***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: OBJECTIVE To determine whether serum lipid intervention , in addition to conventional diabetes treatment , could alter cardiovascular outcomes in type 2 diabetes . RESEARCH DESIGN AND METHODS There were 164 type 2 diabetic subjects ( 117 men , 47 women ) without a history of clinical cardiovascular disease r and omized to receive either bezafibrate or placebo daily on a double-blind basis in addition to routine diabetes treatment and followed prospect ively for a minimum of 3 years . Serial biochemical and noninvasive vascular assessment s , carotid and femoral artery B-mode ultrasound measurements , and those pertaining to coronary heart disease (CHD)— clinical history , the World Health Organization ( WHO ) cardiovascular question naire , and resting and exercise electrocardiogram (ECG)—were recorded . RESULTS Bezafibrate treatment was associated with significantly greater reductions over 3 years in median serum triglyceride ( −32 vs. 4 % , P = 0.001 ) , total cholesterol ( −7 vs. −0.3 % , P = 0.004 ) , and total−to-HDL cholesterol ratio ( −12 vs. −0.0 % , P = 0.001 ) , and an increase in HDL cholesterol ( 6 vs. −2 % , P = 0.02 ) as compared with placebo . There was a trend toward a greater reduction of fibrinogen ( −18 vs. −6 % , P = 0.08 ) at 3 years . No significant differences between the two groups were found in the progress of ultrasonically measured arterial disease . In those treated with bezafibrate , there was a significant reduction ( P = 0.01 , log-rank test ) in the combined incidence of Minnesota-coded probable ischemic change on the resting ECG and of documented myocardial infa rct ion . CONCLUSIONS Improving dyslipidemia in type 2 diabetic subjects had no effect on the progress of ultrasonically measured arterial disease , although the lower rate of “ definite CHD events ” in the treated group suggests that this might result in a reduction in the incidence of coronary heart disease Few studies have evaluated the efficacy of cholesterol-lowering interventions in a community setting and have included a control or comparison group . As part of a preventive health demonstration project in rural Pennsylvania , Medicare beneficiaries underwent cholesterol screening to identify high-risk individuals with serum cholesterol levels > or = 240 mg/dL. These high-risk individuals were r and omized to a  cholesterol-lowering intervention  through either local hospitals or physicians ' offices or to a control group . Baseline and follow-up serum cholesterol levels collected two to three years later were compared according to service location ( hospital versus physician 's office ) , intervention attendance , degree of participation , baseline heart disease history , and cholesterol-lowering medication use at follow-up . Serum cholesterol levels decreased between 5.7 % and 6.6 % in the hospital-based and physician-based groups , as well as in a control group not offered the intervention .  Participation rates did not differ between treatment groups , nor did participation affect serum cholesterol levels . Attendance level and heart disease history were not associated with a greater decrease in serum cholesterol levels . Individuals reporting cholesterol-lowering drug use at follow-up had significantly higher baseline serum cholesterol levels and a significantly greater decrease in total serum cholesterol ( P < .0001 ) than those not on medication . Both nonpharmacological ( diet ) and pharmacological ( drug ) interventions will reduce serum cholesterol levels and heart attack risk . The study results suggest that , at least for older individuals , the impact of nonpharmacological interventions on the community is minimal . We conclude that only very aggressive treatment will significantly loser serum cholesterol levels in older individuals at risk for heart attack Abstract Objective : To describe , and to test against trial data , a simple and flexible computer program for calculating cardiovascular risk in individual patients as an aid to managing risk factors and prescribing drugs to lower cholesterol concentration and blood pressure . Design : Descriptive comparison of actual cardiovascular risk in r and omised controlled trials of cholesterol reduction  with risk predicted by a computer program based on the Framingham risk equation . Comparison of the program 's performance with that of tables and guidelines by means of hypothetical case examples . Main outcome measures : Average risk of coronary heart disease and myocardial infa rct ion . Results : The computer program accurately predicted baseline absolute risk in a UK population as well as the relative and absolute reduction in risk from cholesterol lowering for primary prevention of coronary heart disease . The program also allowed a more refined estimate of absolute risk of coronary heart disease than some existing tables and enabled the impact of prescribing decisions to be quantified and costed . Conclusions : This simple computer program to estimate individuals ' cardiovascular disease risk and display the benefits of intervention should help clinicians and patients decide on the most effective packages of risk reduction and identify those most likely to benefit from modulation of risk factors CONTEXT Although cholesterol-reducing treatment has been shown to reduce fatal and nonfatal coronary disease in patients with coronary heart disease ( CHD ) , it is unknown whether benefit from the reduction of low-density lipoprotein cholesterol ( LDL-C ) in patients without CHD extends to individuals with average serum cholesterol levels , women , and older persons . OBJECTIVE To compare lovastatin with placebo for prevention of the first acute major coronary event in men and women without clinical ly evident atherosclerotic cardiovascular disease with average total cholesterol ( TC ) and LDL-C levels and below-average high-density lipoprotein cholesterol ( HDL-C ) levels . DESIGN A r and omized , double-blind , placebo-controlled trial . SETTING Outpatient clinics in Texas . PARTICIPANTS A total of 5608 men and 997 women with average TC and LDL-C and below-average HDL-C ( as characterized by lipid percentiles for an age- and sex-matched cohort without cardiovascular disease from the National Health and Nutrition Examination Survey [ NHANES ] III ) . Mean ( SD ) TC level was 5.71 ( 0.54 ) mmol/L ( 221 [ 21 ] mg/dL ) ( 51 st percentile ) , mean ( SD ) LDL-C level was 3.89 ( 0.43 ) mmol/L ( 150 [ 17 ] mg/dL ) ( 60th percentile ) , mean ( SD ) HDL-C level was 0.94 ( 0.14 ) mmol/L ( 36 [ 5 ] mg/dL ) for men and 1.03 ( 0.14 ) mmol/L ( 40 [ 5 ] mg/dL ) for women ( 25th and 16th percentiles , respectively ) , and median ( SD ) triglyceride levels were 1.78 ( 0.86 ) mmol/L ( 158 [ 76 ] mg/dL ) ( 63rd percentile ) . INTERVENTION Lovastatin ( 20 - 40 mg daily ) or placebo in addition to a low-saturated fat , low-cholesterol diet . MAIN OUTCOME MEASURES First acute major coronary event defined as fatal or nonfatal myocardial infa rct ion , unstable angina , or sudden cardiac death . RESULTS After an average follow-up of 5.2 years , lovastatin reduced the incidence of first acute major coronary events ( 1 83 vs 116 first events ; relative risk [ RR ] , 0.63 ; 95 % confidence interval [ CI ] , 0.50 - 0.79 ; P<.001 ) , myocardial infa rct ion ( 95 vs 57 myocardial infa rct ions ; RR , 0.60 ; 95 % CI , 0.43 - 0.83 ; P=.002 ) , unstable angina ( 87 vs 60 first unstable angina events ; RR , 0.68 ; 95 % CI , 0.49 - 0.95 ; P=.02 ) , coronary revascularization procedures ( 157 vs 106 procedures ; RR , 0.67 ; 95 % CI , 0.52 - 0.85 ; P=.001 ) , coronary events ( 215 vs 163 coronary events ; RR , 0.75 ; 95 % CI , 0.61 - 0.92 ; P = .006 ) , and cardiovascular events ( 255 vs 194 cardiovascular events ; RR , 0.75 ; 95 % CI , 0.62 - 0.91 ; P = .003 ) . Lovastatin ( 20 - 40 mg daily ) reduced LDL-C by 25 % to 2.96 mmol/L ( 115 mg/dL ) and increased HDL-C by 6 % to 1.02 mmol/L ( 39 mg/dL ) . There were no clinical ly relevant differences in safety parameters between treatment groups . CONCLUSIONS Lovastatin reduces the risk for the first acute major coronary event  in men and women with average TC and LDL-C levels and below-average HDL-C levels . These findings support the inclusion of HDL-C in risk-factor assessment , confirm the benefit of LDL-C reduction to a target goal , and suggest the need for re assessment of the National Cholesterol Education Program guidelines regarding pharmacological intervention BACKGROUND The atherosclerotic progression-reducing effect of LDL cholesterol ( LDL-C ) lowering has been established in subjects with severe atherosclerotic disease but not in persons with elevated LDL cholesterols without severe atherosclerosis . KAPS ( Kuopio Atherosclerosis Prevention Study ) is the first population -based trial in the primary prevention of carotid and femoral atherosclerosis . METHODS AND RESULTS The eligibility requirements were serum LDL-C > or = 4.0 mmol/L and total cholesterol < 7.5 mmol/L. Out of a geographically defined population , 447 men aged 44 to 65 years ( mean , 57 ) were r and omized to pravastatin ( 40 mg/d  ) or placebo for 3 years . Less than 10 % of the subjects had prior myocardial infa rct ion . Thirty-nine men discontinued study medication ; however , efficacy data were available for 424 men . The primary outcome was the rate of carotid atherosclerotic progression , measured as the linear slope over annual ultrasound examinations in the average of the maximum carotid intima-media thickness ( IMT ) of the far wall of up to four arterial segments ( the right and left distal common carotid artery and the right and left carotid bulb ) . For the carotid arteries , at the overall mean baseline IMT of 1.66 mm , the rate of progression of carotid atherosclerosis was 45 % ( 95 % CI , 16 to 69 % ) less in the pravastatin ( 0.017 mm/y ) than the placebo ( 0.031 mm/y ) group ( P = .005 ) . In the common carotid artery there was a treatment effect of 66 % ( 95 % CI , 30 to 95 % ; pravastatin 0.010 mm/y ; placebo 0.029 mm/y ; P < .002 ) at the overall mean baseline IMT of 1.35 mm . A treatment effect of 30 % ( 95 % CI , -1 % to 54 % ) was found for the carotid bulb ( pravastatin , 0.028 ; placebo , 0.040 ; P = .056 ) at the overall mean baseline IMT of 2.0 mm . The treatment effect was larger in subjects with higher baseline IMT values , in smokers and in those with low plasma vitamin E levels . There was no significant treatment effect on atherosclerotic progression in the femoral arteries . CONCLUSIONS These data establish the antiatherogenic effect of LDL-C lowering by pravastatin in hypercholesterolemic men in a primary prevention setting and suggest a greater effect in smokers than in nonsmokers BACKGROUND Familial combined hyperlipidaemia ( FCH ) , characterized by elevated very-low-density lipoprotein ( VLDL ) and /or low-density lipoprotein ( LDL ) , is associated with an increased prevalence of premature cardiovascular disease . Therefore , lipid-lowering is frequently indicated . METHODS We evaluated in a parallel , double-blind r and omized fashion the effect of gemfibrozil ( 1200 mg/day ) ( n = 40 ) or simvastatin ( 20 mg/day ) ( n = 41 ) on lipids , apolipoprotein-B (apo-B)-containing lipoproteins , apo-CIII and lipoprotein(a ) [ Lp(a ) ] , in 81 well-defined FCH patients . RESULTS While both drugs lowered plasma cholesterol and triglyceride levels , gemfibrozil lowered plasma triglycerides more effectively by reduction of triglycerides in VLDL and LDL , whereas simvastatin was more effective in its reduction of total plasma cholesterol by exclusively decreasing LDL cholesterol . High-density lipoprotein ( HDL ) increased to an equal extent on both therapies . Total serum apo-B 
    Output:
    
When statin drugs were considered alone , no substantial differences in results were found .
Treatment with lipid lowering drugs lasting five to seven years reduces coronary heart disease events but not all cause mortality in people with no known cardiovascular disease