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.     

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.     

Acute myocardial infarction: intracoronary application of nitroglycerin and streptokinase.

In five patients with acute myocardial infarction, the effects of both intracoronary nitroglycerin (NTG) and subsequent intracoronary streptokinase application were evaluated. In addition, transluminal recanalization was performed in one of these patients. Injection of NTG into the infarct-related coronary artery resulted in improved distal filling of the subtotally occluded left circumflex artery in one patient, and in transient patency of the completely occluded right coronary artery in a second patient. In a third patient patency of the totally occluded left anterior descending artery (LAD) was achieved by transluminal recanalization with a guide wire. In a forth patient with occulsion of the LAD, there was no response to intracoronary NTG and mechanical recanalization was not attempted. Subsequent intracoronary infusion of streptokinase (1,000--2,000 U/min for 15--60 min) resulted in a further and long-term reduction of narrowing at the site of acute occlusion in patients I-III and in opening of the completely occluded LAD in patient IV. Improvement of lumen was paralleled by alleviation of symptoms. In a fifth patient, in whom the LAD was subtotally occluded, the degree of coronary obstruction could not be changed by intracoronary application of NTG or by lysis. In this patient, symptoms and ECG changes improved with reduction of pathologically elevated blood pressure values. The findings suggest that myocardial infarction had been caused by thrombotic occulsion in four patients, and that spasm of the infarct vessel could have been an additional factor in two of these patients. In the fifth patient, an increase of afterload in the presence of a subtotal lesion might have caused the critical imbalance between oxgen supply and demand, resulting in cell death.     

Coronary arteriographic findings during early hours of acute myocardial infarction: response to intracoronary injection of nitrates

We performed coronary arteriography and gave intracoronary injection of nitrates within 8 hours after the onset of symptoms of acute myocardial infarction in eighteen patients. Improved distal filling or patency of the total occluded coronary artery after intracoronary injection of nitrates occurred in 4 of 18 patients. In one of four patients the first intracoronary nitrates injection failed to release the initial total occlusion, but after intracoronary Urokinase administration, the second nitrates injection succeeded to dilate the completely occluded coronary artery. Coronary arteriography was again performed in sixteen patients in the chronic stage (4-15 weeks after the onset of acute myocardial infarction) and ergonovine maleate was injected intravenously in seven patients. Focal spasm was induced by ergonovine injection in three patients in one of whom intracoronary nitrates failed to release the complete obstruction in the acute stage. We conclude that coronary spasm as well as intracoronary thrombosis plays an important role in the production of acute myocardial infarction.     

Results of using percutaneous transluminal coronary angioplasty in patients with stable and unstable angina pectoris and acute myocardial infarct

Transcutaneous transluminal coronary angioplastics (TTCA) was performed in 28 coronary heart disease patients (8 patients had stable and 5 others labile angina, 15 presented acute myocardial infarction, AMI). The patients with AMI received intracoronary thrombolytic treatment prior to TTCA. Successful dilatation was performed in one patient with narrowing of the main trunk of the left coronary artery, in 14 of 21 patients with the stenosis of the anterior interventricular branch and in 5 of 6 patients with the narrowing of the right coronary artery. In three cases TTCA was carried out in the presence of the occluded coronary artery, with two patients benefiting from the operation. In 5 patients with AMI in whom an attempt to dilate the lumen of the coronary artery was unsuccessful, emergency surgery for aorto-coronary shunting was conducted. This operation was also performed in the planned order in 2 angina patients. In 7 patients the failure of TTCA was explained by the impossibility to pass the dilatary sound through the stenosis of the coronary artery and in 1 case by the failure to enter the ostium of the left coronary artery with the guiding catheter.     

A case of myocardial infarction due to the left main trunk lesion, in which percutaneous coronary recanalization and emergency coronary-aorto bypass graft, and subsequent percutaneous coronary angioplasty were effective not only from a viewpoint of survival but from comeback to social life

A case of acute myocardial infarction due to the lesion in the left main coronary artery was reported. A 50-year male was referred to our department for suspected acute myocardial infarction. Physical examination on admission revealed slight cyanosis with cold sweating due to severe chest pain. Pulse was irregular and heart rate was 78 beats/min. Blood pressure was 100/80 mmHg. A series of electrocardiograms (ECG) and laboratory data provided the diagnosis of wide-ranged anterolateral infarction in the left ventricle. Emergency coronary angiograms taken without delay showed a subtotal occlusion (99% stenosis) of the left main coronary trunk (LMT) before the initiation of intracoronary thrombolysis (PTCR). Following the intracoronary infusion of urokinase of 1,200,000 units, symptoms and ECG changes transiently improved but worsened later, and LMT stenotic lesion and delayed filling of myocardium were similar with before PTCR. Emergency coronary-aorto bypass graft (CABG) was undertaken without a significant delay to both the left anterior descending artery (LAD) and left circumflex coronary artery (LCX). With these treatments, the patient could survive despite the wide area of infarction due to LMT lesion. Coronary angiograms performed 37 days after the CABG showed that the graft to LAD was completely occluded and the LCX graft was patent with partial stenosis. Treadmill test at this time induced an anginal episode with ischemic ECG changes on moderate exercise, indicating the presence of significant area of ischemic myocardium. For salvage of the ischemic myocardium, percutaneous transluminal coronary angioplasty (PTCA) was successfully performed for the LMT stenosis, resulting in no episode of angina nor ischemic ECG changes during exercise loading.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

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.     

Acute anterior myocardial infarction due to aortosaphenous vein graft occlusion with very large thrombus burden

A 75-year-old man, with a previous history of myocardial infarction and three-vessel coronary artery bypass grafting, presented with an acute anterior ST-elevation myocardial infarction. The vein graft to the left anterior descending artery was occluded with heavy thrombus burden, and the other grafts were patent. After administering a bolus dose of tirofiban and then undergoing percutaneous coronary intervention without stenting to the left anterior descending artery saphenous vein graft, intracoronary thrombolytic infusion was performed to maintain the patency of the vein graft. The patient was asymptomatic after medical follow-up. This may be an effective treatment option in patients with large thrombus burden and requires further investigation through large-scale trials.     

Intracoronary streptokinase thrombolytic recanalization and subsequent surgical bypass of remaining atherosclerotic stenosis in acute myocardial infarction: Complementary combined approach effecting reduced infarct size,preventing reinfarction,and improving left ventricular function

In 48 patients with acute myocardial infarction (AMI) the acutely thrombus-occluded coronary artery was successfully recanalized nonsurgically via catheter with intracoronary streptokinase (SK) infusion after a mean occlusion time of 3.1 ± 1.6 hours. In all cases residual high-grade fixed atherosclerotic stenosis remained after percutaneous transluminal coronary recanalization (PTCR). Subsequent aortocoronary bypass surgery (ACBS) circumventing the stenotic coronary artery was performed during the acute stage of myocardial infarction (within 10 days of AMI onset) in 34 patients and electively (longer than 10 days after AMI onset) in 14 patients. No patient died from early PTCR or from ACBS intervention. There were two late post-ACBS arrhythmogenic deaths, two patients suffered nonfatal reinfarction post ACBS several months after hospital discharge, only two had occasional post-ACBS angina pectoris, and one patient had post-ACBS mild heart failure. The remaining 41 post-ACBS patients were completely asymptomatic throughout long-term follow-up evaluation. In the left ventricular (LV) segment supplied by the initially occluded coronary artery, which was recanalized early by means of SK therapy and subsequently grafted, wall motion improved significantly from the acute to the postoperative stage in patients who underwent early surgery (from 13.6% ± 1.9% to 40.3% ± 2.7%, p < 0.001) and in the electively operated group (from 18.0% ± 7.1% to 48.2% ± 6.3%, p < 0.001). Ischemic wall motion was improved irrespective of whether or not the bypass graft circumventing the residual stenosis of the infarct vessel remained patent. Wall motion of nonischemic segments remained essentially unchanged. In the patients who underwent surgery in the early stage, the closure rate of the bypass graft to the infarct-related vessel was 17%, and in the electively operated group no graft was found to be occluded. In conclusion, coronary artery recanalization, achieved by means of early SK-PTCR therapy with subsequent ACBS, can be performed safely in patients with AMI, and the result will be marked improvement in LV segmental wall motion and global function, diminished reinfarction rate, and reduced incidence of angina pectoris, all benefits that are consistently maintained during long-term evaluation.     

Bedside intracoronary thrombolysis in the coronary care unit

Using a mobile X-ray unit in the coronary care unit (CCU), intracoronary streptokinase (IC STK) administration was performed in 20 patients with acute myocardial infarction who arrived 2 to 5 hours after onset of symptoms. IC STK was infused at a rate of 4000 U/min. Of 20 patients, 17 had complete and 3 subtotal occlusion of the infarct-related artery. The IC STK infusion resulted within 15 to 80 min in reperfusion in 12 of 17 patients with occluded artery (70%). One patient died, 4 patients underwent early bypass grafting, in one PTCA was attempted and in one a femoral A-V fistula caused by the procedure required surgical revision. IC STK infusion is much more economical if performed in the CCU and the 24-hour coverage can be provided by an experienced invasive cardiologist on call service.     

经皮冠状动脉介入术后心肌灌注评价方法的比较

目的比较经冠状动脉超声心肌声学造影(MCE)与校正的心肌梗死溶栓临床试验(TIMI)帧数计数(CTFC)及冠状动脉血流速度方法对经皮冠状动脉介入术(PCI)后心肌灌注的评价,并探讨相关临床意义。方法68例住院患者根据选择性冠状动脉造影结果,按血管狭窄程度分组A组,正常对照组;B组,血管狭窄75%~95%;C组,血管狭窄>95%;D组,急性血管闭塞。对各病变血管均进行PCI治疗,并恢复TIMI3级血流。采用定量经冠状动脉MCE、CTFC及冠状动脉血流速度方法对术后心肌灌注状况进行检测。其中,经冠状动脉MCE有关定量参数分别为造影剂峰值密度(A)反映心肌血容量;峰值时间(TP)反映心肌灌注速度;曲线下面积(AUC)反映心肌血流量。结果PCI后心外膜血管恢复正常血流的前提下,各狭窄病变血管组CTFC与对照组差异无统计学意义;而闭塞血管组冠状动脉血流速度较对照组低;在MCE检测中,C组的心肌血容量及血流量较对照组低,而D组反映心肌灌注的3个参数值均较对照组差异均有统计学意义。结论经冠状动脉MCE通过多个参数进行定量分析,较其他两种方法能更精确地评价PCI后心肌灌注状况。     

Percutaneous transluminal coronary angioplasty immediately after intracoronary streptolysis of transmural myocardial infarction

Percutaneous transluminal coronary angioplasty (PTCA) was performed in 21 patients with acute myocardial infarction (AMI) treated by intracoronary infusion of streptokinase within 8 hours after the onset of symptoms. Streptolysis therapy began a mean of 3.6 +/- 1.2 hours (+/- SD) after the onset of symptoms. The vessel was occluded in 14 patients and highly stenosed in seven. After the infusion of 67,300 +/- 63,200 IU of streptokinase over 26.1 +/- 21.5 minutes, patency of the occluded vessels was reached. PTCA as performed 20-60 minutes after the end of streptokinase treatment in 19 patients and 24 and 31 hours after treatment in two patients. The dilation was successful in 17 patients (81%). The degree of vessel obstruction was reduced from 90.2 +/- 7.3% to 58.6 +/- 19.5% (area method) and from 71.4 +/- 12.4% to 39.2 +/- 19.7% (diameter method). The improvement was 31.5 +/- 18.4% and 32.2 +/- 19.3%, respectively. No reocclusion was induced by PTCA. Twenty patients were discharged. One died during hospitalization; at autopsy, the treated vessel was still patent. During the follow-up period, two reinfarctions and one asymptomatic reocclusion occurred. The clinical findings during the hospital course and the follow-up period were compared with those of a control group of 18 patients with AMI and comparable coronary stenoses who were treated only with streptokinase infusion. Four of these patients had a reinfarction during the hospital course, and three died during the follow-up period. PTCA can be performed safely and successfully immediately after intracoronary infusion of streptokinase in patients with AMI. By reducing the subtotal stenosis, this treatment contributes to the reperfusion of the ischemic myocardium, diminishes the risk of a reocclusion and seems to improve the prognosis.     

Acute electrocardiographic changes associated with successful coronary thrombolysis in acute myocardial infarction

In this study ECG changes were analyzed to assess the acute effects of antegrade blood flow on the ECG in patients with AMI. The study population consisted of 22 patients with MI in whom the totally occluded left anterior descending artery (LAD) or right coronary artery (RCA) was recanalized by intracoronary urokinase infusion (recanalized group) and 14 patients in whom the occluded coronary artery was not successfully recanalized (control group). No significant difference was found in the sum of ST segment elevation (V2-V4 leads for the LAD-occluded group, II, III and aVF leads for the RCA-occluded group) before urokinase infusion. In the recanalized group sigma ST abruptly increased in 5 min after recanalization in 13 of 16 LAD-occluded patients from 1.49 +/- 0.89 mV to 2.44 +/- 1.67 mV (p less than 0.005), and in 4 of 6 RCA-occluded patients from 0.66 +/- 0.12 mV to 1.42 +/- 0.52 mV (p less than 0.01). However increased sigma ST in the recanalized group was reduced to the control value existing before recanalization within 30 min after recanalization and continued to decline more rapidly than in the control group. These transient ST segment elevations were not correlated with long-term angiographic determinants of left ventricular function. We conclude that ST segment shows abrupt augmentation after successful thrombolysis and that continuous ST segment monitoring is useful for assessing thrombolysis in AMI.     

Myocardial ischemia due to coronary artery spasm during dobutamine stress echocardiography

Dobutamine stress echocardiography (DSE) is a useful and safe provocation test for myocardial ischemia. Until now, the test has been focused only on the organic lesion in the coronary artery, and positive DSE has indicated the presence of significant fixed coronary artery stenosis. The aim of the present study is to examine whether myocardial ischemia due to coronary spasm is induced by dobutamine. We performed DSE on 51 patients with coronary spastic angina but without significant fixed coronary artery stenosis. All patients had anginal attacks at rest with ST elevation on the electrocardiogram (variant angina). Coronary spasm was induced by intracoronary injection of acetylcholine, and no fixed coronary artery stenosis was documented on angiograms in all patients. DSE was performed with intravenous dobutamine infusion with an incremental doses of 5, 10, 20, 30, and 40 microg/kg/min every 5 minutes. Of the 51 patients, 7 patients showed asynergy with ST elevation. All 7 patients (13.7%) had chest pain during asynergy, and both chest pain and electrocardiographic changes were preceded by asynergy. These findings indicate that dobutamine can provoke coronary spasm in some patients with coronary spastic angina. When DSE is performed to evaluate coronary artery disease, not only fixed coronary stenosis, but also coronary spasm should be considered as a genesis of asynergy.     

A complication of prolonged urokinase infusion into a chronically occluded aortocoronary saphenous vein graft

Recanalization of a chronically occluded aortocoronary saphenous vein graft was performed, using a prolonged intracoronary infusion of urokinase followed by percutaneous transluminal coronary angioplasty (PTCA). Despite an angiographically successful result, the patient developed acute myocardial infarction, presumably secondary to distal migration of partially lysed thrombus. One week after successful angioplasty, the graft was once again proximally occluded.     

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.     

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.