Brachial approach to emergency cardiac catheterization during thrombolytic therapy for acute myocardial infarction. TAMI Study Group

The use of the brachial approach to acute coronary intervention has not been previously studied. In the course of the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) trials, we used the transbrachial approach to cardiac catheterization with or without angioplasty in 202 of 704 (28.6%) patients. The baseline characteristics of age, sex, risk factors, medical history, time from symptom onset to therapy, and left ventricular function were similar for the 2 different approaches. Time from therapy to coronary angiography was not delayed by the brachial approach compared with the femoral approach: 97.1 +/- 26 min vs. 99.9 +/- 133.8 min, respectively. Chemical patency was established in 78 vs. 73% of patients and technical success with acute PTCA with the brachial approach was 89% vs. 78% with the femoral approach. Clinical outcomes were quite similar with respect to death (6 vs. 6%), reocclusion (10 vs. 14%), and emergency coronary bypass surgery (5 vs. 6%). Baseline hematocrit was 43.9 +/- 4.4 and 43.5 +/- 4.8, respectively with a nadir of 32.9 +/- 5.6 vs. 33.0 +/- 5.4. The need for vascular repair occurred in 1% vs. 3% of patients and retroperitoneal hemorrhage was documented in 1% vs. 1% of patients. This study indicates that in the hands of experienced operators the transbrachial approach to acute coronary intervention in the acute phase of treatment with thrombolytic therapy can be used with equal risks and efficacy as the femoral approach.     

Relation of temporal creatine kinase-MB release and outcome after thrombolytic therapy for acute myocardial infarction. TAMI Study Group

Measuring biochemical marker release after acute myocardial infarction helps in estimating infarct size and prognosis. We sought to relate in-hospital outcomes and curve-fitted creatine kinase (CK)-MB variables after thrombolysis. We measured CK-MB mass initially and at 30 and 90 minutes, and at 3, 8, and 20 hours after thrombolysis in 130 patients also undergoing cardiac catheterization at 90 minutes and at 5 to 7 days. Data were fitted, and maximums and curve areas calculated. CK-MB maximums related to infarct location (p = 0.014) and time to therapy (p = 0.002); curve area did not. Neither maximums nor curve area related to Thrombolysis in Myocardial Infarction trial flow grade at 90 minutes. Maximums related to ejection fraction at 90 minutes (p = 0.0004) and at 5 to 7 days (p = 0.0014), as did curve area (p = 0.0076 and 0.030, respectively). Maximums related to infarct zone function at 90 minutes (p = 0.024) and at 5 to 7 days (p = 0.042); curve area related only at 90 minutes (p = 0.027). Both maximums and curve area predicted congestive heart failure (p = 0.008 and p = 0.042, respectively) and a composite of congestive heart failure or death (p = 0.004 and p = 0.047, respectively); however, after adjusting for maximums, curve area no longer predicted congestive heart failure (p = 0.92). Maximums predicted the composite outcome after adjustment for curve area, and showed a trend toward predicting congestive heart failure (p = 0.089). We conclude that CK-MB maximums relate to infarct zone function, left ventricular function, and in-hospital outcomes after thrombolysis for acute myocardial infarction.     

Consequences of reocclusion after successful reperfusion therapy in acute myocardial infarction. TAMI Study Group

To determine the clinical consequences of reocclusion of an infarct-related artery after reperfusion therapy, we evaluated 810 patients with acute myocardial infarction. Patients were admitted into four sequential studies with similar entry criteria in which patency of the infarct-related artery was assessed by coronary arteriography 90 minutes after onset of thrombolytic therapy. Successful reperfusion was established acutely in 733 patients. Thrombolytic therapy included tissue-type plasminogen activator (t-PA) in 517, urokinase in 87, and a combination of t-PA and urokinase in 129 patients. All patients received aspirin, intravenous heparin and nitroglycerin, and diltiazem during the recovery phase. A repeat coronary arteriogram was performed in 88% of patients at a median of 7 days after the onset of symptoms. Reocclusion of the infarct-related artery occurred in 91 patients (12.4%), and 58% of these were symptomatic. Angiographic characteristics at 90 minutes after thrombolytic therapy that were associated with reocclusion compared with sustained coronary artery patency were right coronary infarct-related artery (65% versus 44%, respectively) and Thrombolysis in Myocardial Infarction (TIMI) flow 0 or 1 (21% versus 10%, respectively) before further intervention. Median (interquartile value) degree of stenosis in the infarct-related artery at 90 minutes was similar between groups: 99% for reoccluded (value, 90/100%) compared with 95% for patent (value, 80/99%). Patients with reocclusion had similar left ventricular ejection fractions compared with patients with sustained patency at follow-up. However, patients with reocclusion at follow-up had worse infarct-zone function at -2.7 (value, -3.2/-1.8) versus -2.4 (SD/chord) (value, -3.1/-1.3) (p = 0.016). The recovery of both global and infarct-zone function was impaired by reocclusion of the infarct-related artery compared with maintained patency; median delta ejection fraction was -2 compared with 1 (p = 0.006) and median delta infarct-zone wall motion was -0.10 compared with 0.34 SD/chord (p = 0.011), respectively. In addition, patients with reocclusion had more complicated hospital courses and higher in-hospital mortality rates (11.0% versus 4.5%, respectively; p = 0.01). We conclude that reocclusion of the infarct-related artery after successful reperfusion is associated with substantial morbidity and mortality rates. Reocclusion is also detrimental to the functional recovery of both global and infarct-zone regional left ventricular function. Thus, new strategies in the postinfarction period need to be developed to prevent reocclusion of the infarct-related artery.     

The thrombolysis and angioplasty in myocardial infarction (TAMI) trial: review and nursing implications

The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Trial was a multicenter, randomized trial designed with the purpose of determining the clinical impact of immediate or deferred angioplasty on left ventricular function following successful myocardial reperfusion with tissue plasminogen activator (t-PA). Results from this trial indicate that immediate coronary angioplasty following successful thrombolysis, when coronary artery anatomy is suitable, offers no advantage over delayed elective angioplasty. The purpose of this article is to discuss and critically review the TAMI trial. Details of the trial will be discussed followed by a critique and implications for nursing.     

Coronary bypass surgery improves global and regional left ventricular function following thrombolytic therapy for acute myocardial infarction. TAMI Study Group

Coronary bypass surgery was performed prior to hospital discharge in 303 (22%) of 1387 consecutive patients enrolled in the TAMI 1 to 3 and 5 trials of intravenous thrombolytic therapy for acute myocardial infarction. Bypass surgery was of emergency nature (less than 24 hours from treatment with intravenous thrombolytic therapy) in 36 (2.6%) and was deferred (greater than 24 hours) in 267 (19.3%) patients. The indications for bypass surgery included failed angioplasty (12%); left main or equivalent coronary disease (9%); complex or multivessel coronary disease (62%); recurrent postinfarction angina (13%); and refractory pump dysfunction, mitral regurgitation, ventricular septal rupture or abnormal predischarge functional test (1% each). Although patients having bypass surgery were older (59.5 +/- 9.8 versus 56.0 +/- 10.2 years, (p less than 0.0001), had more extensive coronary artery disease (46% with three-vessel disease versus 11%, (p less than 0.0001), had more frequent diabetes mellitus (19% versus 15%, (p = 0.048), had more prior infarctions (p less than 0.0001), had more severe initial depression in global left ventricular ejection fraction (48.0 +/- 11.9% versus 51.8 +/- 11.9%, p = 0.0002), and regional infarct zone (-2.7 +/- 0.94 versus -2.5 +/- 1.1 SD/chord, p = 0.02) and noninfarct zone function (-0.36 +/- 1.8 versus 0.43 +/- 1.6 SD/chord, p less than 0.0001) than patients not having coronary bypass surgery, no difference in the incidence of death in hospital (7% surgical versus 6% nonsurgical) or death at long-term follow-up of hospital survivors (7% surgical versus 6% nonsurgical) was noted between groups. Surgical patients demonstrated a greater degree of recovery in left ventricular ejection fraction (3.4 +/- 9.8% versus 0.16 +/- 8.5%, p = 0.036) and infarct zone regional function (0.71 +/- 1.1 versus 0.34 +/- 0.99 SD/chord, p = 0.001) when immediate (90 minutes following initiation of thrombolytic therapy) and predischarge (7 to 14 days after treatment) contrast left ventriculograms were compared than did patients who received only intravenous thrombolytic therapy with or without coronary angioplasty. These data suggest a beneficial influence of coronary bypass surgery on left ventricular function and possibly on the clinical outcome of patients initially treated with intravenous thrombolytic therapy for acute myocardial infarction.     

Combined thrombolytic therapy and coronary angioplasty for acute myocardial infarction

From September, 1983, to August, 1984, combined thrombolytic therapy and percutaneous transluminal coronary angioplasty was used to treat 22 cases of acute myocardial infarction. Initial coronary angiograms showed total obstruction in 13 and severe stenosis in 9. Intracoronary infusion of urokinase reopened 7 of 13 totally occluded lesions but left a residual severe stenosis. Coronary angioplasty opened all of the remaining totally obstructed lesions and decreased the stenosis in 14 of 16 stenosed lesions. These procedures were performed 0.5 to 24 hours after the onset of chest pain. Lesions were not successfully dilated in two patients, because of arterial dissection in one and rethrombus formation in the other. One patient died from progressive hypotension beginning during the procedure, despite technically successful coronary angioplasty. Eighteen of the 20 successfully dilated lesions were patent at repeat angiography performed 1 to 3 weeks later. One successfully dilated lesion occluded 8 days after the procedure and was redilated by a larger sized balloon.     

急诊冠状动脉腔内成形术与溶栓治疗急性心肌梗塞的临床分析

目的　探讨急诊冠状动脉腔内成形术 (PTCA)对急性心肌梗塞 (AMI)的临床疗效。方法　对 5 2例AMI患者行急诊PTCA治疗 (PTCA组 ) ,5 8例AMI患者行溶栓治疗 (溶栓组 ) ,比较两组住院和随诊期间的情况。结果　PTCA组住院期间死亡 3例 ,抢救成功率为 94 2 % ,平均住院天数为 14 6天(9 5± 4 2天 ) ,左室射血量数 (LVEF)为 45 5 %± 4 3% ;随诊 2～ 18个月 ,心绞痛发作 3例 ,择期再次PTCA 3例。溶栓组住院期间死亡 8例 ,抢救成功率为 86 2 % ,平均住院天数为 2 6 4天 (17 2± 7 5天 ) ,LVEF为 37 6 %± 6 2 % ;随诊 2～ 18个月 ,心绞痛发作 17例 ,行择期PTCA 17例。结论　急性心肌梗塞急诊PTCA可即时开通梗塞相关血管 (IRA) ,大大降低AMI的住院死亡率 (P <0 0 1) ,缩短住院天数 (P <0 0 1) ,有效保护心脏功能 (P <0 0 5 )。     

Complete atrioventricular block complicating inferior wall acute myocardial infarction treated with reperfusion therapy. TAMI Study Group

Previous studies report larger myocardial infarcts and increased in-hospital mortality rates in patients with inferior wall acute myocardial infarction (AMI) and complete atrioventricular block (AV), but the clinical implications of these complications in patients treated with reperfusion therapy have not been addressed. The clinical course of 373 patients--50 (13%) of whom developed complete AV block--admitted with inferior wall AMI and given thrombolytic therapy within 6 hours of symptom onset was studied. Acute patency rates of the infarct artery after thrombolytic therapy were similar in patients with or without AV block. Ventricular function measured at baseline and before discharge in patients with complete AV block showed a decrement in median ejection fraction (-3.5 vs -0.4%, p = 0.03) and in median regional wall motion (-0.14 vs +0.24 standard deviations/chord, p = 0.05). The reocclusion rate was higher in patients with complete AV block (29 vs 16%, p = 0.03). Patients with complete AV block had more episodes of ventricular fibrillation or tachycardia (36 vs 14%, p less than 0.001), sustained hypotension (36 vs 10%, p less than 0.001), pulmonary edema (12 vs 4%, p = 0.02) and a higher in-hospital mortality rate (20 vs 4%, p less than 0.001), although the mortality rate after hospital discharge was identical (2%) in the 2 groups. Multivariable logistic regression analysis revealed that complete AV block was a strong independent predictor of in-hospital mortality (p = 0.0006). Thus, despite initial successful reperfusion, patients with inferior wall AMI and complete AV block have higher rates of in-hospital complications and mortality.     

Reperfusion therapy in elderly patients with acute myocardial infarction: a randomized comparison of primary angioplasty and thrombolytic therapy

OBJECTIVES: This study sought to determine the short- and long-term outcome of primary coronary angioplasty and thrombolytic therapy for acute myocardial infarction (AMI) in patients older than 75 years of age. BACKGROUND: The benefit of reperfusion therapy in elderly patients with AMI is uncertain, although elderly people account for a large proportion of deaths. METHODS: We randomly assigned a total of 87 patients with an AMI who were older than 75 years to treatment with angioplasty or intravenous (IV) streptokinase. Clinical outcome was measured by taking the end points of death and the combination of death, reinfarction or stroke during follow-up. RESULTS: The primary end point, a composite of death, reinfarction or stroke, at 30 days had occurred in 4 (9%) patients in the angioplasty group as compared with 12 (29%) in the thrombolysis group (p = 0.01, relative risk [RR]: 4.3, 95% confidence interval [CI]: 1.2 to 20.0). At one year the corresponding figures were 6 (13%) and 18 (44%), respectively (p = 0.001, RR: 5.2, 95% CI: 1.7 to 18.1). CONCLUSIONS: In this series of patients with AMI who were older than 75 years, primary coronary angioplasty had a significant clinical benefit when compared with IV streptokinase therapy.     

Intracoronary thrombolytic therapy in acute myocardial infarction: a prospective, randomized, controlled trial

A prospective, randomized trial was designed to assess the efficacy of intracoronary thrombolytic therapy with streptokinase (STK) in acute myocardial infarction. Sixty-four patients with acute myocardial infarction were randomized within 6 hours of onset of symptoms to 1 of 3 groups. Sixteen patients were treated by conventional means (control group). Nineteen patients underwent coronary arteriography and received corticosteroids and intracoronary and intravenous nitroglycerin (NTG group). Twenty-nine patients received management identical to that of the NTG group, with the addition of intracoronary STK therapy (STK group). Recanalization was demonstrated in 21 of 29 patients (72%) in the STK group. Global and regional ejection fraction (EF) was determined by radionuclide ventriculography before any intervention and 7 to 10 days later. No significant improvement in global EF was achieved in the control and NTG groups. In STK patients as a group, global EF did not increase significantly; however, in patients recanalized with STK, EF improved from 42 +/- 17% to 49 +/- 16% (p = 0.023). All groups showed wide variability of response. Improvement in global EF of more than 5% was noted in 44% of patients recanalized with STK. When subgrouped on the basis of initial global EF of 45% or less or more than 45%, only patients recanalized with STK with an initial EF of 45% or less had an improved global EF (from 30 +/- 10% to 42 +/- 10%, p = 0.015).(ABSTRACT TRUNCATED AT 250 WORDS)     

Sequential combination thrombolytic therapy for acute myocardial infarction: results of the pro-urokinase and t-PA enhancement of thrombolysis (PATENT) trial

Objectives. The present study was designed to test the efficacy and safety of a sequential combination of recombinant tissue-type plasminogen activator (rt-PA) and pro-urokinase in patients with acute myocardial infarction.Background. Efforts continue to identify a thrombolytic regimen that induces rapid, complete and sustained coronary artery patency in acute myocardial infarction. The two endogenous plasminogen activators rt-PA and pro-urokinase have been shown experimentally to induce fibrinolysis by sequential and complementary mechanisms. As a result, certain combinations of these activators have been found to be synergistic in vitro and in vivo.Methods. In a multicenter observational study with core facilities for angiographic and laboratory analysis, 101 patients with acute myocardial infarction were enrolled and gives a low dose bolus of rt-PA (5 to 10 mg) followed by a 90-min infusion of pro-urokinase (40 mg/h). All patients received intravenous heparin and oral aspirin. Coronary angiography was performed in all patients at 90 min.Results. Angiography at 90 min showed the infarct-related artery to be patent (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3 flow) in 77% of patients, and 60% achieved TIMI grade 3 flow. At one center, angiography was repeated at 24 h to detect a possible reocclusion. All 28 patients with a patent infarct-related artery at 90 min had patency at 24 h (82% achieved TIMI grade 3 flow). Treatment was well tolerated, with bleeding complications essentially confined to arterial puncture site hematomas. There was only one in-hospital death.Conclusions. A sequential combination of low dose rt-PA and reduced-dose pro-urokinase produced a high TIMI 3 patency rate, was well tolerated and was associated with a low reocclusion rate.     

Prognostic implications and predictors of enhanced regional wall motion of the noninfarct zone after thrombolysis and angioplasty therapy of acute myocardial infarction. The TAMI Study Groups

Although impairment of left ventricular function in acute myocardial infarction is closely related to extent of necrosis, function in the noninfarct 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 Infarction (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 noninfarct 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 noninfarct zone was the absence of multivessel disease (p = 0.0001). Clinical factors that were related weakly to noninfarct zone function included female gender (p = 0.08) and higher flow in the infarct artery (p = 0.03). Neither the degree of infarct zone dysfunction nor infarct location was associated with hyperkinesis of the noninfarct zone. In hospital, mortality was closely related to function in the noninfarct zone (p = 0.006), ejection fraction (p = 0.025), and the number of diseased vessels (p = 0.009) but was not related to infarct zone function (p = 0.128).(ABSTRACT TRUNCATED AT 250 WORDS)     

Delays in thrombolytic therapy for acute myocardial infarction in Finland. Results of a national thrombolytic therapy delay study

Objective To determine lengths and causes of pre- and in-hospital delaysin thrombolytic treatment. Design A prospective national survey covering 48 of the 51 Finnishuniversity, central and general hospitals to obtain basic databefore the start of a public campaign to shorten patient-relateddelay in acute myocardial infarction. Subjects One thousand and twelve consecutive patients with acute myocardialinfarction who received thrombolytic therapy over 3 months in1995 and who represent 40% of all patients with confirmed acutemyocardial infarction. Results The median interval between onset of infarction symptoms andinitiation of thrombolytic therapy was 160min (30–647).Only 13% of the patients received thrombolysis within 60minand 38% within 120min. The median time from the onset of symptomsto the call for help was 60min (5–491), and no differencewas found in patients with or without a history of previousmyocardial infarction (60 and 64min, respectively). Only 52%of the patients called to the dispatch centre. The median delayfrom calling for help to hospital arrival was 40min (10–170).The median in-hospital door-to-needle thrombolysis delay was40min (12–196). In 13% of hospitals the median delay wasmore than 60min. The emergency physician encountered difficultiesin decision making in 33% of cases. Conclusions Only 38% of the patients received thrombolysis within 2h ofonset of symptoms. Patient-related delay before they soughthelp accounted for the major portion of the total treatmentdelay. Thus the findings emphasize the importance of promptaction when people are confronted with an acute heart attack.Reorganizing the emergency medical service and emergency departmentroutines is also a necessary target to shorten thrombolysisdelays. The delay attributable to transporting patients couldbe shortened by initiating thrombolytic treatment in the pre-hospitalsetting. In Finnish hospitals, door-to-needle delay was acceptablein cases with clear indications for thrombolysis. However, emergencyphysicians often had diagnostic difficulties, which led to remarkablylonger in-hospital delays.     

Evaluation of lesions suitable for percutaneous transluminal coronary angioplasty after thrombolytic therapy of acute myocardial infarction

Forty-two patients of acute myocardial infarction (AMI) and clinically successful thrombolysis underwent coronary angiography 7.6 +/- 3.6 days after the AMI. The infarct related artery was patent in 33 of 42 (78.5%) patients, and 27 of these 33 (82%) had residual diameter stenosis of 70 per cent or more. Arteries showing more than 70 per cent luminal diameter narrowing were considered suitable for percutaneous transluminal coronary angioplasty (PTCA) if the lesion was less than 1 cm in length and there was no significant left main or distal lesion. Based on the above criteria, 22 of the 33 patients (66%) with recanalised infarct-related artery were found to have lesions suitable for PTCA. Thus, after successful thrombolysis, significant proportion of patients of acute myocardial infarction have residual lesions that are suitable for PTCA.     

不同溶栓药物和剂量治疗急性心肌梗塞239例对比分析

２３９例急性心肌梗塞（ＡＭＩ）患者接受溶栓治疗，其中采用日本尿激酶（ＵＫ）９６万Ｕ３５例，１５０万Ｕ５５例；国产ＵＫ９６万Ｕ１５例，１５０万Ｕ５３例；德国链激酶（ＳＫ）１５０万Ｕ６６例；国产重组链激酶（ｒＳＫ）１５０万Ｕ１５例。对不同剂量及不同溶栓剂的疗效与安全性进行对比分析发现：１９９２年前国产ＵＫ９６万Ｕ比日本进口ＵＫ９６万Ｕ血管再通率低（２０．０％ｖｓ５１．４％Ｐ＜０．０１）。１９９２年后国产ＵＫ剂量增至１５０万Ｕ，血管再通率显著提高（５６．６％ｖｓ２０．０％Ｐ＜０．０１），与进口ＵＫ１５０万Ｕ的疗效与安全性相近（Ｐ＞０．０５）；国产ｒＳＫ１５０万Ｕ与进口ＳＫ１５０万Ｕ的血管再通率相似（７３．３％ｖｓ６５．２％Ｐ＞０．０５）；且比国产ＵＫ１５０万Ｕ的血管再通率明显提高（７３．３％ｖｓ５６．６％Ｐ＜０．０５），虽然ｒＳＫ轻度出血高于ＵＫ（２６．７％ｖｓ９．４％Ｐ＜０．０１），偶有低血压发生，但不影响疗效。国产ｒＳＫ与ＵＫ比进口ＳＫ和ＵＫ价格低２～４倍。因此认为，国产ｒＳＫ和ＵＫ是较为有效、安全、价廉且适合我国国情的溶栓药物。     

Long-term follow-up of patients with acute myocardial infarction treated with primary angioplasty or thrombolysis. Results of the MITRA trial

Long-term follow-up after treatment with primary angioplasty compared to treatment with thrombolysis in patients with acute myocardial infarction (AMI) remains still to be determined. We therefore analyzed the data of the "Maximal Individual Therapy" in Acute Myocardial Infarction (MITRA-1) Registry. Follow-up data for a median of 17 months after discharge were available in 2090 out of 2195 (95%) AMI patients treated with thrombolysis, as well as 293 out of 312 patients (94%) treated with primary angioplasty. There were only small differences in patient characteristics between the two treatment groups. Compared to patients treated with thrombolysis, those treated with primary angioplasty had a higher prevalence of prior myocardial infarction (16.4% versus 12.2%, p = 0.04), longer prehospital delay: 10 minutes (130 minutes versus 120 minutes, p = 0.002), and a longer door-to-treatment time: 45 minutes (p < 0.001). Primary angioplasty patients were more likely to be treated with beta-blockers (primary angioplasty 79.8% versus thrombolysis 66.2%, p < 0.001) or statins (24.5% versus 16.5%, p < 0.001). There was no difference between the treatment groups for total mortality (p = 0.90) nor for the combined endpoint of death or re-infarction (p = 0.85). However, the combined endpoint of death, re-infarction or percutaneous coronary intervention or coronary bypass surgery was significantly lower in the primary angioplasty group (primary angioplasty 25.6% versus thrombolysis 32.3%, univariate odds ratio 0.72, 95% CI: 0.55-0.95, p = 0.02). This result was confirmed by multivariate analysis after adjusting for confounding parameters (multivariate odds ratio: 0.62, 95% CI: 0.42-0.91). The beneficial effect of primary angioplasty compared to thrombolysis achieved during the hospital stay after an AMI is maintained during a 17 month follow-up. AMI patients treated with thrombolysis were more likely to be treated with either percutaneous coronary intervention or coronary bypass surgery after discharge.     

A prospective, placebo-controlled, randomized trial of intravenous streptokinase and angioplasty versus lone angioplasty therapy of acute myocardial infarction.

BACKGROUND. The value of routine administration of intravenous thrombolytic agents during percutaneous transluminal coronary angioplasty (PTCA) therapy of acute myocardial infarction (MI) has not been determined. Therefore, we prospectively randomized 122 patients with evolving MI to PTCA therapy with or without adjunctive intravenous streptokinase therapy. METHODS AND RESULTS. Patients with ECG ST segment elevation who presented within 4 hours of symptom onset, had no contraindication to thrombolytic therapy, and were not in cardiogenic shock were enrolled. They were treated immediately with intravenous heparin (10,000 units) and oral aspirin (325 mg) and randomized to treatment with placebo or streptokinase (1.5 M units) administered intravenously over 30 minutes. Patients then were taken immediately to the catheterization laboratory, and those with suitable coronary anatomy underwent immediate PTCA. Subsequent clinical course, serial radionuclide ventriculography, and 6-month repeat angiography were analyzed. A total of 106 patients were treated with PTCA. Use of PTCA was similar for placebo (92%) and streptokinase (83%) groups. Angioplasty was successful in 95% of patients, with no difference in placebo (93%) and streptokinase (98%) groups. Serial radionuclide ventriculography demonstrated no difference in 24-hour (52 +/- 12% versus 50 +/- 12%) or 6-week (51 +/- 12% versus 51 +/- 13%) ejection fraction values for placebo and streptokinase groups, respectively. Contrast ventriculography demonstrated improvement in immediate (54 +/- 12%) versus 6-month (60 +/- 15%, p < 0.05) values for the overall group. No differences in 6-month values were present (58 +/- 15% versus 62 +/- 15%, p = NS) for placebo and streptokinase groups, respectively. Coronary angiography was performed in 75% of the 90 patients eligible for restudy. Arterial patency was 87% at 6 months, and coronary restenosis was present in 38% of patients. No differences in chronic patency or restenosis were detected for the two treatment groups. Although adjunctive intravenous streptokinase therapy did not improve outcome, it did complicate the hospital course. Hospitalization was longer (9.3 +/- 5.0 versus 7.7 +/- 4.4 days, p = 0.046) and more costly ($25,191 +/- 15,368 versus $19,643 +/- 7,250, p < 0.02). Transfusion rate was higher (39% versus 8%, p = 0.0001) and need for emergency coronary bypass surgery was greater (10.3% versus 1.6%, p = 0.03) for the streptokinase-treated patients. CONCLUSIONS. Adjunctive intravenous streptokinase therapy does not enhance early preservation of ventricular function, improve arterial patency rates, or lower restenosis rates after PTCA therapy of acute MI. Hospital course is longer, more expensive, and more complicated. For these reasons, PTCA therapy of acute MI should not be routinely performed with adjunctive intravenous streptokinase therapy.