***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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    Input: BACKGROUND Post-trial monitoring of patients in the United Kingdom Prospect i ve Diabetes Study ( UKPDS ) examined whether risk reductions for microvascular and macrovascular disease , achieved with the use of improved blood-pressure control during the trial , would be sustained . METHODS Among 5102 UKPDS patients with newly diagnosed type 2 diabetes mellitus , we r and omly assigned , over a 4-year period beginning in 1987 , 1148 patients with hypertension to  tight or less-tight blood-pressure control regimens .  The 884 patients who underwent post-trial monitoring  were asked to attend annual UKPDS clinics for the first 5 years , but no attempt was made to maintain their previously assigned therapies . Annual question naires completed by patients and general practitioners were used to follow patients who were unable to attend the clinic in years 1 through 5 , and question naires were used for all patients in years 6 to 10 . Seven prespecified aggregate clinical end points were examined on an intention-to-treat basis , according to the previous r and omization categories . RESULTS Differences in blood pressure between the two groups during the trial disappeared within 2 years after termination of the trial . Significant relative risk reductions found during the trial for any diabetes-related end point , diabetes-related death , microvascular disease , and stroke in the group receiving tight , as compared with less tight , blood-pressure control were not sustained during the post-trial follow-up . No risk reductions were seen during or after the trial for myocardial infa rct ion or death from any cause , but a risk reduction for peripheral vascular disease associated with tight blood-pressure control became significant ( P=0.02 ) . CONCLUSIONS The benefits of previously improved blood-pressure control were not sustained when between-group differences in blood pressure were lost . Early improvement in blood-pressure control in patients with both type 2 diabetes and hypertension was associated with a reduced risk of complications , but it appears that good blood-pressure control must be continued if the benefits are to be maintained . ( UKPDS 81 ; Current Controlled Trials number , IS RCT N75451837 . OBJECTIVES This study investigated whether the beneficial effects of intensive glycemic control and fenofibrate treatment of dyslipidemia in reducing retinopathy progression demonstrated in the Action to Control Cardiovascular Risk in Diabetes ( ACCORD ) Eye Study persisted beyond the clinical trial . RESEARCH DESIGN AND METHODS The ACCORD Study ( 2003–2009 ) r and omized participants with type 2 diabetes to intensive or st and ard treatment for glycemia ( A1C level at < 6.0 % [ 42 mmol/mol ] vs. 7.0–7.9 % [ 53–63 mmol/mol ] ) , systolic blood pressure ( < 120 vs. 140 mmHg ) , and dyslipidemia ( fenofibrate [ 160 mg ] plus simvastatin or placebo plus simvastatin ) . ACCORD Eye Study participants , who had baseline and year 4 eye examinations and fundus photographs , were reexamined in the ACCORD Follow-On ( ACCORDION ) Eye Study ( 2010–2014 ) 4 years after the ACCORD trial closeout . The outcome measure was diabetic retinopathy progression of three or more steps on the Early Treatment Diabetic Retinopathy Study scale . RESULTS Diabetic retinopathy progressed in 5.8 % with intensive glycemic treatment versus 12.7 % with st and ard ( adjusted odds ratio [ aOR ] 0.42 , 95 % CI 0.28–0.63 , P < 0.0001 ) , 7.5 % with intensive blood pressure treatment versus 6.0 % for st and ard ( aOR 1.21 , 95 % CI 0.61–2.40 , P = 0.59 ) , and 11.8 % with fenofibrate versus 10.2 % with placebo ( aOR 1.13 , 95 % CI 0.71–1.79 , P = 0.60 ) in ACCORDION Eye participants ( n = 1,310 ) . CONCLUSIONS Prior intensive glycemic control continued to reduce diabetic retinopathy progression , despite similar A1C levels , when the ACCORD Study ended . This is the first study in people with type 2 diabetes of 10 years ’ duration and established cardiovascular disease , unlike the newly diagnosed participants of the UK Prospect i ve Diabetes Study , to demonstrate this effect . The benefit of fenofibrate , however , did not persist . Intensive blood pressure control had no effect Background —We have previously demonstrated that ramipril reduces vascular events and new diagnoses of diabetes when given for a 4.5-year period . However , it is not known whether the benefits are observed in subgroups of patients at varying risk or on other proven therapies and whether the benefits are sustained beyond the current trial . The 2 aims of this investigation were to assess whether the benefits observed during the HOPE trial were ( 1 ) maintained after trial cessation during an additional 2.6 years of follow-up and ( 2 ) observed in subgroups based on risk and ancillary treatments . Methods and Results —Of the initial 267 study centers and 9297 patients , 174 centers and 4528 patients agreed to further follow-up . The rates of use of angiotensin-converting-enzyme inhibitors ( ACEIs ) in the 2 groups ( 72 % ramipril versus 68 % placebo ) were similar after the end of the trial . During the posttrial follow-up , patients allocated to ramipril had a 19 % further lower relative risk ( RR ) of myocardial infa rct ion ( 95 % confidence interval [ CI ] , 0.65 to 1.01 ) , a 16 % lower RR ( 95 % CI , 0.70 to 0.99 ) of revascularization , and a 34 % lower RR of a new diagnosis of diabetes ( 95 % CI , 0.46 to 0.95 ) . Similar RR reductions in vascular events were observed during and after the active phase of the trial , regardless of baseline risk ( RR of 0.76 , 0.89 , and 0.83 for low- , medium- , and high-risk patients , respectively ) or ancillary treatments ( RR of 0.90 for aspirin , 0.76 for & bgr;-blockers , and 0.84 for lipid-lowering medication ) . Conclusions —The benefits of ramipril observed during the active period of the HOPE trial were maintained during posttrial follow-up for cardiovascular death , stroke , and hospitalization for heart failure . Additional reductions in myocardial infa rct ion , revascularization , and the development of diabetes were observed during the follow-up phase despite similar rates of ACEI use in the 2 r and omized groups . These benefits were consistent regardless of patient risk or ancillary treatments There is controversy regarding whether strict blood pressure control is indicated in chronic kidney disease ( CKD ) since the primary results of r and omized controlled trials failed to show any impact on progression of kidney disease with this strategy . However , strict blood pressure control may have other beneficial effects beyond reducing risk of end-stage renal disease ( ESRD ) , such as lowering mortality after ESRD onset . The Modification of Diet in Renal Disease ( MDRD ) trial r and omized 840 patients with CKD to strict ( mean arterial pressure under 92 mm Hg ) versus usual ( mean arterial pressure under 107 mm Hg ) blood pressure control between 1989–1993 . Here we extended follow-up of study enrollees by linkage with United States Renal Data System and National Death Index to ascertain ESRD and vital status through 2010 . Overall , 627 patients developed ESRD through 2010 with median follow-up of 19.3 years . After ESRD onset , there were 142 deaths in the strict blood pressure arm and 182 deaths in the usual blood pressure arm ( significant unadjusted hazard ratio for death 0.72 ( 95 % CI 0.58–0.89 ) ) . Overall , there were 212 deaths in the strict blood pressure control arm and 233 deaths in the usual arm ( significant unadjusted hazard ratio for death 0.82 ( 95 % CI 0.68–0.98 ) ) . Thus , although strict blood pressure control did not delay progression of CKD to ESRD , this strategy was associated with a lower risk of death after ESRD . Hence , long-term post-ESRD outcomes should be considered when formulating blood pressure targets for CKD OBJECTIVE Early initiation of intensive diabetes therapy aim ed at achieving near-normal glycemia reduces the early development of vascular complications in type 1 diabetes . We now assess whether intensive therapy compared with conventional therapy during the Diabetes Control and Complications Trial ( DCCT ) affected the incidence of cardiovascular disease over 30 years of follow-up . RESEARCH DESIGN AND METHODS The DCCT r and omly assigned 1,441 patients with type 1 diabetes to  intensive versus conventional therapy for a mean of 6.5 years , after which 93 % were subsequently monitored during the observational Epidemiology of Diabetes Interventions and Complications ( EDIC ) study . Cardiovascular disease ( nonfatal myocardial infa rct ion and stroke , cardiovascular death , confirmed angina , congestive heart failure , and coronary artery revascularization ) was adjudicated using st and ardized measures . RESULTS During 30 years of follow-up in DCCT and EDIC , 149 cardiovascular disease events occurred in 82 former intensive treatment group subjects versus 217 events in 102 former conventional treatment group subjects . Intensive therapy reduced the incidence of any cardiovascular disease by 30 % ( 95 % CI 7 , 48 ; P = 0.016 ) , and the incidence of major cardiovascular events ( nonfatal myocardial infa rct ion , stroke , or cardiovascular death ) by 32 % ( 95 % CI −3 , 56 ; P = 0.07 ) . The lower HbA1c levels during the DCCT/EDIC statistically account for all of the observed treatment effect on cardiovascular disease risk . Increased albuminuria was also independently associated with cardiovascular disease risk . CONCLUSIONS Intensive diabetes therapy during the DCCT ( 6.5 years ) has long-term beneficial effects on the incidence of cardiovascular disease in type 1 diabetes that persist for up to 30 years BACKGROUND An impaired glomerular filtration rate ( GFR ) leads to end-stage renal disease and increases the risks of cardiovascular disease and death .  Persons with type 1 diabetes are at high risk for kidney disease , but there are no interventions that have been proved to prevent impairment of the GFR in this population . METHODS In the Diabetes Control and Complications Trial ( DCCT ) , 1441 persons with type 1 diabetes were r and omly assigned to 6.5 years of intensive diabetes therapy aim ed at achieving near-normal glucose concentrations or to conventional diabetes therapy aim ed at preventing hyperglycemic symptoms . Subsequently , 1375 participants were followed in the observational Epidemiology of Diabetes Interventions and Complications ( EDIC ) study . Serum creatinine levels were measured annually throughout the course of the two studies . The GFR was estimated with the use of the Chronic Kidney Disease Epidemiology Collaboration formula . We analyzed data from the two studies to determine the long-term effects of intensive diabetes therapy on the risk of impairment of the GFR , which was defined as an incident estimated GFR of less than 60 ml per minute per 1.73 m(2 ) of body-surface area at two consecutive study visits . RESULTS Over a median follow-up period of 22 years in the combined studies , impairment of the GFR developed in 24 participants assigned to intensive therapy and in 46 assigned to conventional therapy ( risk reduction with intensive therapy , 50 % ; 95 % confidence interval , 18 to 69 ; P=0.006 ) . Among these participants , end-stage renal disease developed in 8 participants in the intensive-therapy group and in 16 in the conventional-therapy group . As compared with conventional therapy , intensive therapy was associated with a reduction in the mean estimated GFR of 1.7 ml per minute per 1.73 m(2 ) during the DCCT study but during the EDIC study was associated with a slower rate of reduction in the GFR and an increase in the mean estimated GFR of 2.5 ml per minute per 1.73 m(2 ) ( P<0.001 for both comparisons ) . The beneficial effect of intensive therapy on the risk of an impaired GFR was fully attenuated after adjustment for glycated hemoglobin levels or albumin excretion rates . CONCLUSIONS The long-term risk of an impaired GFR was significantly lower among persons treated early in the course of type 1 diabetes with intensive diabetes therapy than among those treated with conventional diabetes therapy . ( Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and others ; DCCT/EDIC Clinical Trials.gov numbers , NCT00360815 and NCT00360893 . ) Background Evidence on long term effectiveness of public health strategies for lowering blood pressure ( BP ) 
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We judged the memory phenomenon to be positive when the cardiovascular outcome at the end of the post-trial follow-up period in the intervention group was significantly superior even though the favorable control of a risk factor ( blood glucose , blood pressure or lipid level ) during the trial period was lost after the cessation of the intervention .
Transient intensive glucose lowering rather easily induced memory for the suppression of diabetic microangiopathies , while memory for the suppression of macroangiopathies tended to be first evident in the post-trial follow-up period .
Transient intensive blood pressure lowering  was generally effective in the formation of memory for the suppression of cardiovascular events and had an especially strong impact on risk reduction of chronic heart failure .
Transient intensive LDL cholesterol lowering  clearly had a long-term beneficial effect on risk reduction of cardiovascular events .
Our systematic review revealed the clinical relevance of cardiometabolic memory