***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: Although impairment of left ventricular function in acute myocardial infa rct ion is closely related to extent of necrosis , function in the noninfa rct zone also contributes to global performance and thus may be of prognostic importance . We evaluated left ventricular regional wall motion by the centerline chord method in 332 patients treated with intravenous tissue-type plasminogen activator ( t-PA ) in the multicenter Thrombolysis and Angioplasty in Myocardial Infa rct ion ( TAMI ) I trial . All patients had acute contrast ventriculograms of suitable quality for analysis , and 266 patients had paired acute and day 7 ventriculograms .  Enhanced function of the noninfa rct zone was present during acute catheterization ( + 0.3 SD/chord ) and was associated with preservation of the acute ejection fraction ( p = 0.0001 ) . Multiple linear regression analysis revealed the most powerful clinical factor associated with enhanced function of the noninfa rct zone was the absence of multivessel disease ( p = 0.0001 ) . Clinical factors that were related weakly to noninfa rct zone function included female gender ( p = 0.08 ) and higher flow in the infa rct artery ( p = 0.03 ) . Neither the degree of infa rct zone dysfunction nor infa rct location was associated with hyperkinesis of the noninfa rct zone . In hospital , mortality was closely related to function in the noninfa rct zone ( p = 0.006 ) , ejection fraction ( p = 0.025 ) , and the number of diseased vessels ( p = 0.009 ) but was not related to infa rct zone function ( p = 0.128 ) . ( ABSTRACT TRUNCATED AT 250 WORDS OBJECTIVES To test our hypothesis that the development of vulnerable plaques is not limited to the culprit lesions , but is a pan-coronary process , we directly observed all three major coronary arteries by angioscopy and evaluated the prevalence of yellow plaques in patients with myocardial infa rct ion ( MI ) . BACKGROUND Although pathologic studies have suggested that the disruption of atheromatous plaque plays a major role in the development of acute MI , the prevalence of yellow plaques in the whole coronary arteries of patients with MI has not been clarified . METHODS Thirty-two patients undergoing follow-up catheterization one month after the onset of MI were prospect ively and consecutively enrolled in this study . The prevalence of yellow plaques and thrombus in the major coronary arteries was successfully evaluated in 20 patients ( 58 coronary arteries , 21 culprit lesions ) by coronary angioscopy .  The diameter stenosis ( DS ) of the culprit lesions and the maximal diameter stenosis ( maxDS ) of nonculprit segments were angiographically measured for each coronary artery . RESULTS The DS of the culprit lesions and maxDS were 27 + /- 17 % and 19 + /- 13 % , respectively . Yellow plaques and thrombus were detected in 19 ( 90 % ) and 17 ( 81 % ) of 21 culprit lesions , respectively . Yellow plaques were equally prevalent in the infa rct -related and non-infa rct -related coronary arteries ( 3.7 + /- 1.6 vs. 3.4 + /- 1.8 plaques/artery ) . However , thrombus was only detected in the nonculprit segments of one ( 2 % ) coronary artery . CONCLUSIONS In patients with MI , all three major coronary arteries are widely diseased and have multiple yellow though nondisrupted plaques . Acute MI may represent the pan-coronary process of vulnerable plaque development Results of recent studies have suggested that routine cardiac catheterization may be unnecessary after reperfusion therapy for acute myocardial infa rct ion . Therefore to better define the short-term prognostic value of early coronary angiography , and specifically the prognostic significance of multivessel coronary artery disease , the angiographic findings of 855 patients consecutively enrolled in five phases of the TAMI study were correlated with their in-hospital outcome . All patients received intravenous thrombolytic therapy ( tissue plasminogen activator , urokinase , or both agents ) and underwent cardiac catheterization within 90 minutes of the initiation of therapy . Multivessel disease , defined as the presence of greater than or equal to 75 % luminal diameter stenosis in two or more major epicardial arteries , was documented in 236 patients . When compared with the group of patients without multivessel disease , this group had a higher prevalence of coronary risk factors and more frequently had a history of antecedent ischemic chest pain . Although the severity of the infa rct zone dysfunction was similar in the two groups ( -2.77 + /- 1.00 vs -2.50 + /- 1.09 SD/chord , p = NS ) , global left ventricular ejection fraction was lower in the group with multivessel disease ( 48.6 + /- 12.4 % vs 51.8 + /- 10.6 % , p less than 0.01 ) . This was associated with a significant difference in the function of the noninfa rct zone . Whereas this region was hyperkinetic in the group with minimal or single-vessel disease , it was hypocontractile or dyskinetic in those with multivessel disease ( + 0.66 + /- 1.53 vs -0.52 + /- 1.73 SD/chord , p = 0.0001 ) . ( ABSTRACT TRUNCATED AT 250 WORDS OBJECTIVES This study was design ed to assess the prevalence and clinical significance of exaggerated nonculprit lesion stenosis in the setting of acute ( < 12 h ) myocardial infa rct ion ( AMI ) . BACKGROUND Although microvascular spasm may reduce nonculprit artery flow during AMI , it is unknown whether increased tone may exaggerate nonculprit lesion severity . METHODS In patients with additional angiography within nine months of AMI , and significant nonculprit lesions imaged in matching views , stenosis severity was compared between studies in a r and om blinded fashion using vali date d quantitative coronary angiography software . Baseline demographics , medications , hemodynamics at each study , and clinical status at follow-up ( infa rct /unstable angina/stable angina ) were used to determine the independent influence of the infa rct presentation on stenosis exaggeration . RESULTS From 548 patients with AMI ( 1/99 to 6/01 , 321 with multivessel disease ) , 112 had additional angiography ; of these 48 had 59 lesions suitable for analysis . Between infa rct and noninfa rct angiograms there was a significant change in minimal lumen diameter ( 1.53 + /- 0.51 mm vs. 1.78 + /- 0.65 mm , p < 0.001 ) and percentage stenosis ( 49.3 + /- 14.5 % vs. 40.4 + /- 16.6 % , p < 0.0001 ) of the nonculprit lesion without significant change in reference segment diameter , which was not predicted by changes in medication or hemodynamics . Twenty-one percent of patients had lesions > 50 % at AMI that were < 50 % at non-AMI angiography . Infa rct versus noninfa rct setting was the only significant independent predictor of change in nonculprit stenosis . CONCLUSIONS Significant exaggeration of nonculprit lesion stenosis severity occurs at infa rct angiography , which may affect revascularization decision making in an appreciable number of patients Background Few reports described outcomes of complete compared with infa rct -related artery (IRA)-only revascularisation in patients with ST-elevation myocardial infa rct ion ( STEMI ) and multivessel coronary artery disease ( CAD ) . Moreover , no studies have compared the simultaneous treatment of non-IRA with the IRA treatment followed by an elective procedure for the other lesions ( staged revascularisation ) . Methods The outcomes of 214 consecutive patients with STEMI and multivessel CAD undergoing primary angioplasty were studied . Before the first angioplasty patients were r and omly assigned to three different strategies : culprit vessel angioplasty-only ( COR group ) ; staged revascularisation ( SR group ) and simultaneous treatment of non-IRA ( CR group ) . Results During a mean follow-up of 2.5 years , 42 ( 50.0 % ) patients in the COR group experienced at least one major adverse cardiac event ( MACE ) , 13 ( 20.0 % ) in the SR group and 15 ( 23.1 % ) in the CR group , p<0.001 . Inhospital death , repeat revascularisation and re-hospitalisation occurred more frequently in the COR group ( all p<0.05 ) , whereas there was no significant difference in re-infa rct ion among the three groups . Survival free of MACE was significantly reduced in the COR group but was similar in the CR and SR groups . Conclusions Culprit vessel-only angioplasty was associated with the highest rate of long-term MACE compared with multivessel treatment . Patients scheduled for staged revascularisation experienced a similar rate of MACE to patients undergoing complete simultaneous treatment of non-IRA AIMS To examine the incidence of and propensity for non-culprit interventions performed at the time of the  primary percutaneous coronary intervention ( PCI )  and its association with 90-day outcomes . METHODS AND RESULTS We examined the incidence , propensity for , and associated 90-day outcomes following non-culprit interventions performed at the time of primary PCI among ST-elevation myocardial infa rct ion patients with multi-vessel coronary artery disease ( MVD ) . Of the 5373 patients who underwent primary PCI in the APEX-AMI trial , 2201 had MVD . Of those , 217 ( 9.9 % ) underwent non-infa rct -related arteries ( IRA ) PCI , whereas 1984 ( 90.1 % ) underwent PCI of the IRA alone . Ninety-day death and death/CHF/shock were higher in the non-IRA group compared with the IRA-only PCI group ( 12.5 vs. 5.6 % , P ( log-rank ) < 0.001 and 17.4 vs. 12.0 % , P ( log-rank ) = 0.020 , respectively ) . After adjusting for patient and procedural characteristics as well as propensity for performing non-IRA PCI , this procedure remained independently associated with an increased hazard of 90-day mortality [ adjusted hazard ratio 2.44 , 95 % CI ( 1.55 - 3.83 ) , P < 0.001 ] . CONCLUSION Non-culprit coronary interventions were performed at the time of primary PCI in 10 % of MVD patients and were significantly associated with increased mortality . Our data support current guideline recommendations discouraging the performance of such procedures in stable primary PCI patients . Prospect i ve r and omized study of this issue may be warranted BACKGROUND AMI reperfusion by thrombolysis does not improve TIMI flow and LV function . The role of infa rct -related artery ( IRA ) stenosis and superimposed changes in coronary vasomotor tone in maintaining LV dysfunction must be eluci date d. METHODS AND RESULTS Forty patients underwent diagnostic angiography 24 hours after thrombolysis .  Seventy-two hours after thrombolysis , the culprit lesion was dilated with coronary stenting . During angioplasty , LV function was monitored by transesophageal echocardiography . Percent regional systolic thickening was quantitatively assessed before PTCA , soon after stenting , 15 minutes after stenting , and after phentolamine 12 microg/kg IC ( n=10 ) , the alpha1-blocker urapidil 600 microg/kg IV ( n=10 ) , or saline ( n=10 ) . Ten patients pretreated with beta-blockers received urapidil 10 mg IC . Coronary stenting significantly improved thickening in IRA-dependent and in non-IRA-dependent myocardium ( from 27+/-15 % to 38+/-16 % and from 40+/-15 % to 45+/-15 % , respectively ) . Simultaneously , TIMI frame count decreased from 39+/-11 and 40+/-11 in the IRA and non-IRA , respectively , to 23+/-10 and 25+/-7 ( P<0.05 ) . Fifteen minutes after stenting , thickening worsened in both IRA- and non-IRA-dependent myocardium ( to 19+/-14 % and 28+/-14 % , P<0.05 ) , and TIMI frame count returned , in both the IRA and non-IRA , to the values obtained before stenting . Phentolamine and urapidil increased thickening to 36+/-17 % and 41+/-14 % in IRA and to 48+/-11 % and 49+/-17 % in non-IRA myocardium respectively , and TIMI frame count decreased to 16+/-6 and to 17+/-5 , respectively . Changes were attenuated with beta-blocker pretreatment . CON 
    Output:
    
There is paucity of r and omized data to guide management of STEMI patients with multivessel disease .
SS-PCI group in cohort studies has higher baseline risk compared to IRA-PCI .
The primary end point is higher for SS-PCI in observational cohort studies but this difference did not persist after exclusion of shock patients and for analysis limited to r and omized controlled trials .