Evolving concepts in the treatment of acute myocardial infarction

Recent studies in patients with transmural acute myocardial infarction have demonstrated that intravenous thrombolytic therapy with streptokinase or tissue plasminogen activator improves left ventricular function and reduces mortality. To accomplish this, these agents must be infused early, ie, within 3 to 4 hours of the onset of chest pain; later administration of the agents exerts no significant beneficial effect. Tissue plasminogen activator appears to be the most effective and safest of the available thrombolytic agents: its intravenous administration is followed by coronary reperfusion in about 70% of patients, and its use is not associated with allergic reactions, a systemic fibrinolytic state, or a prolonged fibrinolytic effect. Once reperfusion has been established with an intravenous thrombolytic agent, intravenous heparin is given for several days, followed by oral aspirin to prevent reocclusion. Since many of these patients have a residual high-grade coronary artery stenosis in the infarct-related artery, mechanical alleviation of the residual stenosis with angioplasty or bypass surgery is an attractive therapy 2 to 4 days after reperfusion, and preliminary data indicate that elective coronary angioplasty 3 days after thrombolytic therapy is beneficial. However, further studies are needed to assess more definitively the use of such an aggressive therapeutic strategy.     

Advances in intracoronary thrombolysis treatment

Based on the results of intracoronary thrombolysis in 30 patients with initial onset of anterior myocardial infarction, we concluded that: (1) left ventricular function and clinical features are markedly improved when reperfusion is accomplished within four hours after coronary artery occlusion; and (2) intracoronary thrombolysis therapy should be considered possible up to 10 hours after the onset of myocardial infarction to prevent expansion of infarct sizes and to preserve ventricular functions. Not infrequently, there is a significant stenosis at the site of initial occlusion after thrombolytic therapy, which results in an immediate reocclusion. Consequently, percutaneous transluminal coronary angioplasty (PTCA) is now widely performed after thrombolytic treatment to achieve more definite revascularization. Our early experiences showed that PTCA following thrombolytic treatment has an increased potential for reinfarction rather than added benefits for left ventricular functions. More recently, however, since our PTCA technique has been improved so as to achieve sufficient dilatation of the stenosed coronary artery, there has been less tendency to immediate reinfarction after the procedure for acute myocardial infarction. Whether PTCA should be added to thrombolytic therapy during the acute phase of myocardial infarction is controversial. The alternative is to wait until it can be performed on an elective basis. It is obvious that early revascularization is essential for preserving left ventricular functions after acute myocardial infarction. For this reason, thrombolytic agents such as tissue plasminogen activator and plasminogen proactivator, which can be administered intravenously, are being intensively sought using molecular biological techniques. The ideal thrombolytic agents should have more fibrin-specific properties with longer half-lives than currently-available substances. However, so far none of these novel agents, have been studied in patients.     

Early treatment of acute myocardial infarction with intravenous streptokinase. A high-risk syndrome

Fifty-one successive patients treated with intravenous streptokinase 1.7 +/- 0.8 (mean +/- SD) hours after onset of symptoms of acute myocardial infarction were evaluated during a three-month posthospital follow-up period. Coronary angiography was performed four to nine days after the initial hospital admission. Twenty-eight patients had a second late angiogram. Forty-one patients had successful reperfusion but only 25% of all patients were without significant clinical cardiovascular manifestations during this period. Postmyocardial infarction angina pectoris occurred in 21 patients, an abnormal stress test result was present in 28 patients, eight patients developed congestive heart failure, and five patients had reinfarction. An intervention with percutaneous transluminal coronary angioplasty or coronary artery bypass graft was performed in 15 (37%) of 41 reperfused patients. A significantly higher intervention rate was present in patients treated with streptokinase within one hour following the onset of symptoms. Early reocclusion (within three months of the infarct) was noted in patients with 60% or more residual stenosis in their infarct-related coronary artery. These patients also had a significantly greater incidence of angina pectoris. Our findings indicate that early thrombolytic therapy of acute myocardial infarction preserves myocardium, and since the infarct-related artery is patent, but narrowed, the jeopardized area is responsible for a high-risk syndrome with an increased likelihood of ischemic symptoms. An early aggressive approach may be indicated, especially for patients with greater than 60% residual stenosis in their infarct-related coronary artery.     

After thrombolytic therapy: angiography, angioplasty, or surgery?

Thrombolytic therapy has been found to improve the prognosis of selected patients with acute myocardial infarction. Many investigators advocate that combined emergency coronary angiography and percutaneous transluminal coronary angioplasty be performed immediately after thrombolytic therapy. Emergency angiography documents the anatomic extent of coronary artery disease, shows whether reperfusion has occurred, and indicates whether emergency angioplasty is necessary. In this setting, emergency catheterization without angioplasty is associated with relatively little additional risk. However, a number of prospective trials have compared emergency angioplasty to more conservative treatment strategies, and emergency angioplasty has been not found to offer any advantage in terms of improved prognosis or preservation of left ventricular function. Therefore, it is probable that most patients with evolving Q-wave myocardial infarction are best treated with conservative strategies after initial thrombolytic therapy, although there may still be a role for emergency angioplasty in a relatively small subset who present with evolving myocardial infarction and severely depressed left ventricular function. Emergency coronary artery bypass surgery also appears to have a limited role in patients treated with thrombolytic therapy. Nevertheless, in occasional patients with a poor prognosis at hospital presentation, in whom thrombolytic therapy and emergency angioplasty have failed or are contraindicated, prompt emergency coronary artery bypass grafting may salvage the ischemic myocardium and improve the prognosis.     

Recurrent ischemia without warning. Analysis of risk factors for in-hospital ischemic events following successful thrombolysis with intravenous tissue plasminogen activator

Ischemic events after successful thrombolysis have been reported to occur in 18-32% of patients treated for acute myocardial infarction with thrombolytic therapy, and previous studies in which patients received streptokinase suggest that risk of early recurrent ischemia is closely related to the presence of a high-grade residual stenosis. If these events are predictable after intravenous recombinant tissue-plasminogen activator (rt-PA) thrombolytic therapy, then further intervention after its use could be targeted at selected patients. One-hundred ninety-two patients from the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) I and TAMI III trials had successful rt-PA-mediated thrombolysis without immediate coronary angioplasty (PTCA). One-hundred seventy-four of these patients (92%) had prehospital discharge angiography. The mean age was 56 +/- 11 years; 81% were men; the infarct-related artery was the left anterior descending in 76 (39.8%), the left circumflex in 24 (12.6%), and the right coronary artery in 91 (47.6%). Thrombolysis with rt-PA resulted in a residual 73 +/- 13% diameter and 0.95 +/- 0.51 mm stenosis by quantitative coronary arteriography, and Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 in 59.2% and 3 in 40.8% of stenoses as assessed on angiograms obtained 90 minutes after the initiation of rt-PA therapy. Recurrent ischemic events (ischemia requiring emergency percutaneous transluminal coronary angioplasty or urgent bypass surgery, reocclusion of the infarct-related artery, or cardiac death) occurred in 41 patients (21.3%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiographic findings and catheterization laboratory events in patients with primary coronary angioplasty or streptokinase therapy for acute myocardial infarction

Background: The purpose of this study was to evaluate catheterizationlaboratory events and angiographic findings in patients randomlyassigned to undergo primary coronary angioplasty or to receiveintravenous streptokinase for acute myocardial infarction. Methods: We analysed angiographic data in 301 patients withacute myocardial infarction, randomly assigned to undergo primarycoronary angioplasty without antecedent thrombolytic therapyor to receive intravenous streptokinase therapy. Follow-up coronaryangiography was preferably performed after 3 months. AII angiogramswere analysed with a quantitative coronary analysis system. Results: Of the 152 patients assigned to angioplasty treatment,140 underwent this procedure with a success rate of 97%. Theresidual diameter stenosis of the infarct-related vessel immediatelyafter angioplasty was 27 ± 15% and there were major eventsin 14% of the patients in the catheterization laboratory. Atfollow-up angiography after a mean interval of 92 days in theangioplasty assigned patients, a diameter stenosis of 35 ±22% was observed in this group. The restenosis rate was 28%and the reocclusion rate 5%. A Thrombolysis in Myocardial Infarction(TIMI) grade 2 flow immediately after angioplasty was predictivefor reocclusion at follow-up (P= 0.001). In the streptokinaseassigned patients (149) the infarct-related vessel was patentat follow-up angiography after a mean of 22 days in 66% of thepatients with a mean residual diameter stenosis of 77 ±20%. Conclusion: Primary coronary angioplasty is a highly effectiveand safe reperfusion modality for patients with acute myocardialinfarction. However, TIMI grade 2 flow through the infarct-relatedvessel immediately after angioplasty is a predictor of reocclusion.     

Acute myocardial infarction: immediate coronary angioplasty for failure or contra-indications of thrombolytic therapy. Apropos of a series of 100 cases

One hundred patients admitted to a centre of interventional cardiology with acute myocardial infarction of less than 6 hours, underwent coronary angioplasty of first intention because of contra-indications to thrombolytic therapy (n = 20) or after thrombolytic therapy with streptokinase (n = 54), acylenzymes (n = 12) or tissue type plasminogen activator (n = 14). The indication of angioplasty were those of the TIMI (Thrombolysis in Myocardial Infarction) classification (occluded artery, TIMI grade 0) (n = 60) (suboccluded artery, TIMI grade 1) (n = 40). The criterion of success of angioplasty was an increase greater than 1 of TIMI grade. Reperfusion of the coronary artery was obtained by angioplasty in 95% of failures of thrombolysis and in 90% of patients with contra-indications to thrombolytic therapy. The early reocclusion rate at D1 was 2%. Repeat angioplasty at D1 was successful in both these cases and the arteries were still patent at D21. The reocclusion rate at the third week in 75 patients who underwent control coronary angiography was 5.3%. In patients with arterial occlusion, immediate angioplasty attained two objectives in the same procedure: a high rate of emergency myocardial reperfusion and a low rate of reocclusion. The average left ventricular ejection fraction (all arteries) significantly improved (+9.2% in absolute values) when the artery remained patent (p less than 0.001), especially when the initial ejection fraction was low. In the patients who had occluded arteries at control angiography at 3 weeks, the ejection fraction decreased (-4% in absolute values) (NS). The following complications were observed: 4 coronary artery dissections and haematomas at the site of femoral puncture in patients who had received thrombolytic therapy (10 drained surgically). The hospital mortality was 3% and global mortality after an average follow-up period of 19.6 months was 5%. Coronary angioplasty in acute myocardial infarction carries a low risk and seems to be beneficial in patients with contra-indications to or failure of thrombolysis.     

What is established in thrombolytic therapy of acute myocardial infarction? Pharmacological approaches

Summary Thrombolytic therapy by early reopening of an occluded coronary vessel, and hence re-establighing oxygen delivery, can significantly reduce infarct size. The result depends both on the duration of ischemia and the presence of collaterals. By early initiation of intravenous thrombolytic therapy and shortening the ischemic period, the functional results may be improved. PTCA has to considered in order to avoid reocclusion of the infarct vessel, mainly in patients with high-grade residual stenosis and viable myocardium in the poststenotic area. The benefit of early thrombolytic therapy in acute myocardial infarction has been proven in randomized trials. However, to achieve statistical significance, a large number of patients had to be included. It is mainly the patients with previous myocardial infarction with a large area at infarct risk and/or anterior myocardial infarction that derive most benefit from this intervention.     

Prognosis following interventional therapy for acute myocardial infarction: utility of dipyridamole thallium scintigraphy.

A variety of methods for risk stratification after acute myocardial infarction have been successfully employed, however, little attention has been focused on patients who have received reperfusion therapy. The present report examines the utility of dipyridamole thallium scintigraphy in the prediction of late cardiac death or recurrent myocardial infarction in patients who have received thrombolytic therapy. Prospectively, 71 patients who presented with myocardial infarction and were treated with recombinant tissue plasminogen activator (and frequently percutaneous transluminal coronary angioplasty) were enrolled in the study. The primary end points during the follow-up period of nearly 2 years were recurrent infarction or death, which occurred in 10 patients. Although cardiac events were significantly related to either the performance of late myocardial revascularization or the presence of a residual coronary artery stenosis at discharge, no scintigraphic variable was found to be predictive of myocardial infarction or death. Thus, this report is the first to suggest limitation of scintigraphic techniques with regard to prognostic value in myocardial infarction survivors treated with reperfusion techniques. This selected population may have physiologic differences as compared with post-infarction studies performed before the advent of thrombolytic agents. Caution is therefore advised in extrapolating results of earlier reports to the ever increasing percentage of patients receiving recannalization therapy.     

The results of large clinical trials comparing primary angioplasty and thrombolysis]

One of the main cardiological debate is about which one, between primary angioplasty (PTCA) and thrombolysis, is to prefer for the therapy of acute myocardial infarction. The data available in the literature do not show that one of these two therapeutical choices is definitely better than the other one. Since the main therapeutical goal in patients with acute myocardial infarction is the early and persisting recovery of the anterograde coronary flow, the best therapy for every patient is the one that can be performed more quickly and safely. Therefore, PTCA has to be preferred whenever it can be done quickly, by expert personnel and with cardiosurgical support, especially in patients considered to be at high risk or with contraindications to thrombolysis. Otherwise, thrombolytic therapy should be better. Stent implantation seems to be better than conventional angioplasty, in particular for the reduction of restenosis and reocclusion. These conclusions, however, derive from small studies and require further evidences. Moreover, there are not trials directly comparing primary PTCA and stent implantation with thrombolysis. Rescue PTCA, after failure of thrombolytic therapy, is useful when the coronary flow of the culprit lesion is TIMI 0 or 1, but not when the flow is TIMI 2; there are neither indications to early, but not rescue, angioplasty in all the patients already thrombolyzed. Finally, for patients with acute myocardial infarction and cardiogenic shock, the data currently available, derived more from observational than from randomized studies, suggest revascularization by PTCA.     

Antiplatelet and anticoagulant therapy during coronary thrombolysis

Plasminogen activators reduce mortality in patients with acute myocardial infarction primarily by inducing reperfusion at a time when the myocardium is still viable. Consequently, important determinants of the clinical response to thrombolytic therapy include the patency rate, the timing of reperfusion, and the frequency of coronary reocclusion. With present thrombolytic agents, coronary patency is not achieved in 30%-50% of patients and reperfusion is often delayed for more than 60 min after initiating thrombolytic therapy. Even in those that achieve patency, reperfusion flow, an important determinant of myocardial salvage, may be limited by incomplete clot lysis and residual coronary stenosis. Finally, reocclusion has been reported in 15%-25% of patients and has serious clinical consequences. Experimental and clinical evidence suggests that many of these problems reflect ongoing platelet activation and thrombosis. Thus, there is a rational basis to assume that the clinical benefit of thrombolytic therapy will be enhanced by the addition of antiplatelet and anticoagulant agents.     

Reinfarction after thrombolytic therapy for acute myocardial infarction followed by conservative management: incidence and effect of smoking

A group of 456 consecutive patients seen less than or equal to 6 h after the onset of acute myocardial infarction associated with ST segment elevation received thrombolytic therapy and were followed up for 12 months. Intravenous streptokinase was given to 315 patients and recombinant tissue-type plasminogen activator (rt-PA) to 141 patients. Reinfarction rate and risk factors for reinfarction were assessed. Management after thrombolysis was conservative; revascularization procedures were reserved for patients with symptoms refractory to medical therapy or for those with left main coronary artery stenosis. Coronary artery surgery or angioplasty was performed in only 3.7% of patients during the first 30 days after thrombolysis and in only 8.6% by 1 year. Most patients (79%) underwent coronary arteriography. Twenty-six patients (5.7%) exhibited signs of threatened reinfarction at 1 month after thrombolytic therapy as did 43 patients (9.4%) by 1 year. Reinfarction was prevented in four of these patients by early readministration of thrombolytic therapy. Multivariate analysis of possible risk factors for reinfarction identified at the time of initial infarction showed current cigarette smoking to be the only predictive factor (reinfarction occurred in 12.5% of smokers versus 6.3% of nonsmokers, p = 0.04). A second analysis of risk factors identified 3 weeks after initial infarction, including the severity of residual stenosis at coronary arteriography and exercise test variables, again showed continued cigarette smoking to be the only factor predictive of reinfarction. Twenty percent of patients who continued to smoke developed reinfarction compared with 5.1% of those who stopped (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Primary angioplasty for cardiogenic shock complicating acute myocardial infarction.

To evaluate the role of primary percutaneous transluminal coronary angioplasty in cardiogenic shock, 53 patients admitted with the diagnosis of acute myocardial infarction and cardiogenic shock were studied. Thirty-five (66.0%) patients received intravenous thrombolytic therapy (streptokinase 15 lac units) and 18 (34.0%) underwent primary percutaneous transluminal coronary angioplasty. There was no significant difference in the mean age, risk factor profile, presence of prior myocardial infarction, site of myocardial infarction and cardiac enzyme levels at presentation between the two groups. More male patients were present in the group undergoing primary percutaneous transluminal coronary angioplasty (94.44% vs 68.57%; p = 0.04). The time delay between the onset of symptoms and presentation to the hospital did not differ significantly between the two groups (318.9 vs 320.0 minutes; p = NS). In the primary percutaneous transluminal coronary angioplasty group, 17 patients had a single infarct-related artery and one had both left anterior descending and right coronary artery occlusion. Thus in 18 patients, 19 vessels were attempted. Angiographic success (< 50% residual stenosis) was achieved in 15 (78.94%) vessels of which TIMI III flow was achieved in 10 (52.63%) vessels and TIMI II flow in five (26.31%). Intra-aortic balloon pump was needed in five (27.77%) patients undergoing coronary angioplasty. In-hospital mortality was 27.77 percent in patients undergoing primary percutaneous transluminal coronary angioplasty and 57.14 percent in patients receiving intravenous thrombolytic therapy (p = 0.04). In the thrombolytic therapy group, mortality was higher (85.91%) in patients presenting six hours or later after the onset of symptoms as compared to those presenting in less than six hours of the onset of symptoms (50%). In primary percutaneous transluminal coronary angioplasty group, mortality was 21.42 percent in patients with successful and 50 percent in patients with failed angioplasty. Thus, in patients with acute myocardial infarction and cardiogenic shock, an aggressive invasive strategy with primary percutaneous transluminal coronary angioplasty, as compared to intravenous thrombolytic therapy, is helpful in reducing in-hospital mortality.     

Significance of residual coronary artery stenosis after reperfusion therapy in acute myocardial infarction

We evaluated the efficacy of reperfusion therapy in acute myocardial infarction in terms of postinfarction angina (PIA), reinfarction and coronary reocclusion. In 99 hospitalized patients with acute myocardial infarction within 6 hours after the onset of symptoms, 67 were treated using intracoronary thrombolysis (ICT) alone (Group T) and the remaining 32 using ICT followed by percutaneous transluminal coronary angioplasty (PTCA) (Group T + A). PTCA was performed for the arteries with high grade residual stenosis (TIMI grade 0, 1, 2) after ICT. Recatheterization was performed 28 +/- 12 days after hospitalization in 93% (62/67) of Group T and in all of Group T + A. There were no significant differences in age, sex, time interval from the onset to reperfusion, the extents of coronary artery disease and the Cohn grade of collaterals. However, anteroseptal infarction was more frequent in Group T than in Group T + A (p less than 0.05). Residual stenosis (diameter) at the end of intervention was 81 +/- 14% in Group T, and 48 +/- 15% in Group T + A, (p less than 0.01). Residual stenosis at recatheterization was 70 +/- 23% in Group T, and 55 +/- 22% in Group T + A (p less than NS). The incidence of PIA did not differ between the two groups (20.1% vs 6.2%). However, the incidence was higher in patients with residual stenosis of 70% or more than in those with residual stenosis of less than 70% (23.8% vs 2.9%, p less than 0.05). The incidence of reinfarction (re-elevation of CPK) did not differ between the two groups (7.4% in Group T, 6.2% in Group T + A); and neither did the incidence of coronary reocclusion at the time of recatheterization (14.5% vs 3.1%). We concluded that higher degree of residual stenosis at the end of intervention has a greater risk of PIA and reocclusion. Although differences were not statistically significant, the patients treated with ICT followed by PTCA seemed to have lower incidence of PIA and reocclusion compared with those treated with ICT alone, thus having better hospital prognosis.     

Reocclusion: The flip side of coronary thrombolysis

Since the introduction of thrombolytic therapy for acute myocardial infarction, the incidence of coronary artery reocclusion has been intensively studied. Also, the prediction and diagnosis of reocclusion by angiographic and clinical variables, as well its invasive and pharmacologic prevention, have gained much attention.By angiographic definition, reocclusion requires three angiographic observations: one with an occluded artery, one with a reperfused artery and a third for the assessment of subsequent occlusion (true reocclusion). Since the introduction of early intravenous reperfusion therapy, most studies use only two angiograms: one with a patent and one with a nonpatent infarct-related artery. A search for all published reocclusion studies revealed 61 studies (6,061 patients) with at least two angiograms. The median time interval between the first angiogram after thrombosis and the second was 16 days (range 0.1 to 365). Reocclusion was observed in 666 (11%) of 6,061 cases. Interestingly, the 28 true reocclusion studies showed an incidence of reocclusion of 16 ± 10% (mean ± SD), and the 33 studies with only two angiograms 10 ± 8% (p = 0.04), suggesting that proven initial occlusion of the infarct-related artery is a risk factor for reocclusion after successful thrombolysis. The other predictors for reocclusion are probably severity of residual stenosis of the infarct-related artery after thrombolysis and perhaps the flow state after lysis. Reocclusion is most frequently seen in the early weeks after thrombolysis. The clinical course in patients with reocclusion is more complicated than in those without complication. Left ventricular contractile recovery after thrombolysis is hampered by reocclusion.Routine invasive strategies have not been proven effective against reocclusion. In the prevention of reocclusion, both antiplatelet and antithrombin strategies have been tested, including hirudin and hirulog, but the safety of these agents in thrombolysis is still questionable.Thus, reocclusion after thrombolysis is an early phenomenon and is more frequent after proven initial occlusion of the infarct-related artery. Reocclusion can be predicted by angiography after thrombolysis. Because reocclusion is detrimental, strategies to prevent it should be developed and carried out after thrombolytic therapy for acute myocardial infarction as soon as they are deemed safe.     

Identification and transport of patients with acute myocardial infarction for thrombolytic therapy

The concepts of acute, potentially reversible coronary artery thrombosis and myocardial salvage by early coronary thrombolysis using pharmacologic agents and/or percutaneous transluminal coronary angioplasty have evolved rapidly since 1980. Broad, general application of these methods awaited clear data on efficacy and safety of proposed treatment regimens, and in May 1987 streptokinase was recommended for approval by the Food and Drug Administration for intravenous use in patients with acute myocardial infarction. A second, more promising drug, recombinant tissue-type plasminogen activator, was approved by the FDA in November 1987. Thrombolysis is now accepted therapy for patients with acute myocardial infarction. Rapid identification of the patient with acute myocardial infarction plays an important role in treatment, because thrombolytic therapy is maximally effective if begun within four hours of the onset of symptoms. Care must be taken in selecting patients for treatment to ensure that an acute myocardial infarction is in evolution and that a medical condition predisposing to hemorrhage is not present. Cost of treatment and risk of complications must be considered before initiating therapy. In many patients, thrombolytic therapy can be considered only the first step in treatment, because of the relatively frequent occurrence of reocclusion and reinfarction after initial thrombolysis. If cardiac catheterization, angioplasty, and open heart surgery facilities are not readily available, transfer to a tertiary care center is indicated for high-risk patients, such as those with large anterior infarction, vacillating pain, or previous myocardial infarction. Transfer is safe if carried out promptly by critical care transport teams experienced in cardiac care.     

Coronary stent implantation in acute vessel closure 48 hours after an unsatisfactory coronary angioplasty

We report the implantation of a balloon-expandable stent in a patient with acute vessel closure in the state of evolving myocardial infarction following 48 hr after unsatisfactory coronary angioplasty. The stent was implanted after successful recanalization of an occluded left anterior descending artery, with repeated unsatisfactory results of balloon angioplasty. Adjunct thrombolytic therapy was contraindicated. No residual stenosis was documented in immediate control angiograms, or after 24 hr, 3 weeks, and 4 months.     

Intravenous streptokinase during acute myocardial infarction. A prospective open study

To evaluate the efficacy of intravenous streptokinase in acute myocardial infarction (AMI) 108 patients received a high-dose (1.5 million units), short-term infusion (60 minutes) within 6 hours after onset of symptoms, followed by anticoagulation. Before discharge a submaximal exercise test and a coronary arteriography were performed in 100 surviving patients. Sixty-seven patients had a patent infarct-related vessel. Clinical reocclusion occurred in 21 patients. Left ventricular function was slightly, but not significantly, better in patients with patent infarct-related vessels: ejection fraction 59.5 +/- 13% versus 57.4 +/- 13%. Additional procedures were performed in 20 patients: percutaneous transluminal coronary angioplasty (PTCA) in 8 and coronary artery bypass surgery (CABG) in 12. The results indicate that streptokinase applicated during a 6 hour-time window is a potent thrombolytic agent in acute myocardial infarction with limited effect on global left ventricular function. Pre-discharge evaluation is necessary to screen patients for residual ischemia.     

Percutaneous transluminal coronary angioplasty after intracoronary streptokinase in evolving acute myocardial infarction

To achieve optimal myocardial revascularization and prevent rethrombosis of the infarct-related coronary artery, percutaneous transluminal coronary angioplasty (PTCA) was attempted in 18 patients with evolving acute myocardial infarction (9 anterior and 9 inferior) after administration of intracoronary streptokinase. PTCA was attempted 338 +/- 151 minutes after the onset of symptoms. After thrombolytic therapy, 11 patients had a severe residual stenosis and 7 a persistent total occlusion of the infarct-related coronary artery. PTCA was successful in 13 of 18 patients: in 9 of 11 with coronary stenoses and in 4 of 7 with total coronary occlusions. PTCA reduced the severity of the coronary lesion from 91 +/- 2% to 27 +/- 7% (p less than 0.001), and the transstenotic pressure gradient from 38 +/- 5 to 6 +/- 2 mm Hg (p less than 0.01). One patient in cardiogenic shock died during urgent coronary surgery after unsuccessful PTCA. After PTCA, all patients received heparin and antiplatelet agents. One patient had reinfarction with reocclusion of the infarct-related artery 5 days after PTCA. The other 12 patients had an uneventful hospital course, and cardiac catheterization before hospital discharge (8 to 17 days) revealed reocclusion of the infarct-related coronary artery in 3 and persistent patency in 9. Persistent patency of the infarct-related artery was associated with preservation of left ventricular end-diastolic volume (initial 86 +/- 6 ml/m2, follow-up 91 +/- 6 ml/m2), and improvement in left ventricular ejection fraction in some patients.     

Combination thrombolytic therapy: a comparison of simultaneous and sequential regimens of tissue plasminogen activator and urokinase

Coronary angioplasty following unsuccessful tissue plasminogen activator (t-PA) therapy for acute myocardial infarction has been associated with a high incidence of subsequent reocclusion of the infarct-related artery, and a relatively high in-hospital mortality. In contrast, the combination of t-PA and urokinase, when given intravenously prior to coronary angiography, appears to be associated with a low incidence of post-rescue angioplasty reocclusion. In order to determine whether intraprocedural urokinase, given at the time of rescue coronary angioplasty for failed t-PA therapy, improves long-term patency of the infarct vessel to the same extent as preangiographic, combination t-PA/urokinase therapy, three thrombolytic treatment strategies were retrospectively compared. The first group included 86 patients undergoing rescue angioplasty after t-PA monotherapy (t-PA alone). The clinical and angiographic outcomes of these patients were compared with those of 24 patients who received intravenous or intracoronary urokinase during rescue angioplasty following unsuccessful t-PA therapy (sequential t-PA/urokinase therapy), and with those of 34 patients undergoing rescue coronary angioplasty following unsuccessful therapy with the combination of intravenous t-PA and urokinase (simultaneous therapy). There was no difference in postangioplasty patency rate of the infarct-related artery between the three groups. However, the sequential t-PA/urokinase regimen was associated with a subsequent reocclusion rate that was lower than the rate that occurred in the t-PA monotherapy group but higher than the rate in the simultaneous t-PA/urokinase group (13 versus 29 versus 2%, respectively; p = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)