Early positive technetium-99m stannous pyrophosphate images as a marker of reperfusion after thrombolytic therapy for acute myocardial infarction

Fourteen patients with transmural acute myocardial infarction (AMI) were treated with intravenous streptokinase a mean of 4 +/- 1 hours after chest pain and underwent technetium-99m stannous pyrophosphate (Tc-99m-PPi) imaging 7 +/- 2 hours after the onset of chest pain. The early Tc-99m-PPi images were obtained to test the hypothesis that an early, strongly abnormal Tc-99m-PPi image suggests reperfusion. Eleven of 14 patients had early peaking (within 16 hours) serum creatine kinase isoenzyme levels (CK-B) at a mean of 11 +/- 3 hours. Ten of 14 patients had 3+ or 4+ acute Tc-99m-PPi images. Eight of 11 patients had patent infarct-related vessels at cardiac catheterization 15 days after AMI. One patient who had both an early positive Tc-99m-PPi image and CK-B peak level had an occluded infarct-related artery at catheterization. Acute left ventricular (LV) ejection fraction (EF) by radionuclide ventriculography was compared with LVEF on day 15, and improved from 0.37 +/- 0.13 to 0.50 +/- 0.16 (p = 0.004) in the 10 patients with strongly positive acute Tc-99m-PPi images. LVEF also improved from 0.37 +/- 0.12 to 0.49 +/- 0.15 (p = 0.003) in the 11 patients with early peaking serum CK-B values. Three patients without evidence of reperfusion failed to improve the LVEF from the initial value to the one obtained at hospital discharge. Six control patients had acute Tc-99m-PPi images 10 +/- 2 hours after chest pain; none had strongly positive acute Tc-99m-PPi images, and the mean time to peak CK-B was 19 +/- 5 hours.(ABSTRACT TRUNCATED AT 250 WORDS)     

Noninvasive markers of intravenous streptokinase coronary thrombolysis

Early creatine kinase (CK) enzyme peaking, rapid electrocardiographic (EKG) changes toward normal, reperfusion arrhythmias, pain disappearance, and 201thallium myocardial scintigraphy appear useful to identify the success or failure of intravenous (i.v.) thrombolytic therapy in patients with acute myocardial infarction (AMI). Most patients with AMI are treated currently in community hospitals which do not possess coronary angiographic capabilities. Recent evidence indicates that early intravenous streptokinase results in coronary thrombolysis in the majority of patients treated. A composite of noninvasive markers of coronary reperfusion was assessed in two similar patients with transmural AMI. One received intravenous streptokinase (STK) 750,000 U 90 min after AMI onset; the other received intracoronary (i.c.) STK 4000 U/min 140 min after onset. Within one hour each showed a sudden change in elevated EKG ST segments toward normal, followed by frequent premature ventricular beats and pain disappearance. Posttreatment angiograms documented recanalization of each infarct-related artery. Early CK peaking occurred at 10 hours after the onset of chest pain in the first patient and at 12 hours in the second. This contrasts with delayed CK peaking at 26.4 hours among 384 patients reviewed with untreated AMI. Early CK peaking appears the most accurate indirect marker of successful coronary thrombolysis.     

Management of Patients with Heparin-Induced Thrombocytopenia: Focus on Recombinant Hirudin

It remains controversial whether percutaneous transluminal coronary angioplasty (PTCA) performed 24 hours after the onset of acute myocardial infarction (AMI) in coronary arteries with 99% stenosis is useful in preserving left ventricular function. We investigated the effectiveness of PTCA in preventing left ventricular remodeling when it was performed 24 hours after the onset of AMI in infarct-related coronary arteries (IRCAs) having 99% stenosis and thrombolysis in myocardial infarction (TIMI) grade 3 flow. The subjects were 19 patients with AMI (anterior wall, 9 patients; inferior wall, 7 patients; and non-Q, 3 patients) who, within 24 hours of the onset of AMI, underwent coronary angiography and left ventriculography during the acute and/ or chronic phases. The patients were divided into a PTCA group, comprised of patients in whom PTCA was successfully performed 24 hours after the onset of AMI (n = 10), and a non-PTCA group (n = 9). The non-PCTA group included patients who were successfully reperfused by thrombolysis and did not include patients who had spontaneous reperfusion or reperfusion after PTCA. In the non-PTCA group, the left ventricular end-diastolic volume (mean ± SD) was significantly increased in the chronic phase (86 ± 23 mL/m² as compared with the acute phase (67 ± 13 mL/m², whereas in the PTCA group no significant difference was observed between end-diastolic volumes in the acute and chronic phases (67 ± 26 and 68 ± 13 mL/m², respectively). Left ventricular remodeling is prevented by PTCA when it is performed 24 hours after the onset of AMI in IRCAs with 99% stenosis and TIMI grade 3 flow.     

Shunt between the ventricular chamber and coronary arteries preserves left ventricular function in acute myocardial infarction.

It is controversial whether newly created channels made by transmyocardial laser revascularization are functionally significant, so the present study evaluated the shunt flow from the left ventricular (LV) cavity to the ischemic myocardium in 51 patients with acute myocardial infarction (AMI) caused by complete occlusion of the proximal left anterior descending coronary artery. All patients underwent left heart catheterization within 24 h of onset and all underwent successful coronary reperfusion using primary coronary angioplasty with no angiographic restenosis on follow-up coronary angiography (CAG). The presence of the LV shunt flow was evaluated by selective left CAG after successful reperfusion. The LV global ejection fraction (EF) and regional function (centerline method) were analyzed by ventriculography in both the acute and chronic phases. The patients were divided into the 3 groups (Group A, no LV shunt without collaterals, n=20; Group B, no LV shunt with collaterals, n=24; Group C, LV shunt with collaterals, n=7). There was no difference in the grade of collateral circulation between Groups B and C. The improvements in LVEF and regional function from the acute phase to the chronic phase were significantly greater in Group C than in Groups A and B. Not only collateral circulation but also LV shunt contributes to the functional recovery of infarct myocardium in patients with AMI.     

Importance of early initiation of intravenous streptokinase therapy for acute myocardial infarction

The importance of timing of intravenous streptokinase (SK) administration in patients with acute myocardial infarction (AMI) was evaluated. Intravenous SK, 750,000 U, was administered within 4 hours of the onset of ischemic chest pain to 72 consecutive patients having their first AMI. Six days later, cardiac catheterization was performed to calculate global ejection fraction (EF), and computer-derived infarct-related regional EF and dysfunction index were also determined; electrocardiograms were recorded, from which QRS scores could be calculated to estimate infarct size. Of 19 patients who had an anterior AMI, 12 (63%) who received intravenous SK within 2 hours after onset of pain sustained only minimal damage in terms of global EF, infarct-related EF, dysfunction index and QRS score. All 10 patients who received SK 2 to 4 hours after pain onset had large infarcts (p less than 0.001). Of the former group, 11 of 12 patients (91%) whose pain was relieved within 1.5 hours of intravenous SK administration (presumably due to successful reperfusion) had a good outcome, whereas all 7 whose pain lasted longer did poorly (p less than 0.001). Furthermore, among patients with anterior AMI, 11 of 14 (79%) whose pain was relieved within 3.5 hours of onset had small infarcts, compared with none of the 12 patients whose pain lasted longer (p less than 0.0001). In inferior AMI, the critical time between onset of pain and initiation of intravenous SK was 1.5 hours (p less than 0.05). The timing of initiation of thrombolytic therapy and the total pain duration are critical in determining outcome in AMI, and time intervals vary depending on infarct localization.     

Electrically induced ventricular arrhythmias in acute myocardial infarction treated with thrombolytic agents

Ninety-two patients underwent programmed ventricular stimulation 12 +/- 3 days after acute myocardial infarction (AMI) treated with thrombolytic agents (streptokinase, recombinant tissue plasminogen activator, or both). Cardiac catheterization was performed in all patients on admission to hospital and was repeated in 97% of them 13 +/- 5 days later. Sustained ventricular arrhythmias--either tachycardia (VT) or fibrillation--were induced in 20 (22%) patients, with nonsustained VT induced in another 12 (13%). Multivariate analysis was used to identify predictors of induction of sustained VT, with short right ventricular effective refractory period (p = 0.0061), site of AMI (inferior or posterior, p = 0.008), infarct-related artery (right or circumflex coronary artery, p = 0.018), multivessel coronary artery disease (p = 0.043) and male sex (p = 0.028) being significant predictors of sustained VT. Neither successful reperfusion, time to reperfusion, nor residual stenosis in the infarct-related artery was significant. All patients in whom VT was induced were treated with electrophysiologically guided antiarrhythmic therapy. Cardiac mortality after hospital discharge was 1% over 30 +/- 16 months.     

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.     

Importance of early and complete reperfusion to achieve myocardial salvage after thrombolysis in acute myocardial infarction.

The importance of the timing and completeness of coronary artery reperfusion for limitation of acute myocardial infarction (AMI) size after intravenous thrombolytic therapy was studied in 39 patients. All had electrocardiographic epicardial injury and acute coronary angiography performed < 8 hours after symptom onset. Acutely jeopardized myocardium was estimated at baseline, and before and after angiography by quantitative ST-segment analysis. The AMI size was estimated on the final electrocardiogram by the Selvester QRS score. Left ventricular ejection fraction was measured at the time of acute angiography and before discharge in 31 of these patients. In the 21 patients with normal flow (Thrombolysis in Myocardial Infarction [TIMI] trial grade 3) in the infarct-related artery, the amount of jeopardized myocardium decreased from baseline to that before and after angiography (17 to 11 and 11%, respectively; p < 0.00005), and the median final AMI size was reduced (17 to 9%; p = 0.0004). In 6 patients with suboptimal flow (TIMI grade 2), the median amount of jeopardized myocardium decreased slightly from baseline to that before to after angiography (15 to 12%); however, the median final AMI size was not reduced (17%). In 12 patients with no reperfusion (TIMI 0 to 1) flow, the median amount of jeopardized myocardium remained unchanged from baseline to that before angiography (21%), and the final AMI size was not significantly reduced. There was a significant inverse correlation between the change in global left ventricular function and the difference between electrocardiographic estimated jeopardized and final AMI size (rs = -0.53; p = 0.008).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of the collateral circulation on myocardial salvage in patients with acute myocardial infarction]

The effects of the extent of coronary collateral circulations, the duration of myocardial ischemia and recanalization of infarct-related vessels on left ventricular function were evaluated in 43 patients with acute anteroseptal myocardial infarction. All patients had complete occlusions of their proximal left anterior descending coronary arteries and were treated with intra-coronary thrombolytic therapy within 8 hours after the onset of their chest pain. The 43 patients were categorized in 4 groups based on the extent of their coronary collaterals in the early period of myocardial infarction and the results of thrombolysis. Group A consisted of 11 patients with well-developed collaterals who had successful thrombolysis. Group B was comprised of 14 patients with poorly developed or no collaterals, and successful thrombolysis. In group C, there were 9 patients with well-developed collaterals and unsuccessful thrombolysis. In group D, there were 9 patients who had poorly or not developed collaterals, and all had unsuccessful thrombolysis. Four weeks after the intervention, ejection fraction (EF) and regional wall motion (RWM) were calculated from the data of the left ventricular angiograms. There was no significant difference in patients' age, sex, nor in peak serum creatine kinase among the 4 groups or the duration of myocardial ischemia between groups A and B. Patients with successful thrombolysis (groups A and B) had significantly higher EF and preserved RWM of infarct areas compared to patients with unsuccessful thrombolysis (groups C and D, p less than 0.05). Thirteen patients with early reperfusion (within 4 hours after the onset of chest pain) had significantly higher EF and better RWM than did 12 patients with late reperfusion and 18 patients with unsuccessful thrombolysis (p less than 0.01). However, there was no significant correlation between the duration of myocardial ischemia and RWM of the infarct areas among 25 patients who had successful thrombolysis (r = -0.3, NS). Patients in group A had higher EF and better RWM of infarct areas than did patients in groups B, C and D (p less than 0.01). In addition, 3 patients with well-developed collaterals had good RWM despite late reperfusion which occurred more than 4 hours after the onset of symptoms. These results suggest that the extent of coronary collaterals during the early period of myocardial infarction and the time delay from the onset of symptoms to the initiation of thrombolytic therapy are important factors for the salvage of left ventricular function in patients with myocardial infarction.     

Radionuclide evaluation of postextrasystolic potentiation of left ventricular function induced by atrial and ventricular stimulation

Postextrasystolic potentiation of left ventricular function induced by ventricular and atrial stimulation was compared in 10 patients using radionuclide ventriculography. After insertion of pacing wires, a preliminary radionuclide ventriculogram was obtained and then ventricular and atrial trigeminy was induced in random order, each with identical R-R coupling intervals, each for 6 to 10 minutes. During the stimulation studies, radionuclide data were acquired in electrocardiographic gated list mode format. Left ventricular ejection fraction and relative end-diastolic and end-systolic volume changes were measured for each reformatted composite sinus, atrial and ventricular premature beat and potentiated beat. The volume changes were normalized to the count-based values obtained for the sinus beat of the appropriate study. Postextrasystolic potentiation induced by either ventricular or atrial stimulation was characterized by similar significant increases in left ventricular ejection fraction (mean ± standard deviation 7 ± 3 percent, p < 0.01 versus 7 ± 5 percent, p < 0.01; difference not significant [NS]) and decreases in relative end-systolic volume (?12 ± 12 percent, p < 0.01 versus ?12 ± 8 percent, p < 0.01; NS) but little change in relative end-diastolic volume (+5 ± 10 percent, NS versus +4 ± 7 percent, NS; NS). This was despite a longer compensatory pause (1,120 ± 220 versus 1,050 ± 190 ms, p < 0.01) after the ventricular premature beat. It is concluded that there is no difference in the postextrasystolic potentiation induced by atrial or ventricular premature stimulation.     

Reperfusion phenomenon is a strong predictor of left ventricular remodeling after acute myocardial infarction.

BACKGROUND:Many clinicians have seen the reperfusion phenomenon, a paradoxical response that includes a transient increase of chest pain, additional ST-segment elevation or ventricular arrhythmias immediately after coronary reperfusion, in patients with acute myocardial infarction (AMI). The aim of the present study was to investigate the impact of this phenomenon during coronary reperfusion on left ventricular (LV) remodeling in patients with AMI. METHODS AND RESULTS: One hundred and thirty-eight consecutive patients with a first anterior-wall AMI, undergoing coronary reperfusion treatment within 24 h of onset were prospectively evaluated for reperfusion phenomenon and followed up with scheduled evaluations of LV function and morphology with left ventriculography for 1 year. Of the 138 enrolled patients, 77 underwent serial left ventriculography at the acute, subacute and 1-year phases. Of these 77 patients, 39 demonstrated the reperfusion phenomenon. The LV end-diastolic volume index significantly increased from the acute to subacute phase and to the 1-year phase, but was unchanged in the 38 patients without reperfusion phenomenon. In multivariate analysis, reperfusion phenomenon was the only determinant of LV dilatation after AMI. CONCLUSIONS: Reperfusion phenomenon was a strong predictor of LV remodeling after reperfusion therapy for AMI.     

Preservation of global and regional left ventricular function after early thrombolysis in acute myocardial infarction

The effect of early myocardial reperfusion (within 4 hours after onset of symptoms) on regional left ventricular function in patients with acute myocardial infarction has been quantitated by analysis of segmental wall motion. Of 533 patients randomized either to conventional coronary care unit therapy or to a reperfusion strategy, in 332 high quality angiograms were obtained 2 to 8 weeks after the onset of myocardial infarction. In those assigned to thrombolytic therapy, angiographic data were also available after acute reperfusion. Analysis on an "intention to treat" basis revealed significant preservation of left ventricular function after thrombolytic therapy (ejection fraction 53%) compared with conventional treatment (ejection fraction 47%). In addition, wall motion analysis showed significant improvement of regional function in the infarct zone in both inferior and anterior infarction. In addition, significant changes occurred in regional function of the remote "noninfarct zone" in the acute as well as the chronic stage. It is concluded that improved regional and global left ventricular function can be achieved with early reperfusion and that this is the likely explanation for the reduction of early and late mortality after thrombolysis observed in this study.     

Intracoronary streptokinase in evolving acute myocardial infarction

Intracoronary application of thrombolytic agents, particularly streptokinase, can recanalize arteries that had been totally occluded in patients with evolving acute myocardial infarction (AMI). Numerous uncontrolled trials have testified to the effectiveness of thrombolytic therapy in most patients in reestablishing flow to the infarct-related coronary artery. Follow-up of patients in whom reperfusion has been established has often demonstrated small but significant increases in the left ventricular ejection fraction. In contrast, in other patients in whom thrombolytic therapy failed to reopen the occluded vessel, the left ventricular ejection fraction usually does not change during follow-up. In most reported uncontrolled trials, few complications are described and the mortality rate in patients treated by this therapy may be lower than expected. These data have been used as the basis for widespread application of this technique in many catheterization laboratories around the world. Our initial experience at the University of Florida in 23 patients has not been as successful as other uncontrolled trials previously reported. Reperfusion was accomplished in only 12 patients. Of 17 who survived their AMI, only five demonstrated an improved left ventricular ejection fraction of at least 10%. Serious complications, including bleeding from catheterization sites or allergic reactions to streptokinase, occurred. Controlled trials to critically evaluate this new therapy are needed and are in progress.     

Indices of reperfusion in patients with acute myocardial infarction using characteristics of the CK-MB time-activity curve

The purpose of this study was to identify indices of coronary artery reperfusion in patients treated with thrombolytic therapy for acute myocardial infarction (AMI) by means of characteristics from the serum creatine kinase (CK) isoenzyme MB time-activity curve. Frequent blood sampling as performed in three groups with a first AMI: 29 patients treated with intravenous thrombolytic therapy who had a patent infarct-related artery with normal flow (TIMI-3) at acute catheterization (reperfusion group); four patients with a persistently closed infarct-related artery (no reperfusion group); and 44 patients who did not receive any therapy aimed at coronary reperfusion (no thrombolytic therapy group). In the latter group we prospectively estimated that 25% would have spontaneous reperfusion. A physiologically based computer-calculated multi-compartment method was used to determine the characteristics of the serum CK-MB time-activity curve. In addition to demonstrating an earlier increase, a shorter time to peak of serum CK-MB and a lower estimated infarct size in the reperfusion group (p = 0.025 to 0.00001), the appearance rate constant (k1) and time from estimated initial increase to peak of CK-MB in the blood stream (tRP) were significantly different from those values in the no thrombolytic therapy group (p less than 00001). A cutoff level indicating reperfusion if k1 was greater than 0.185 or tRP was less than 16.5 hours demonstrated overlapping values between these two groups in only four patients (k1), two patients (tRP), and six patients with a combination.(ABSTRACT TRUNCATED AT 250 WORDS)     

急性心肌梗死后存活心肌对梗死相关血管晚期血运重建术后左室功能的影响

目的探讨存活心肌对急性心肌梗死(AMI)后梗死相关血管(IRA)晚期血运重建术后远期左室功能以及左室重构的影响.方法69例AMI未接受早期再灌注治疗者,于发病10～21 d行IRA经皮冠状动脉血运重建(PCI)术,术前于AMI发病后5～10 d应用小剂量多巴酚丁胺(5和10μg·min-1·kg-1)超声心动图负荷试验检测存活心肌,并分别测定和计算给药前后左室腔大小、左室射血分数(LVEF)以及室壁运动积分(WMS).按有无存活心肌分为存活心肌组和无存活心肌组,超声心动图随访术后6个月时两组左室腔大小、LVEF和WMS的变化.结果157个运动异常节段中89个节段(57%)有存活心肌,有存活心肌组26例(占38%),无存活心肌组43例(占62%).存活心肌组术后6个月LVEF较术前明显提高(P＜0.05),收缩末期容积指数(LVESVI)和WMS明显降低(P＜0.05和P＜0.01);而无存活心肌组LVEF较术前明显降低(P＜0.01),LVESVI和左室舒张末期容积指数(LVEDVI)较术前明显增加(P＜0.05),WMS无明显变化.存活心肌组多巴酚丁胺负荷时的LVEF和WMS明显改善,且与6个月时的测定值相近;而无存活心肌组PCI前应用多巴酚丁胺LVEF和WMS均无明显变化.结论AMI后有存活心肌者晚期血运重建有利于改善远期左室功能和减少左室重构.心肌梗死后早期小剂量多巴酚丁胺负荷状态下左室收缩功能的提高预示晚期血运重建术后心功能改善.     

Planar myocardial scintigraphy with 99mTc sestamibi for the evaluation of the infarct area and the efficacy of the thrombolytic therapy]

BACKGROUND: Nuclear cardiology permits the estimation of myocardial infarction size and the result of the thrombolytic therapy. The aim of the study was to demonstrate the feasibility of the planar myocardial scintigraphy with tecnetium-99m-sestamibi in the coronary intensive care unit for the early identification of the infarct size and the results of the thrombolytic therapy. MATERIAL AND METHODS: We studied 15 patients affected by a first acute myocardial infarction (AMI), 10 anterior and 5 inferior wall, treated with thrombolysis (APSAC 30U i.v.) within and interval of 3 hours from the symptoms onset, tecnetium-99m-sestamibi was injected before thrombolysis and after 3 +/- 1 hours the planar imaging was registered with a mobile gamma-camera. Scintigraphic evaluation was repeated after 24 hours and before patient discharge. Within 48 hours from the thrombolytic therapy the coronary angiography was performed for the demonstration of patency of the infarct-related artery. The left ventricle myocardial perfusion was divided in the 3 planar projections into 13 segments. The perfusion in each segment was evaluated with a perfusion score: 0 = normal, 1 = moderately reduced, 2 = severely reduced, 3 = absent. The sum of the hypoperfused segments represented the infarct size. A perfusion score improvement greater than 40% was considered a marker of reperfusion. RESULTS: The infarct size involved 4.2 +/- 1.5 segments in the anterior and 2 +/- 0.8 segments in the inferior wall infarctions (p < 0.05). The scintigraphic imaging made 24 hours after AMI allowed the diagnosis of coronary reperfusion in 10 patients. The coronarography demonstrated the infarct related artery patency in 14 patients. The nuclear imaging at patient discharge provided the diagnosis or reperfusion in 11 cases and demonstrated an improvement of the myocardial perfusion score in 8 cases. CONCLUSIONS: In patients with AMI treated with thrombolysis the scintigraphic imaging with tecnetium-99m-sestamibi is feasible with a mobile gamma-camera in the intensive coronary care unit. The quality of planar imaging is good and allows the evaluation of myocardial infarct size and the efficiency of thrombolytic therapy. An earlier scintigraphic imaging should be taken into consideration for a more timely non-invasive evaluation of patients who need coronary angiography and, if necessary, a rescue-PTCA.     

Influence of coronary collateral vessels on myocardial infarct size in humans. Results of phase I thrombolysis in myocardial infarction (TIMI) trial. The TIMI Investigators

BACKGROUND. The influence of coronary collateral vessels on infarct size in humans remains controversial, partly because no previous study has examined the impact of collaterals present at the onset of acute myocardial infarction on infarct size. METHODS AND RESULTS. The present study used the data base of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial to correlate the presence or absence of angiographically documented collaterals in the initial hours of myocardial infarct evolution with the size of the infarct as assessed by serial measurements of serum creatine kinase (CK). To avoid the confounding effects of reperfusion on enzymatic estimates of infarct size, this report is limited to those 125 patients who failed to recanalize at 90 minutes after administration of tissue plasminogen activator or streptokinase. Patients with angiographically documented collaterals (group A, n = 51) had significantly lower values of peak serum CK than patients without collaterals (group B, n = 74) (1,877 +/- 216 versus 2,661 +/- 212 IU/l, respectively [mean +/- SEM], p = 0.004). Similarly, CK-derived infarct size estimates were significantly lower in group A than in group B (20.6 +/- 2.5 versus 31.4 +/- 2.8 CK gram equivalents, p = 0.001). The infarct size observed in patients with collaterals was less for anterior infarctions as well as for infarctions of other locations; thus, the beneficial effects of collaterals were independent of the site of the infarct. In 65 of the 125 patients who failed to reperfuse, left ventricular ejection fraction (LVEF) was assessed by contrast ventriculography both at initial cardiac catheterization (before thrombolytic therapy) and at hospital discharge. Among the patients who had both studies, global LVEF tended to increase from pretreatment to hospital discharge in group A (from 50.6 +/- 1.8% to 53.4 +/- 1.8%, p = 0.10) but decreased in group B patients (from 50.3 +/- 1.8% to 47.8 +/- 1.7%, p = 0.02). At hospital discharge, global LVEF was greater in patients with coronary collaterals (53.5 +/- 1.7% versus 49.6 +/- 1.7%, p = 0.01). CONCLUSIONS. The results demonstrate that, in patients in whom thrombolytic therapy fails to induce reperfusion, the presence of coronary collateral vessels at the onset of myocardial infarction is associated with limitation of infarct size as assessed enzymatically and with improved ventricular function on discharge as assessed by LVEF.     

Effects of intravenous sm-9527 (double-chain tissue plasminogen activator) on left ventricular function in the chronic stage of acute myocardial infarction

Clinical effects of thrombolytic agent SM-9527 (double-chain tissue plasminogen activator) on left ventricular (LV) function were assessed in patients with acute myocardial infarction (AMI). A dose of 30 × 10⁶ IU SM-9527 was given intravenously to patients with AMI within 6 h after onset Of 159 candidates, 20 were excluded from the trial due to diseases other than myocardial infarction or failure to meet the protocol requirements; 114 of the remaining 139 were subjected to LV function analysis. The following results were obtained: (1) Patients with successful reperfusion in response to SM-9527 in the acute stage without later reocclusion revealed a significant improvement of LV function in the chronic stage. (2) Adverse effects were noted in 15 patients (10.8%), but none were serious; all were bleeding related to catheterization. (3) Hemagglutination fibrinolysis system test revealed no problems. It is concluded that early thrombolytic therapy with intravenous SM-9527 for AMI provides significant improvement of LV function in the chronic stage.     

Viable Myocardium Impact on Left Ventricular Function after Late Revascularization of Infarct-related Artery in Acute Myocardial Infarction

Objectives The long-term benefit of late reperfusion of infarct-related artery (IRA) after acute myocardial infarction (AMI) is controversial, and the benefit mechanisms remain uncertain. Low dose dobutamine stress echocardiography (LDSE) can identify viable myocardium and predict improvement of wall motion after revascularization. Methods Sixty-nine patients with first AMI who did not received early reperfusion therapy were studied by LDSE at 5 to 10 days after AMI. Wall motion abnormality and left ventricular size were measured at the same time. Successful PCI were done in all patients at 10 to 21 days after AMI onset. Patients were divided in two groups based on the presence or absence of viable myocardium. Echocardiography was repeated six months later. Results There were 157 motion abnormality segments. 89 segments (57%) were viable during LDSE. 26 patients (38%) with viability and 43 (62%) without. In viable group, left ventricular ejection fraction (LVEF) was increased (P < 0.05), and left ventricular end systolic volume index (LVESVI) and wall motion score (WMS) were decreased (P < 0.05 and P < 0.01) significantly at 6 months compared with baseline. But in patients without viability, LVEF was decreased (P < 0.01), and LVESVI and left ventricular end diastolic volume index (LVEDVI) were increased (P<0.05) significantly after 6 months, and the WMS did not changed (P > 0.05). LVEF increased (P< 0.05) and WMS decreased (P < 0.05) on LDSE during acute phase in patients with viability, but they were not changed in the nonviable group. Conclusions Late revascularization of IRA in patients with presence of viable myocardium after AMI is associated with long-term preservation left ventricular function and less ventricular remodeling. Improvement of left ventricular systolic function on LDSE indicates late phase recovery of left ventricular function after late revascularization.     

High-dose intravenous thrombolytic therapy in acute myocardial infarction: efficiency, tolerance, complications and influence on left ventricular performance

Ten patients with acute myocardial infarction (AMI) underwent coronarographic studies before, immediately after and ten days after an intravenous infusion of 1 500 000 I.U. streptokinase (STK). Mean time between onset of symptoms to initiation of STK infusion was 03 hours 34 minutes. Occlusion of the infarct-related vessel was present in all of them and successful thrombolysis was obtained in 8 of the patients. Systemic fibrinolytic activity was present in 9 patients, one of whom required a transfusion of blood because of severe bleeding. At ventriculography, the global left ventricular ejection fraction and the regional ventricular ejection fraction, whatever the area involved, showed no significant improvement 10 days after the procedure. This suggests that high-dose intravenous STK in AMI, although causing an effective thrombolysis, does not seem to improve early myocardial function.