemia ( P < 0.001 ) , renal insufficiency ( P = 0.009 ) and aspirin dose < or = 100 mg ( P = 0.004 ) . Multivariate analysis revealed hemoglobin ( odds ratio [ OR ] 0.6 ; 95 % confidence interval [ CI ] 0.51 to 0.69 ; P < 0.001 ) and aspirin dose < or = 100 mg ( OR 2.23 ; 95 % CI 1.12 to 4.44 ; P = 0.022 ) to be independent predictors of aspirin resistance . Daily aspirin dose < or = 100 mg was associated with increased prevalence of aspirin resistance compared with 150 mg and 300 mg daily ( 30.2 % vs 16.7 % vs 0 % , P = 0.0062 ) . CONCLUSION A 100 mg or less daily dose of aspirin , which may have lower side effects , is associated with a higher incidence of aspirin resistance in patients with coronary artery disease . Prospect i ve r and omized studies are warranted to eluci date the optimal aspirin dosage for preventing ischemic complications of atherothrombotic disease BACKGROUND Acetylsalicylic acid , or aspirin , is widely used in secondary prevention of coronary artery diseases , but the inhibition of platelet aggregation is not uniform in all individuals . OBJECTIVE To investigate the prevalence of aspirin resistance at rest and during exercise in coronary artery disease patients . MATERIAL S AND METHODS Fifty patients with stable coronary artery disease were prospect ively studied . All patients received aspirin ( 75 - 300 mg/day for > 1 month ) and no other antiplatelet therapy . Aspirin resistance was studied , at rest and immediately after a stress test , using the st and ardized platelet function analyzer ( PFA-100(R ) , Dade-Behring ) . Aspirin resistance was defined as a normal collagen/epinephrine closure time ( < 186 s ) . RESULTS Ten patients ( 20 % ) were  aspirin-resistant  at rest . Out of the 40 patients who were aspirin-sensitive at rest , 9 ( 22 % ) were aspirin-resistant immediately after the exercise stress test . There were no differences in aspirin sensitivity regarding gender , age , diabetes , hypertension , dyslipidemia , platelet count , medical treatment or number of the coronary arteries involved . CONCLUSIONS Aspirin resistance is detected , at rest , in 20 % of our patients with stable coronary artery disease .  Aspirin treatment does not seem to protect against exercise-induced platelet activation in 22 % of such patients , despite aspirin sensitivity at rest Background and Purpose — Recent studies suggest that patients who do not respond to aspirin ( ASA ) therapy may be at increased risk of ischemic vascular events . The availability of simple to use point-of-care ( POC ) platelet function tests now potentially allows aspirin nonresponsiveness to be identified in routine clinical practice . However , there are very few data on whether the different tests produce consistent results . We therefore compared 2 POC tests ( PFA-100 device and the Ultegra-RPFA [ RPFA ] ) with conventional light transmission aggregometry ( LTA ) . Methods — Platelet function was assessed by all 3 tests in 100 patients receiving low-dose ASA therapy after transient ischemic attack ( TIA ) or ischemic stroke . Results — The incidence of ASA nonresponsiveness was 17 % by the RPFA and 22 % by the PFA-100 , compared with only 5 % by LTA ( ie , as defined with both arachidonic acid and ADP ) . Agreement between the RPFA and the PFA-100 and arachidonic acid induced LTA was poor ( & kgr;=0.16 , 95 % CI , −0.08 to 0.39 , P=0.11 ; and & kgr;=0.09 −0.12 to 0.30 , P=0.32 , respectively ) . Agreement between the 2 POC tests was also poor ( & kgr;=0.14 , −0.08 to 0.36 , P=0.15 ) . Only 2 % of patients were aspirin nonresponders by all 3 tests . Conclusions — The prevalence of apparent ASA nonresponsiveness was higher with both the POC tests than with LTA . However , agreement between the tests was poor and very few patients were ASA nonresponsive by all 3 tests . Aspirin nonresponsiveness is therefore highly test-specific and large prospect i ve studies will be required to determine the prognostic value of each of the separate tests Aspirin , compared with placebo , reduces the risk of cardiovascular events by 25 % in population s of patients with and without known arterial vascular disease . However , the phenomena of ‘ aspirin resistance ’ that has been described in 5–50 % of this population may critically reduce aspirin 's efficacy . One study has suggested that aspirin-resistant patients have a 3.5 times higher risk of cardiovascular death . Presently , there are no established , simple , broadly used methods determining antiplatelet properties of aspirin , while conventional aggregometry requires special equipment and trained personnel . We sought to determine the validity of an Ultegra analyzer with the novel aspirin-sensitive cartridge before and after one pill of non-enteric coated aspirin ( 325 mg ) in subjects with multiple risk factors for coronary artery disease . One hundred and fifty-four volunteers were enrolled into the multicenter study , but six of them were excluded . Data from 148 participants were analyzed . Platelets were assessed twice at baseline ( pre-aspirin ) , and after 2–30 h ( post-aspirin ) . We employed 5 μmol/l epinephrine-induced conventional aggregometry , and aspirin response units stimulated by propyl gallate with the point-of-care Ultegra analyzer . A single pill of aspirin  reduced platelet-rich plasma aggregation from 72  
    Output:
    
agent
Prevalences widely differ between studies reporting on aspirin resistance .
***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 Late venous graft thrombosis , leading to recurrent ischemia , is frequently encountered in old , degenerated vein grafts with advanced atherosclerotic plaque formation . Aspirin has been indicated to maintain venous graft patency in the post-operative period . However , there is considerable evidence that aspirin resistance is of concern in patients with venous grafts . MATERIAL AND METHOD Prospect ively enrolled 14 patients ( 11 male , 3 female , Group 1 ) , who were shown to have at least one occluded saphenous vein graft on their late control coronary angiogram after bypass operation , were compared for the presence of aspirin resistance by PFA-100 with age- and sex-matched 14 patients ( 10 male , 4 female , Group 2 ) , who were found patent and well-functioning vein grafts without wall irregularities on late post-operative coronary angiograms ( mean 6.5+/-2.5 years ) , enrolled as a control group . RESULTS Mean CT of collagen/epinephrine cartridge in Group 1 was 197+/-85 s and significantly less than in Group 2 ( 279+/-44 s ; p=0.011 ) . It was found that 50 % of patients in Group 1 were so-called aspirin resistant , whereas in Group 2 , this ratio was 7.1 % ( p=0.033 ) . BMI ( p=0.038 , Beta=-0.322 ) , uric acid level ( p=0.023 , Beta=-0.355 ) , and CT by collagen/epinephrine cartridge ( p=0.008 , Beta=0.431 ) were independently predicting late occlusion of saphenous vein graft . CONCLUSION Aspirin resistance is highly prevalent in patients with occluded venous grafts at a relatively late period OBJECTIVES This study was design ed to determine if aspirin resistance is associated with clinical events . BACKGROUND Aspirin resistance , defined by platelet function testing and presumed clinical unresponsiveness to aspirin , has been previously reported by our group and others . However , little information exists linking the laboratory documentation of aspirin resistance and long-term clinical events . METHODS We prospect ively enrolled 326 stable cardiovascular patients from 1997 to 1999 on aspirin ( 325 mg/day for > or = 7 days ) and no other antiplatelet agents .  We tested for aspirin sensitivity by optical platelet aggregation using adenosine diphosphate ( ADP ) and arachidonic acid ( AA ) . The primary outcome was the composite of death , myocardial infa rct ion ( MI ) , or cerebrovascular accident ( CVA ) . Mean follow-up was 679 + /- 185 days . Aspirin resistance was defined as a mean aggregation of > or = 70 % with 10 microM ADP and > or = 20 % with 0.5 mg/ml AA . RESULTS Of the patients studied , 17 ( 5.2 % ) were aspirin resistant and 309 ( 94.8 % ) were not aspirin resistant . During follow-up , aspirin resistance was associated with an increased risk of death , MI , or CVA compared with patients who were aspirin sensitive ( 24 % vs. 10 % , hazard ratio [ HR ] 3.12 , 95 % confidence interval [ CI ] 1.10 to 8.90 , p = 0.03 ) . Stratified multivariate analyses identified platelet count , age , heart failure , and aspirin resistance to be independently associated with major adverse long-term outcomes ( HR for aspirin resistance 4.14 , 95 % CI 1.42 to 12.06 , p = 0.009 ) . CONCLUSIONS This study demonstrates the natural history of aspirin resistance in a stable population , documenting a greater than threefold increase in the risk of major adverse events associated with aspirin resistance We report the incidence of  aspirin  nonresponsiveness  in a prospect i ve , multicenter registry ( n=422 patients ) to be 23 % using the Ultegra Rapid Platelet Function Assay-ASA , and determined a history of coronary artery disease to be associated with twice the odds of being an  aspirin nonresponder ( odds ratio 2.01 , 95 % confidence interval 1.189 to 3.411 , p=0.009 ) . Further prospect i ve studies are needed to correlate  aspirin nonresponsiveness to adverse clinical events Background and Purpose — Aspirin is used commonly to prevent ischemic strokes and other vascular events . Although aspirin is considered safe and effective , it has limited efficacy with a relative risk reduction of 20 % to 25 % for ischemic stroke . We sought to determine if aspirin as currently used is having its desired antiplatelet effects . Methods — We ascertained patients with cerebrovascular disease who were taking only aspirin as an antiplatelet agent .  Platelet function was evaluated using a platelet function analyzer ( PFA-100 ) . PFA test results were correlated with aspirin dose , formulation , and basic demographic factors . Results — We ascertained 129 patients , of whom 32 % were taking an enteric-coated aspirin preparation and 32 % were taking low-dose ( ≤162 mg/d ) aspirin .  For the entire cohort , 37 % of patients had normal PFA-100 results , indicating normal platelet function . For the patients taking low-dose aspirin , 56 % had normal PFAs compared with 28 % of those taking ≥325 mg/d of aspirin , while 65 % of patients taking enteric-coated aspirin had normal PFAs compared with 25 % taking an uncoated preparation ( P < 0.01 for both comparisons ) . Similar results were obtained if PFA results were analyzed using mean closure times ( low-dose aspirin , 183 sec ; high-dose aspirin , 233 sec ; enteric-coated , 173 sec ; uncoated , 235 sec ; P < 0.01 for comparisons ) . Older patients and women were less likely to have a therapeutic response to aspirin , independent of aspirin dose or formulation . Conclusions — A significant proportion of  patients taking low-dose aspirin or enteric-coated aspirin  have normal platelet function as measured by the PFA-100 test . If these results correlate with clinical events , they have broad implication s in determining how aspirin is used and monitored PURPOSE We sought to investigate the association of aspirin dose and aspirin resistance in stable coronary artery disease patients measured by a point-of-care assay . METHODS We studied 468 consecutive stable coronary artery disease patients in a referral cardiac center who were taking aspirin 80 to 325 mg daily for > or = 4 weeks .  The VerifyNow Aspirin ( Ultegra RPFA-ASA , Accumetrics Inc , San Diego , Calif ) was used to determine aspirin responsiveness . An aspirin reaction unit ( ARU ) > or = 550 indicates the absence of aspirin-induced platelet dysfunction , based on correlation with epinephrine-induced light transmission aggregometry . Demographic and clinical data were collected to analyze the predictors of aspirin resistance . RESULTS  Aspirin resistance was noted in 128 ( 27.4 % ) patients . Univariate predictors of aspirin resistance include elderly ( P = 0.002 ) , women ( P < 0.001 ) , anemia ( P < 0.001 ) , renal insufficiency ( P = 0.009 ) and aspirin dose < or = 100 mg ( P = 0.004 ) . Multivariate analysis revealed hemoglobin ( odds ratio [ OR ] 0.6 ; 95 % confidence interval [ CI ] 0.51 to 0.69 ; P < 0.001 ) and aspirin dose < or = 100 mg ( OR 2.23 ; 95 % CI 1.12 to 4.44 ; P = 0.022 ) to be independent predictors of aspirin resistance . Daily aspirin dose < or = 100 mg was associated with increased prevalence of aspirin resistance compared with 150 mg and 300 mg daily ( 30.2 % vs 16.7 % vs 0 % , P = 0.0062 ) . CONCLUSION A 100 mg or less daily dose of aspirin , which may have lower side effects , is associated with a higher incidence of aspirin resistance in patients with coronary artery disease . Prospect i ve r and omized studies are warranted to eluci date the optimal aspirin dosage for preventing ischemic complications of atherothrombotic disease BACKGROUND Acetylsalicylic acid , or aspirin , is widely used in secondary prevention of coronary artery diseases , but the inhibition of platelet aggregation is not uniform in all individuals . OBJECTIVE To investigate the prevalence of aspirin resistance at rest and during exercise in coronary artery disease patients . MATERIAL S AND METHODS Fifty patients with stable coronary artery disease were prospect ively studied . All patients received aspirin ( 75 - 300 mg/day for > 1 month ) and no other antiplatelet therapy . Aspirin resistance was studied , at rest and immediately after a stress test , using the st and ardized platelet function analyzer ( PFA-100(R ) , Dade-Behring ) . Aspirin resistance was defined as a normal collagen/epinephrine closure time ( < 186 s ) . RESULTS Ten patients ( 20 % ) were  aspirin-resistant  at rest . Out of the 40 patients who were aspirin-sensitive at rest , 9 ( 22 % ) were aspirin-resistant immediately after the exercise stress test . There were no differences in aspirin sensitivity regarding gender , age , diabetes , hypertension , dyslipidemia , platelet count , medical treatment or number of the coronary arteries involved . CONCLUSIONS Aspirin resistance is detected , at rest , in 20 % of our patients with stable coronary artery disease .  Aspirin treatment does not seem to protect against exercise-induced platelet activation in 22 % of such patients , despite aspirin sensitivity at rest Background and Purpose — Recent studies suggest that patients who do not respond to aspirin ( ASA ) therapy may be at increased risk of ischemic vascular events . The availability of simple to use point-of-care ( POC ) platelet function tests now potentially allows aspirin nonresponsiveness to be identified in routine clinical practice . However , there are very few data on whether the different tests produce consistent results . We therefore compared 2 POC tests ( PFA-100 device and the Ultegra-RPFA [ RPFA ] ) with conventional light transmission aggregometry ( LTA ) . Methods — Platelet function was assessed by all 3 tests in 100 patients receiving low-dose ASA therapy after transient ischemic attack ( TIA ) or ischemic stroke . Results — The incidence of ASA nonresponsiveness was 17 % by the RPFA and 22 % by the PFA-100 , compared with only 5 % by LTA ( ie , as defined with both arachidonic acid and ADP ) . Agreement between the RPFA and the PFA-100 and arachidonic acid induced LTA was poor ( & kgr;=0.16 , 95 % CI , −0.08 to 0.39 , P=0.11 ; and & kgr;=0.09 −0.12 to 0.30 , P=0.32 , respectively ) . Agreement between the 2 POC tests was also poor ( & kgr;=0.14 , −0.08 to 0.36 , P=0.15 ) . Only 2 % of patients were aspirin nonresponders by all 3 tests . Conclusions — The prevalence of apparent ASA nonresponsiveness was higher with both the POC tests than with LTA . However , agreement between the tests was poor and very few patients were ASA nonresponsive by all 3 tests . Aspirin nonresponsiveness is therefore highly test-specific and large prospect i ve studies will be required to determine the prognostic value of each of the separate tests Aspirin , compared with placebo , reduces the risk of cardiovascular events by 25 % in population s of patients with and without known arterial vascular disease . However , the phenomena of ‘ aspirin resistance ’ that has been described in 5–50 % of this population may critically reduce aspirin 's efficacy . One study has suggested that aspirin-resistant patients have a 3.5 times higher risk of cardiovascular death . Presently , there are no established , simple , broadly used methods determining antiplatelet properties of aspirin , while conventional aggregometry requires special equipment and trained personnel . We sought to determine the validity of an Ultegra analyzer with the novel aspirin-sensitive cartridge before and after one pill of non-enteric coated aspirin ( 325 mg ) in subjects with multiple risk factors for coronary artery disease . One hundred and fifty-four volunteers were enrolled into the multicenter study , but six of them were excluded . Data from 148 participants were analyzed . Platelets were assessed twice at baseline ( pre-aspirin ) , and after 2–30 h ( post-aspirin ) . We employed 5 μmol/l epinephrine-induced conventional aggregometry , and aspirin response units stimulated by propyl gallate with the point-of-care Ultegra analyzer . A single pill of aspirin  reduced platelet-rich plasma aggregation from 72  
    Output:
    