***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: CONTEXT The effect of antihypertensive drugs on cardiovascular events in patients with coronary artery disease ( CAD ) and normal blood pressure remains uncertain . OBJECTIVE To compare the effects of amlodipine or enalapril vs placebo on cardiovascular events in patients with CAD . DESIGN , SETTING , AND PARTICIPANTS Double-blind , r and omized , multicenter , 24-month trial ( enrollment April 1999-April 2002 ) comparing amlodipine or enalapril with placebo in 1991 patients with angiographically documented CAD ( > 20 % stenosis by coronary angiography ) and diastolic blood pressure < 100 mm Hg . A sub study of 274 patients measured atherosclerosis progression by intravascular ultrasound ( IVUS ) . INTERVENTIONS Patients were r and omized to receive amlodipine , 10 mg ; enalapril , 20 mg ; or placebo . IVUS was performed at baseline and study completion . MAIN OUTCOME MEASURES The primary efficacy parameter was incidence of cardiovascular events for amlodipine vs placebo . Other outcomes included comparisons of amlodipine vs enalapril and enalapril vs placebo . Events included cardiovascular death , nonfatal myocardial infa rct ion , resuscitated cardiac arrest , coronary revascularization , hospitalization for angina pectoris , hospitalization for congestive heart failure , fatal or nonfatal stroke or transient ischemic attack , and new diagnosis of peripheral vascular disease . The IVUS end point was change in percent atheroma volume . RESULTS Baseline blood pressure averaged 129/78 mm Hg for all patients ; it increased by 0.7/0.6 mm Hg in the placebo group and decreased by 4.8/2.5 mm Hg and 4.9/2.4 mm Hg in the amlodipine and enalapril groups , respectively ( P<.001 for both vs placebo ) . Cardiovascular events occurred in 151 ( 23.1 % ) placebo-treated patients , in 110 ( 16.6 % ) amlodipine-treated patients ( hazard ratio [ HR ] , 0.69 ; 95 % CI , 0.54 - 0.88 [ P = .003 ] ) , and in 136 ( 20.2 % ) enalapril-treated patients ( HR , 0.85 ; 95 % CI , 0.67 - 1.07 [ P = .16 ] . Primary end point comparison for enalapril vs amlodipine was not significant ( HR , 0.81 ; 95 % CI , 0.63 - 1.04 [ P = .10 ] ) . The IVUS sub study showed a trend toward less progression of atherosclerosis in the amlodipine group vs placebo ( P = .12 ) , with significantly less progression in the subgroup with systolic blood pressures greater than the mean ( P = .02 ) . Compared with baseline , IVUS showed progression in the placebo group ( P<.001 ) , a trend toward progression in the enalapril group ( P = .08 ) , and no progression in the amlodipine group ( P = .31 ) . For the amlodipine group , correlation between blood pressure reduction and progression was r = 0.19 , P = .07 . CONCLUSIONS Administration of amlodipine to patients with CAD and normal blood pressure result ed in reduced adverse cardiovascular events . Directionally similar , but smaller and nonsignificant , treatment effects were observed with enalapril . For amlodipine , IVUS showed evidence of slowing of atherosclerosis progression The West of Scotl and Coronary Prevention Study ( WOSCOPS ) showed that pravastatin reduced the risk of coronary heart disease ( CHD ) events in 6,595 middle-aged hypercholesterolaemic men aged 45 - 64 years without prior myocardial infa rct ion followed for an average of 4.9 years . We hypothesised prospect ively ( a ) that baseline levels of haemorheological variables were related to baseline and incident CHD and to mortality ; and ( b ) that reduction in lipoproteins by pravastatin would lower plasma and blood viscosity , a potential contributory mechanism to CHD events . We therefore studied plasma and blood viscosity , fibrinogen , haematocrit , and blood cell counts at baseline and 1 year . At baseline , plasma and blood viscosity were related to risk factors , CHD measures , and claudication . On univariate analysis , baseline levels of all rheological variables ( except platelet count ) were related to incident CHD ; CHD mortality ; and total mortality . On multivariate analysis including baseline CHD and risk factors , plasma and blood viscosity , haematocrit and white cell count each remained significantly associated with incident CHD ; while fibrinogen remained an independent predictor of mortality ( all p < 0.03 ) . After one year , lipoprotein reduction by pravastatin was associated with significant reductions ( about one quarter of a st and ard deviation ) in plasma viscosity ( mean difference 0.02 mPa.s , p < 0.001 ) and in blood viscosity ( mean difference 0.06 mPa.s , p<0.001 ) , but was not associated with significant changes in other rheological variables . We therefore suggest that pravastatin therapy , which reduces elevated lipoproteins in hypercholesterolaemic men , may lower risks of CHD and mortality partly by lowering plasma and blood viscosity . Further studies are required to test this hypothesis To determine the effect of atorvastatin on blood rheology in patients with familial hypercholesterolemia ( FH ) on regular LDL apheresis , we prospect ively studied the rheological variables fibrinogen , plasma viscosity , red cell aggregation , whole blood viscosity , hematocrit and platelet aggregation in 12 patients ( two homozygous , ten heterozygous ) before and during treatment with atorvastatin .  Baseline values of red cell aggregation and whole blood viscosity were increased in FH patients on regular LDL apheresis compared with healthy controls ( P<0.05 ) , whereas fibrinogen , plasma viscosity and hematocrit were similar in the two groups . Treatment with atorvastatin reduced red cell aggregation ( P<0.01 ) , whole blood viscosity ( P<0.01 ) , plasma viscosity ( P<0.01 ) and platelet aggregation ( P<0.05 ) , but caused a slight increase in plasma fibrinogen ( by 5 % ; P<0.01 ) . Our findings suggest that atorvastatin improves blood rheology in patients with FH on regular LDL-apheresis . This improvement in blood flow properties may contribute to the well-known beneficial effects of atorvastatin on cardiovascular risk in patients with severe hyperlipidemia and atherosclerotic vascular disease Background —The Clopidogrel in Unstable angina to prevent Recurrent Events ( CURE ) trial demonstrated that clopidogrel , given early and continued long term , was superior to placebo in patients with non-ST – elevation acute coronary syndromes receiving aspirin . The purpose of the present analysis was to estimate the treatment effect Zof clopidogrel in patients who were stratified according to their risk of future cardiovascular events . Methods and Results — Patients ( n=12 562 ) who presented within 24 hours after the onset of symptoms were r and omized to receive clopidogrel ( 300 mg followed by 75 mg daily ) or placebo in addition to aspirin for 3 to 12 months . Treatment effect was analyzed in various risk groups according to the Thrombolysis in Myocardial Infa rct ion ( TIMI ) risk score . The TIMI risk model was vali date d in the CURE population ( C statistic , 0.634 ) . The primary composite outcome of cardiovascular death , myocardial infa rct ion , or stroke increased proportionally with increasing risk according to the TIMI risk score . The impact of clopidogrel versus placebo on the rate of the primary outcome was as follows : low-risk group ( TIMI score 0 to 2 ) , 4.1 % versus 5.7 % ( relative risk [ RR ] , 0.71 ; 95 % confidence interval [ CI ] , 0.52 to 0.97;P < 0.04 ) , intermediate-risk group ( TIMI score 3 to 4 ) , 9.8 % versus 11.4 % ( RR , 0.85 ; 95 % CI , 0.74 to 0.98;P < 0.03 ) , and high-risk group ( TIMI score 5 to 7 ) , 15.9 % versus 20.7 % ( RR , 0.73 ; 95 % CI , 0.60 to 0.90;P < 0.004 ) . There was no evidence of statistical heterogeneity among the groups . Conclusions —The benefit of clopidogrel demonstrated in the CURE trial is consistent in low- , intermediate- , and high-risk patients with acute coronary syndromes ( as stratified by TIMI risk score ) , thus supporting its use in all patients with documented non – ST elevation acute coronary syndromes OBJECTIVES The Circadian Anti-ischemia Program in Europe ( CAPE II ) compared the efficacy of amlodipine and diltiazem ( Adizem XL ) and the combination of amlodipine/atenolol and diltiazem ( Adizem XL)/isosorbide 5-mononitrate on exercise and ambulatory myocardial ischemia during regular therapy and after omission of medication . BACKGROUND The optimal medical therapy for ischemia suppression and the impact of irregular dosing using agents with different pharmacologic properties has not been established in patients with coronary disease . METHODS Patients with > or = 4 ischemic episodes or > or = 20 min of ST segment depression on 72-h electrocardiogram were r and omized to amlodipine 10 mg once daily or diltiazem ( Adizem XL ) 300 mg once daily in a 14-week double-blind r and omized multicountry study . In the second phase , atenolol 100 mg was added to amlodipine and isosorbide 5-mononitrate 100 mg to diltiazem ( Adizem XL ) . Ambulatory monitoring ( 72 h ) and exercise testing were repeated after both phases , on treatment and after a 24-h drug-free interval . RESULTS Both monotherapy with amlodipine and diltiazem ( Adizem XL ) were effective on symptoms and ambulatory and exercise ischemia . Combination therapy reduced ischemia further , with amlodipine/atenolol superior to diltiazem ( Adizem XL)/isosorbide 5-mononitrate . Amlodipine/atenolol was significantly superior during the drug-free interval with maintenance of ischemia reduction . CONCLUSIONS Amlodipine , with its intrinsically long half-life alone or together with beta-blocker , is likely to produce superior ischemia reduction in clinical practice when patients frequently forget to take medication or dose irregularly BACKGROUND Angiotensin-converting-enzyme inhibitors improve the outcome among patients with left ventricular dysfunction , whether or not they have heart failure . We assessed the role of an angiotensin-converting-enzyme inhibitor , ramipril , in patients who were at high risk for cardiovascular events but who did not have left ventricular dysfunction or heart failure . METHODS A total of 9297 high-risk patients ( 55 years of age or older ) who had evidence of vascular disease or diabetes plus one other cardiovascular risk factor and who were not known to have a low ejection fraction or heart failure were r and omly assigned to receive ramipril ( 10 mg once per day orally ) or matching placebo for a mean of five years . The primary outcome was a composite of myocardial infa rct ion , stroke , or death from cardiovascular causes . The trial was a two-by-two factorial study evaluating both ramipril and vitamin E. The effects of vitamin E are reported in a companion paper . RESULTS A total of 651 patients who were assigned to receive  ramipril ( 14.0 percent ) reached the primary end point , as compared with 826 patients who were assigned to receive placebo ( 17.8 percent ) ( relative risk , 0.78 ; 95 percent confidence interval , 0.70 to 0.86 ; P<0.001 ) . Treatment with ramipril reduced the rates of death from cardiovascular causes ( 6.1 percent , as compared with 8.1 percent in the placebo group ; relative risk , 0.74 ; P<0.001 ) , myocardial infa rct ion ( 9.9 percent vs. 12.3 percent ; relative risk , 0.80 ; P<0.001 ) , stroke ( 3.4 percent vs. 4.9 percent ; relative risk , 0.68 ; P<0.001 ) , death from any cause ( 10.4 percent vs. 12.2 percent ; relative risk , 0.84 ; P=0.005 ) , revascularization procedures ( 16.3 percent vs. 18.8 percent ; relative risk , 0.85 ; P<0.001 ) , cardiac arrest ( 0.8 percent vs. 1.3 percent ; relative risk , 0.62 ; P=0.02 ) , [ corrected ] heart failure (  
    Output:
    
Regarding the repolarization changes on the ECG NSTEMI shows similarities with other clinical symptoms where increased intramyocardial microvascular resistance can be supposed without coronary artery disease : false positive exercise stress test , supraventricular tachycardia , left ventricular strain and conduction disturbances .
CONCLUSION The acute treatment of NSTEMI should aim to improve the blood inflow to the stiff myocardium and /or impaired microvascular system and decrease the high microvascular resistance