Emergency coronary artery bypass surgery after intracoronary thrombolysis for evolving myocardial infarction.

Sixteen patients underwent emergency coronary artery bypass surgery immediately after intracoronary streptokinase infusion for acute evolving myocardial infarction. Of these, 11 patients had 70% residual stenosis in the recanalised vessel, and in five thrombolysis was unsuccessful. There were no hospital deaths. All the patients sustained myocardial necrosis, the peak activity of creatine phosphokinase correlating with the time to reperfusion. Chest tube drainage (mean 960 ml) was significantly higher than for control patients but did not correlate with the total dosage of streptokinase. No patients had further myocardial infarction or developed recurrent angina. Selected patients may benefit from coronary bypass surgery after intracoronary streptokinase infusion. If necessary this may be performed immediately with low mortality and morbidity.     

Thrombolytic therapy in acute myocardial infarction: Review of clinical trials

Intracoronary infusion of streptokinase is associated with recanalization rates of 60 to 90% immediately after the procedure. Mortality data in published trials are conflicting. In 125 registry patients who had paired contrast ventriculograms before streptokinase infusion and hospital discharge, improvement in ejection fraction correlated with incomplete coronary obstruction before angiography, the presence of collateral vessels to the infarct area and recanalization of complete obstruction. In assessing the risk/benefit ratio of intracoronary streptokinase infusion, the risks of angiography in the setting of acute myocardial infarction, reocclusion, bleeding and such secondary interventions as angioplasty or bypass surgery must be considered. Intravenous infusion of conventional doses of streptokinase was associated with improved survival in some trials in which therapy began within 12 hours after the onset of infarction. Immediate recanalization rates in patients who received large doses of intravenous streptokinase were lower than those associated with intracoronary streptokinase infusion. The risks and benefits of high-dose intravenous streptokinase administration must still be assessed.     

Quantitative coronary angiography during intracoronary streptokinase in acute myocardial infarction: how long to continue thrombolytic therapy?

An intracoronary infusion of streptokinase is often administered in patients with acute myocardial infarction. To address the question of how long intracoronary streptokinase should be infused, we studied 13 patients with symptoms and electrocardiographic findings suggesting an evolving myocardial infarction. We used subselective catheterization techniques and made quantitative angiographic measurements of the percentage of reduction of coronary artery (CA) diameter before intracoronary streptokinase therapy, immediately after reperfusion was established, and at the completion of streptokinase infusion. Before intracoronary streptokinase and after intracoronary nitroglycerin, nine patients had 100% obstruction of the CA in the "infarct-related vessel." In seven patients reperfusion was established (25 +/- 21 min, mean +/- SD) at which time CA diameter was reduced by 77 +/- 22%. The streptokinase infusion was then continued until repeated films (every 10 to 15 min) suggested no further change at the site of CA obstruction (93 +/- 68 min). The percentage of CA diameter reduction when streptokinase infusion was discontinued was 55 +/- 32%; this value was less (P less than 0.05) than that observed early after reperfusion. These data show that after initial reperfusion was achieved by the use of intracoronary streptokinase, additional streptokinase lessened the reduction of CA diameter. Residual thrombus may be present at the narrowed CA site early after reperfusion, and further "cleanup" can be achieved by prolonging streptokinase infusion.     

Thrombolysis in an aortocoronary saphenous vein graft

Selective intracoronary infusion of streptokinase during the acute phase of myocar-dial infarction may reduce myocardial necrosis. Thrombolytic therapy of acute myocardial infarction has been primarily applied to the native coronary circulation. We are reporting successful thrombolysis in an aortocoronary saphenous vein graft 39 months after bypass surgery. Thrombosis may have developed as a complication of catheterization, and streptokinase may also prove useful in the reversal of thrombosis in this setting.     

Quantitative coronary angiography during intracoronary streptokinase in acute myocardial infarction: How long to continue thrombolytic therapy?

An Intracoronary Infusion of streptokinase is often administered in patients with acute myocardial infarction. To address the question of how long intracoronary streptokinase should be infused, we studied 13 patients with symptoms and electrocardiographic findings suggesting an evolving myocardial infarction. We used subselective catheterization techniques and made quantitative angiographic measurements of the percentage of reduction of coronary artery (CA) diameter before intracoronary streptokinase therapy, immediately after reperfusion was established, and at the completion of streptokinase infusion. Before intracoronary streptokinase and after intracoronary nitroglycerin, nine patients had 100% obstruction of the CA in the “infarct-related vessel.” In seven patients reperfusion was established (25 ± 21 min, mean ± SD) at which time CA diameter was reduced by 77 ± 22%. The streptokinase infusion was then continued until repeated films (every 10 to 15 min) suggested no further change at the site of CA obstruction (93 ± 68 min). The percentage of CA diameter reduction when streptokinase infusion was discontinued was 55 ± 32%; this value was less (P < 0.05) than that observed early after reperfusion. These data show that after initial reperfusion was achieved by the use of intracoronary streptokinase, additional streptokinase lessened the reduction of CA diameter. Residual thrombus may be present at the narrowed CA site early after reperfusion, and further “cleanup” can be achieved by prolonging streptokinase infusion.     

Acute coronary artery occlusion during percutaneous transluminal coronary angioplasty: reopening by intracoronary streptokinase before emergency coronary artery surgery to prevent myocardial infarction

Percutaneous transluminal coronary angioplasty (PTCA) was complicated by acute coronary artery occlusion associated with ST elevation and severe chest pain in three patients. Within 10 minutes, the occluded artery was reopened by an intracoronary (i.c.) infusion of streptokinase, resulting in the disappearance of chest pain and normalization of ST segments. To keep the artery patent, i.c. streptokinase had to be continued until emergency bypass surgery was performed. In two patients, no myocardial infarction occurred, as shown by a normal postoperative left ventricular angiogram. ECG and thallium-201 scintigram. In the other patient, who was admitted with an inferior infarction and underwent PTCA after i.c. lysis, no infarct extension was observed. These results show that i.c. streptokinase rapidly opens an acute coronary artery occlusion complicating PTCA, preventing myocardial infarction.     

Intracoronary infusion of streptokinase in patients with acute myocardial infarction: Effects of reperfusion on left ventricular performance

Cardiac catheterization and coronary angiography were performed on hospital admission in 32 consecutive patients with acute myocardial infarction. Twenty-six patients had total occlusion of an infarct-related coronary artery and six had severe proximal stenosis with poor distal flow. In 18 of the 26 patients with total occlusion, intracoronary infusion of Streptokinase resulted in reperfusion of the distal coronary artery. Seventeen of these 18 patients had severe coronary arterial stenosis at the site of the previous total occlusion. Hemodynamic indexes of left ventricular performance and ejection fraction determined by gated cardiac blood pool imaging did not change immediately after reperfusion (p [probability]= not significant [NS]). The mean (± standard deviation) left ventricular ejection fraction increased significantly (p = 0.007) from admission (44 ± 15 percent) to hospital discharge (55 ± 7 percent) in patients evidencing reperfusion of the occluded coronary artery. It did not change (p = NS) in this time span in the patients with severe stenosis alone, in those with total occlusion not demonstrating reperfusion after administration of streptokinase or in an additional 10 control patients with acute myocardial infarction not evaluated with coronary angiography. These data suggest that (1) coronary arterial thrombus is frequent in acute myocardial infarction and can be lysed by intracoronary streptokinase; (2) reperfusion with intracoronary streptokinase in acute myocardial infarction results in improved left ventricular performance between admission and hospital discharge.     

Reperfusion arrhythmia: a marker of restoration of antegrade flow during intracoronary thrombolysis for acute myocardial infarction

We studied the effects of coronary recanalization on arrhythmogenesis in patients undergoing intracoronary thrombolysis during the early hours of myocardial infarction. Catheterization, ventriculography, coronary angiography, and intracoronary streptokinase infusion were performed in 22 patients. Twenty-one of 22 had thrombotic total occlusion of the infarct-related transient thrombolysis with reocclusion by the end of the procedure. In 12 of these 17 patients, restoration of antegrade coronary flow was accompanied by transient arrhythmia. In these 12 patients coronary angiography within seconds of onset of arrhythmia showed vessel patency in a previously totally occluded coronary artery. Two additional patients developed arrhythmias during streptokinase infusion but after reperfusion had already been established. Accelerated idioventricular rhythm was most often noted. Sinus bradycardia and atrioventricular block with hypotension occurred during restoration of flow in arteries supplying the inferoposterior left ventricle. These arrhythmias may be useful noninvasive markers of successful reperfusion during thrombolytic therapy in acute myocardial infarction.     

Intracoronary urokinase as an adjunct to percutaneous transluminal coronary angioplasty in patients with complex coronary narrowings or angioplasty-induced complications.

The effectiveness of intracoronary urokinase infusion as an adjunct to percutaneous transluminal coronary angioplasty (PTCA) was studied in 50 patients who underwent angioplasty for complex coronary narrowings or had thromboembolic complications during PTCA (29 [58%] men, 3 [6%] stable and 37 [74%] unstable angina, and 16 [32%] prior coronary bypass surgery). The primary indications for intracoronary urokinase infusion were intracoronary thrombus in 27 patients (54%), distal coronary embolization in 9 (18%), and abrupt reclosure in 14 (28%). Urokinase was infused in a mean (+/- standard deviation) dosage of 399,000 +/- 194,000 IU (range 150,000 to 1,000,000) at an average rate of 5,000 to 20,000 IU/min. Angiographic success was achieved in 43 patients (86%). Complications included the need for urgent bypass surgery in 3 patients, Q-wave myocardial infarction in 2, and non-Q-wave myocardial infarction in 12 (8 of whom had peak creatine kinase less than twice the upper normal limit). The incidence of myocardial infarction was significantly higher in patients with vein grafts (69%) than in those with PTCA of native vessels (14%). Two patients died (1 massive gastrointestinal necrosis 24 hours after angioplasty, and 1 after urgent bypass surgery). Mean (+/- standard deviation) fibrinogen levels were 355 +/- 73 mg/dl before urokinase infusion, and 361 +/- 70, twelve hours afterward. Three patients had local bleeding, but no transfusions were needed. It is concluded that intracoronary urokinase is a safe and effective adjunct to PTCA in patients with associated thrombi and may improve the success rate in angioplasty complicated by thrombus formation.     

Percutaneous transluminal coronary recanalization: Procedure,results, and acute complications

Percutaneous transluminal coronary recanalization, a new therapeutic procedure used in acute myocardial infarction, offers significant reduction in mortality, as well as more effective limitation of the zone of infarction than has been possible with other pharmacologic treatment employed in the past. The risk of coronary angiography during acute myocardial infarction was surprisingly low, as was the risk of hemorrhagic complications following the intracoronary administration of relatively low doses of thrombolytic substances such as streptokinase. Mechanical recanalization was possible in about one fifth of patients and successful in approximately half of all such attempts, but complications occurred in a small percentage of attempts at this step. Coronary artery spasm was excluded as a possible cause of occlusion in almost all cases. Selective intracoronary infusion of streptokinase produced the highest degree of myocardial reperfusion, and best results were achieved when therapy was initiated shortly after thrombotic occlusion occurred. Residual stenosis of more than 75% luminal diameter narrowing was present in approximately three fourths of cases after complete thrombolysis, and the majority of patients remained appropriate candidates for coronary bypass surgery or for percutaneous transluminal coronary angioplasty (Grüntzig procedure). Although complete analysis of the efficacy of selective recanalization was difficult because it was not possible to establish a suitable control group for purposes of comparison, the mortality of less than 1% in the present group of 232 patients within the first 6 hours following myocardial reperfusion provides an encouraging result.     

Role of coronary artery bypass surgery after intracoronary streptokinase infusion for myocardial infarction

Intracoronary streptokinase infusion has been shown to improve left ventricular function and reduce hospital mortality in patients with acute myocardial infarction. Adjuvant coronary artery bypass surgery is of value in many of these patients who have recurrent angina, circulatory instability, severe coronary artery occlusive disease, or a high risk of reinfarction. There is little, if any, evidence that immediate coronary artery bypass surgery affects the results adversely—either because of recent myocardial infarction or recent streptokinase infusion, and early operation appears to be a safe and worthwhile modality of treatment in this group of patients with myocardial infarction.     

Thrombolytic therapy of acute myocardial infarction

Thrombotic coronary artery occlusion is now recognized as the usual cause of acute myocardial infarction. The thrombus usually forms at the site of intimal disruption over an atherosclerotic plaque. Following coronary occlusion, myocardial necrosis begins within 40 minutes in the subendocardium and progresses outward toward the epicardium over the next several hours. The intracoronary infusion of streptokinase will produce lysis of the occluding thrombus in up to 80% of patients. It appears that reperfusion with streptokinase in the first few hours following the onset of the myocardial infarction produces a small increase in late left ventricular function, though ECG and enzyme evidence of acute myocardial infarction are not prevented. The improvement in left ventricular function is variable from patient to patient and has not been demonstrated in all the randomized studies to date. The time limit for myocardial salvage may not be the same in all patients. The greatest benefit is probably achieved with reperfusion in the first 4-6 hours, although some benefit may occur as late as 18 hours after the onset of infarction. Many patients who receive intracoronary infusion of streptokinase develop a systemic lytic state, though serious bleeding complications in carefully selected patients are infrequent. High-dose IV streptokinase is easier, cheaper, and quicker to initiate than intracoronary streptokinase but is probably less effective than the intracoronary route in producing rapid lysis of the occluding coronary thrombus. The optimal dose and rate of administration of IV streptokinase have not been determined. The final role and ultimate benefit of thrombolytic therapy of myocardial infarction have not yet been determined, but some of the issues may be clarified by the larger randomized trials now under way. It appears, at present, that the use of intracoronary streptokinase may have a role in the treatment of selected patients with acute myocardial infarctions in institutions with the facilities and the personnel necessary to perform this procedure safely. In the future, thrombolytic therapy may also have a place in the treatment of selected patients with unstable angina and post-myocardial infarction angina. The future availability of more selective thrombolytic agents may make the early IV therapy of myocardial infarction a safer, more effective option and expand the indications for thrombolytic therapy.     

Intracoronary thrombolysis in acute myocardial infarction

Forty-seven patients with acute myocardial infarction (MI) underwent intracoronary infusion of Thrombolysin or streptokinase. In 41, a completely reoccluded artery was reopened. Patency was associated with appearance of arrhythmias, relief of pain, gradual return of the ST-segment to the baseline and appearance of abnormal Q waves. Creatine kinase (CK) and MB-CK enzyme levels peaked earlier. Serial thallium scintigrams showed reduction in defect size after reperfusion, and the ejection fraction was higher compared with control. Eighteen patients were recommended for coronary bypass surgery for recurrent pain or severe multivessel disease.     

Systemic versus intracoronary streptokinase infusion in the treatment of acute myocardial infarction

Clinically encouraging results can be obtained with an intravenous high dose short-time infusion of streptokinase in patients with evolving myocardial infarction. The feasibility and efficacy of the intracoronary and the systemic approach of streptokinase therapy in acute myocardial infarction are discussed in this report and include topics such as infarct artery recanalization success rate, coronary thrombus lysis time, benefit for patients with subtotal coronary occlusion, reocclusion rate, the necessity of additional surgical interventions, salvage of ischemic myocardium and side effects. The value of high dose intravenous short-time streptokinase infusion needs to be assessed with properly designed clinical trials against the background afforded by the results observed with direct intracoronary streptokinase infusion.     

Quantitative and qualitative effects of intracoronary streptokinase in unstable angina and non-Q wave infarction

Thrombolytic therapy has been shown to be effective in reopening totally occluded arteries in acute myocardial infarction. Coronary thrombus is also believed to play a role in the pathophysiology of unstable angina and non-Q wave infarction. However, few patients with these two acute coronary syndromes have been treated with intracoronary streptokinase. Therefore, 100,000 to 300,000 IU (mean 177,000 +/- 80,000 IU) of intracoronary streptokinase was infused into 36 consecutive catheterized patients who either presented with an acute episode of unstable angina or had had a recent non-Q wave infarction and in whom a less than 100% occluded ischemia-producing artery could be identified. Qualitative techniques utilizing vessel magnification and quantitative analysis with digital subtraction were performed on the ischemia-producing coronary lesion before and immediately after streptokinase therapy and 3 to 10 days later in 18 patients who were restudied at the time of transluminal coronary angioplasty. Before streptokinase treatment, 24 (67%) of 36 ischemia-producing arteries contained eccentric, irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries averaged 83.8 +/- 8.3% and 94.8 +/- 3.3%, respectively. After streptokinase treatment there were 23 arteries (64%) with eccentric irregular lesions. The percent diameter stenosis and percent area stenosis in all ischemia-producing arteries were similar to pre-streptokinase values (82.9 +/- 5.9% and 93.8 +/- 4.0%, respectively). At restudy, there were also no significant changes in any quantitative or qualitative variable. Five individual patients showed a significant reduction in percent stenosis after streptokinase. This improvement was independent of duration of symptoms, use of heparin before angiography, streptokinase dose or reduction of fibrinogen levels post-streptokinase. Two additional patients deteriorated clinically and developed total occlusion of the ischemia-producing artery within 12 hours of streptokinase infusion. These data suggest that intracoronary streptokinase may be of limited utility in either unstable angina or recent non-Q wave infarction with a less than 100% occluded ischemia-producing artery. In these syndromes, thrombus may be organized or short infusions may be given too late to be effective. In some cases, thrombus may even be absent. Whether longer infusion of streptokinase or other thrombolytic agents will be of benefit remains to be determined.     

Combination therapy for evolving myocardial infarction: Intracoronary thrombolysis and percutaneous transluminal angioplasty

Nonsurgical coronary reperfusion for evolving myocardial infarction is a promising new technique for the salvage of jeopardized myocardium. Successful reperfusion can be established by intracoronary infusion of streptokinase in approximately 75 percent of patients within the first 6 hours of transmural infarction [1,2]. Following recanalization, most patients are left with high grade fixed coronary stenoses which are potential sites for recurrent thrombus formation. Since the underlying site for coronary thrombosis is still present, reocclusion may occur. Indeed, early experience suggests that recurrence of thrombosis is not uncommon [3,4]. Therapy for evolving myocardial infarction should, in some patients, involve not only thrombolysis, but also an attack on the fixed coronary lesion. We describe a patient with evolving myocardial infarction who was treated successfully with combination therapy consisting of intracoronary streptokinase followed by percutaneous transluminal coronary angioplasty [5].     

Intracoronary versus intravenous streptokinase in acute myocardial infarction

To assess the relative efficacy of coronary thrombolysis using intracoronary versus intravenous streptokinase, 32 patients with acute myocardial infarction were randomly assigned to receive intracoronary (n = 17) and intravenous streptokinase (n = 15). All patients underwent selective coronary arteriography before and after administration of streptokinase by either route within 4 hours of the onset of symptoms. Intravenous streptokinase was given as 750,000 units over 30 minutes, while a mean dose of 180,000 units was required for thrombolysis in the group having intracoronary delivery. Recanalization occurred in 71.4% (10 of 14) of patients receiving streptokinase, by the intracoronary group in contrast to only 25% of patients (3 of 12) who received the drug intravenously (P less than 0.05). Spontaneous thrombolysis was seen in 17.6% and 20% of the patients in the groups having intracoronary and intravenous delivery, respectively. Bleeding complications were few in both groups. Thus, when baseline coronary arteriography is performed, recanalization with intracoronary streptokinase is more effective in the treatment of acute myocardial infarction than intravenous streptokinase.     

Prevention of subsequent exercise-induced periinfarct ischemia by emergency coronary angioplasty in acute myocardial infarction: comparison with intracoronary streptokinase

To compare the efficacy of emergency percutaneous transluminal coronary angioplasty and intracoronary streptokinase in preventing exercise-induced periinfarct ischemia, 28 patients presenting within 12 hours of the onset of symptoms of acute myocardial infarction were prospectively randomized. Of these, 14 patients were treated with emergency angioplasty and 14 patients received intracoronary streptokinase. Recatheterization and submaximal exercise thallium-201 single photon emission computed tomography were performed before hospital discharge. Periinfarct ischemia was defined as a reversible thallium defect adjacent to a fixed defect assessed qualitatively. Successful reperfusion was achieved in 86% of patients treated with emergency angioplasty and 86% of patients treated with intracoronary streptokinase (p = NS). Residual stenosis of the infarct-related coronary artery shown at predischarge angiography was 43.8 +/- 31.4% for the angioplasty group and 75.0 +/- 15.6% for the streptokinase group (p less than 0.05). Of the angioplasty group, 9% developed exercise-induced periinfarct ischemia compared with 60% of the streptokinase group (p less than 0.05). Thus, patients with acute myocardial infarction treated with emergency angioplasty had significantly less severe residual coronary stenosis and exercise-induced periinfarct ischemia than did those treated with intracoronary streptokinase. These results suggest further application of coronary angioplasty in the management of acute myocardial infarction.     

Coronary arterial aneurysm formation after balloon angioplasty

The mechanism of coronary stenosis dilatation by percutaneous transluminal coronary angioplasty (PTCA) is incompletely understood. Five men who developed coronary arterial aneurysms at the site of PTCA are described. All patients were in New York Heart Association functional class III or IV at the time of PTCA. In 2 patients acute myocardial infarction was evolving and both had acute coronary occlusion. The other 3 patients had angiographic evidence of intimal disruption or acute coronary reocclusion as a result of PTCA, one of whom had undergone emergency coronary artery bypass grafting. Three patients received intracoronary streptokinase during PTCA. One patient was asymptomatic and 4 were symptomatic when the aneurysms were identified between 11 days and 4 months after PTCA. Other than the complex course and anatomy of these patients before and immediately after PTCA, no other features distinguished them from others undergoing this procedure.     

Selective thrombolytic patency of the coronary arteries in patients with acute myocardial infarction

Urgent selective coronarography followed by intracoronary infusion of nitroglycerin and streptokinase (2000-4000 U/min) was performed in 24 patients with acute myocardial infarction. Mechanical recanalization of an occluded coronary artery was also performed in two patients. The coronary artery supplying the infarcted area was occluded in 22 patients while 2 patients had third-degree stenosis. Following intracoronary drug infusion, antegrade flow was recovered completely in 16 of 22 occluded coronary arteries (72.7%). All patients, however, retained acute coronary arterial stenosis around former occlusions. Aortal-coronary shunting was performed within 1 to 20 days in 6 patients.