Early peak activity of creatine kinase in non-thrombolysed myocardial infarction: prognostic factor?

The time elapsed between the onset of pain and serum creatine kinase (CK) peak activity is an indirect marker of reperfusion in the thrombolytic treatment of myocardial infarction, and some authors regard this time as a prognostic factor in infarctions not treated with thrombolysis. CK activity was measured in 90 consecutive patients (mean age 66.9 +/- 13.7 years) with acute myocardial infarction (anginal pain + ECG signs + CK greater than 160 3U/l, including 40 p. 100 of CK MB). Measurements began at the time of admission to the intensive care unit and were repeated 6-hourly until CK levels returned to normal. Mean time of CK peak activity was 19.30 +/- 7.15 h after the initial pain (8 to 55 hours prior to admission). This time was not influenced by age, sex, presence or absence of risk factors and history of coronary disease, nor by the anterior or transmural location of the infarct. In contrast, an early arrival at the intensive care unit was associated with an early CK peak: patients who reached the unit within 6 hours or less had a peak at 18.15 +/- 6 h, whereas those who arrived after 6 h had a peak at 22.30 +/- 9.30 h (p less than 0.01). In addition, cases of infarction without Q wave and with an initially elevated ST segment had an earlier peak than the others (16.30 +/- 5.30 h vs 19 +/- 6.45 h in transmural infarctions and vs 24.30 +/- 7.30 h in infarctions with initially depressed ST; p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of intracoronary fibrinolysis and conventional treatment of myocardial infarction

57 patients with a complete coronary thrombosis were treated by intracoronary fibrinolysis during the first 6 hours of inaugural myocardial infarction. The artery was revascularised in 37 cases (65 p. 100). Eleven patients had isolated stenosis of the left anterior descending artery and 16 patients isolated stenosis of the right coronary artery. These patients were compared with 27 other patients admitted between the 6th and 18th hours of primary myocardial infarction treated conventionally, in whom coronary angiography performed between the 14th and 21st day after infarction showed isolated left anterior descending disease in 14 cases (9 thromboses and 5 stenoses) and isolated right coronary disease in 13 cases (7 thromboses and 6 stenoses). The haemodynamic data and heart rates were identical in both groups during control coronary angiography between the 14th and the 21st days. Global left ventricular function and regional wall motion were studied by 30 degrees right anterior oblique ventriculography using the Stanford method before fibrinolysis in the first group and at the end of the 3rd week in both groups. In LAD, repermeabilisation by fibrinolysis, significant improvements were observed in ejection fraction (EF p. 100 = 42 +/- 9 vs 50.6 +/- 14 p. 100, p less than 0.05); fractional shortening of the hypokinetic segment (FS p. 100 = 4.5 +/- 4.6 vs 12.4 +/- 8.8 p. 100, p less than 0.001), and in the number of hypokinetic or akinetic segments (6.0 +/- 1.1 vs 4.2 +/- 2.1, p less than 0.05). Segmental and global left ventricular function was much poorer in the group treated conventionally at the 21st day (EF p. 100 = 44 +/- 11 p. 100, p less than 0.05; FS p.t100 = 5.8 +/- 9.7 p.t100, p less than 0.05; number of diseased segments: 6.0 +/- 1.4, p less than 0.01). On the other hand, the improvement was less marked in patients with inferior wall infarction; the results in the two groups were comparable.     

Impact of different reperfusion modalities on ventricular function after acute myocardial infarction

Single-plane contrast ventriculography was performed on admission and before hospital discharge in more than 200 patients with acute myocardial infarction participating in a series of prospective clinical trials including intracoronary streptokinase, percutaneous transluminal coronary angioplasty (PTCA), intravenous tissue plasminogen activator (rt-PA) and thrombolysis (intravenous rt-PA or streptokinase) followed by PTCA. Both global ejection fraction (EF) and regional wall motion of the infarct zone were measured to assess serial changes. Patients treated with intracoronary streptokinase 3.6 +/- 1.8 hours after symptom onset had no increase in EF (mean change 1 +/- 6%, difference not significant [NS]), but patients treated with primary PTCA at 3.0 +/- 1.2 hours did (mean improvement 8 +/- 7%, p less than 0.001). Patients treated with sequential intravenous streptokinase and PTCA 2.6 +/- 1.3 hours after symptom onset showed similar improvement in EF (mean change 6 +/- 12%, p less than 0.002). Patients treated with rt-PA had no change in EF whether treated with rt-PA alone or rt-PA followed by immediate angioplasty (mean change -2 +/- 8% and 0.5 +/- 8%, p = NS, respectively). When angioplasty was used in patients with persistent occlusion after thrombolytic therapy, EF improved in those who had received intravenous streptokinase (mean change 10 +/- 7%, p less than 0.002), but not those who had received rt-PA (+0.5%, p = NS). However, infarct zone regional wall motion improved in patients treated with intracoronary streptokinase (+0.59 +/- 0.79 standard deviation/chord, p less than 0.05), primary PTCA (+1.32 +/- 1.32, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Early reocclusion after in situ coronary desobstruction either with streptokinase or angioplasty during the acute phase of myocardial infarction

The aim of this study was to assess the incidence of early reocclusion after therapeutic reperfusion of coronary arteries in acute myocardial infarction. Seventy four patients underwent intracoronary thrombolysis and 133 patients had immediate coronary angioplasty. The success rates were 70 per cent and 86 per cent respectively (p less than 0.01) and the degree of residual stenosis was 77 +/- 13 percent and 25 +/- 15 per cent respectively (p less than 0.001). The patients in whom coronary reperfusion was successful, 52 after in situ thrombolysis, 48 after angioplasty alone, and 66 after combined angioplasty and intravenous thrombolysis, underwent coronary arteriography 24 to 36 hours later. Reocclusion was asymptomatic in 46 per cent of cases (13/28) and its prevalence was 16.9 per cent: 25.5 per cent for the right coronary compared with 12.8 per cent for the left anterior descending (p less than 0.05) and 11.7 per cent for the left circumflex artery; reocclusion occurred in 8.6 per cent of patients treated before the 3rd hour compared with 22.9 per cent of patients receiving treatment after the 3rd hour (p less than 0.05). The incidence of reocclusion was 17.3 per cent after intracoronary thrombolysis and 16.7 per cent after angioplasty (angioplasty alone 18.7 per cent; associated with thrombolysis 15.2%). The degree of residual stenosis was nil after intracoronary thrombolysis and 16.3 per cent after angioplasty when the stenosis was insignificant, and 20.5 per cent and 18.8 per cent respectively with stenotic lesions greater than 50 per cent.     

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.     

Detection of active left ventricular thrombosis during acute myocardial infarction using indium-111 platelet scintigraphy

Platelet scintigraphy with radioactive indium-111 may be used both to identify and to reflect the activity of thrombin in vivo in man. Forty-one patients with acute myocardial infarction were studied for active left ventricular thrombosis by platelet scintigraphy and followed until in-hospital death, discharge, or same-admission cardiac surgery for evidence of systemic embolization. A total of 4.7 +/- 2.4 X 10(9) platelets (mean +/- 1 SD) labelled with 381 mu Ci +/- 51 mu Ci of indium-111 was injected intravenously at 91 +/- 88 hours following the onset of chest pain. Patients were imaged in multiple views on the day of and three to four days after injection of the platelet suspension. Group 1 (n = 29) had transmural myocardial infarctions, of which 21 were anterior (peak total level of creatine phosphokinase [CPK], 2,272 +/- 2,026 IU; mean +/- 1 SD) and eight were inferior (CPK level, 1,673 +/- 589 IU). Group 2 (n = 12) had subendocardial myocardial infarctions (CPK level 799 +/- 751 IU). Those with subendocardial and transmural inferior myocardial infarctions had neither left ventricular thrombosis nor emboli. Ten (48 percent) of 21 with anterior transmural myocardial infarctions had left ventricular thrombosis by platelet scintigraphy. Three with and one without such thrombosis by scintigraphy had acute neurologic episodes. In the group with anterior myocardial infarctions, seven of ten patients with and four of 11 without left ventricular thrombosis received heparin subcutaneously (chi 2 = 1.22 [Yates correction]; p greater than 0.30). We conclude that platelet scintigraphy may be used to monitor antiplatelet and anticoagulant therapy in patients with anterior transmural myocardial infarctions who are at risk for left ventricular thrombosis and systemic embolization.     

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.     

Effect of thrombolysis (streptokinase) on left ventricular function during acute myocardial infarction

One hundred ninety-two consecutive patients with acute myocardial infarction were enrolled in a prospective trial of coronary thrombolysis in which either intracoronary or intravenous streptokinase was administered. First-pass radionuclide ejection fraction (EF) was measured early (within 24 hours of admission) and late (10 to 14 days after admission) to assess changes in left ventricular (LV) function. In 68 patients in whom reperfusion was successful, mean EF increased from 39 +/- 11% early to 47 +/- 13% late. In 36 patients in whom reperfusion was not successful, the mean EF increase was significantly smaller (from 38 +/- 10% to 42 +/- 11%, p less than 0.025). Patients in whom reperfusion was successful were then grouped according to extent of LV functional change. The extent of EF change (delta EF) was not significantly influenced by time to lysis at intervals up to 7 hours (delta EF = 9.1 +/- 10% at 2 to 3 hours, 8.7 +/- 12% at 3 to 4 hours, 10 +/- 10% at 4 to 5 hours, and 7.0 +/- 10% at 5 to 7 hours; difference not significant [NS]), location of the infarct (delta EF = 8.9 +/- 11% for inferior and 5.7 +/- 8.0% for anterior, NS), or presence of Q waves on the initial electrocardiogram (delta EF = 8.8 +/- 11% in patients with and 7.8 +/- 9.9% in patients without Q waves). Only the initial EF was predictive of subsequent EF change.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary angioplasty after intravenous streptokinase in acute myocardial infarction: influence of restenosis on clinical outcome and left ventricular function

The importance of recurrence of stenosis on clinical outcome and left ventricular function was studied in a consecutive series of patients with acute evolving myocardial infarction (maximal duration of pain 4 h) and thrombolysis (1.5 x 10(6) units of streptokinase intravenously over 60 min) with recanalized single-vessel disease and subsequent successful coronary angioplasty. Coronary angioplasty was performed in 76 patients between 24 hours and 8 days (mean interval 3.3 days) after thrombolysis and was successful in 86% (65/76). The in-hospital reinfarction rate was 5.2% (2 acute and 2 in-hospital reinfarctions). Repeat angiography after a mean interval of 5.9 months revealed a 39% (24/62) restenosis rate (21 restenoses, 3 reocclusions). Restenoses were associated with significantly more clinical complaints (21% vs. 62%; p less than 0.001). Left ventricular function analysis showed significant improvement in the mean global ejection fraction (6.6 +/- 6.0%; p less than 0.001) and mean regional wall motion of the infarct zone (6.2 +/- 8.2%; p less than 0.01) only in patients without restenosis. Recovery of left ventricular function was more evident in inferior than in anterior wall infarctions. In contrast, patients with restenosis had no change in left ventricular function. Thus, the present study demonstrates the adverse influence of restenosis on recovery of left ventricular function and clinical outcome.     

Anterior ST depression in inferior myocardial infarction: correlation with results of intracoronary thrombolysis

Thirty-eight patients underwent left ventricular angiography and coronary arteriography within the first 6 hours of inferior myocardial infarction, in an attempt at intracoronary thrombolysis with streptokinase. Twenty-three of these patients presented with ST segment depression of more than 1 mm on the anterior leads (V1 to V4) of ECGs done immediately before the attempt at thrombolysis (group I), whereas 15 did not (group II). Quantitative analysis of left ventricular angiography showed an ejection fraction significantly lower in group I (51 +/- 10%) than in group II (59 +/- 7%; p less than 0.01). This difference was the result of inferior hypokinesia which was larger both in surface area (group I = 11.5 +/- 6.5 cm2; group II = 4.2 +/- 2.7 cm2; p less than 0.001) and in percentage of ventricular perimeter (group I = 46 +/- 14%; group II = 27 +/- 12%; p less than 0.001). The prevalence of a left anterior descending artery lesion and the degree of stenosis were the same in both groups. The success rate of thrombolysis was not significantly different. However, in cases of persistent success, there was an improvement of regional contraction only in group I, as opposed to absence of change in group II. These results suggest that patients with inferior myocardial infarction and ST anterior depression have an extensive ischemic area rather than anterior wall ischemia. An attempt at coronary thrombolysis seems to be worthwhile only in these patients, as it results in appreciable myocardial salvage when successful.     

Clinical and angiographic results of delayed revascularization by angioplasty or bypass after intravenous thrombolysis in myocardial infarction]

Between 1988 and 1990, 150 patients treated for an infarction by intravenous thrombolysis underwent coronary arteriography. Sixty seven were managed by revascularisation by angioplasty (n = 49) or bypass (n = 18) more than 48 hours after thrombolysis. In this delayed revascularisation group, the time before initial fibrinolysis was 114 +/- 55 minutes. The artery responsible for the infarction was patent in 88 per cent of cases at 12 +/- 9 days, with ejection fraction being 56 +/- 12 per cent. Indications for revascularisation were: recurrence of angina, Thallium stress test showing redistribution (n = 9), diffuse lesions (n = 11) or tight (greater than 75 per cent) proximal stenosis without vessel wall sequelae (n = 10). Comparison of the bypass and angioplasty groups showed a lower ejection fraction in the former than the latter (47% VS 58%, p less than 0.01), more frequent three-vessel disease (50% VS 6%, p less than 0.01) and more frequent revascularisation of the anterior interventricular (100% VS 37%, p less than 0.01). There were 2 deaths and 5 recurrences of infarction at one year. Follow-up arteriography was performed between at 2 and 6 months in 72% of the patients: 16 had restenosis after angioplasty and 4 occlusion of the graft after bypass. A second revascularisation procedure was necessary 15 times (14 angioplasties, 1 bypass). The outcome after bypass or angioplasty was favourable in 90% of cases in this group of patients exposed to a recurrence of infarction.     

Compensatory and noncompensatory left ventricular dilatation after myocardial infarction: time course and hemodynamic consequences at rest and during exercise.

Survival after myocardial infarction decreases with left ventricular dilatation, although dilatation at 4 weeks was found to be compensatory. To study this apparent discrepancy, prospective simultaneous volume and hemodynamic measurements at rest were extended in 39 patients with small and 37 with large myocardial infarctions from 4 (range 2 to 6) days and 4 (range 3 to 5) weeks to 6 (range 5 to 8) months after myocardial infarction and were repeated during exercise. In small myocardial infarctions, end-diastolic volume index (EDVI) decreased from 4 days to 6 months; ejection fraction, stroke volume index (SVI), and end-systolic volume index (ESVI) remained unchanged. SVI increased during exercise at 4 weeks and at 6 months. In large myocardial infarctions (n = 37) ESVI (4 days = 38 +/- 3, 4 weeks = 47 +/- 3,* 6 months = 52 +/- 3*; *p less than 0.05 versus 4 days) and EDVI (4 days = 72 +/- 3, 4 weeks = 86 +/- 5,* 6 months = 92 +/- 5* ; *p less than 0.05 versus 4 days and p less than 0.05 versus 4 weeks) increased at constant wedge pressure. SVI remained unchanged beyond 4 weeks (4 days = 35 +/- 2, 4 weeks = 42 +/- 2*, 6 months = 42 +/- 2*; *p less than 0.05 versus 4 days) and increased during exercise at 4 weeks (rest = 45 +/- 2, exercise = 55 +/- 3; p less than 0.05) but not at 6 months (rest = 42 +/- 3, exercise = 45 +/- 3; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Changes in contractile function of the left ventricle under the effect of thrombolytic reperfusion of the coronary arteries in acute myocardial infarct

A total of 73 patients with myocardial infarction (MI) were included into a prospective study involving intravenous and/or intracoronary streptokinase administration. The total ejection fraction (EF) and the extent of left ventricular dys- and akinetic areas were measured by contrast ventriculography in the first 3-9 hours and 4 weeks after the onset of MI symptoms. Coronary reperfusion performed in the first 3 hours after the onset of symptoms in patients with anterior MI (n = 8) and following 3-9 hours (mean 6.6 +/- 0.89 hours) in patients with inferior MI (n = 17) significantly (p less than 0.05) reduced the extent of dys- and akinetic areas from 20.5 +/- 4.16 to 6.0 +/- 3.99 and 10.0 +/- 1.56 to 5.0 +/- 1.74%, respectively) following 4 weeks. EF significantly (p less than 0.01) increased in the former and tended to show an increase from 51.0 +/- 2.44 to 64.0 +/- 2.26% (p less than 0.1) in the latter. In patients with anterior MI (n = 19) there was a tendency to a decrease in the extent of dys- and akinetic areas from 26.0 +/- 2.85 to 17.0 +/- 3.9 (p less than 0.1) following 3-9 hours. No substantial changes were observed in the values of left ventricular dys- and akinesis and EF in patients with anterior (n = 13) and inferior (n = 16) MI without coronary reperfusion.     

Evolution of systolic function and myocardial perfusion,evaluated by gated-SPECT,in the first year after acute myocardial infarction

INTRODUCTION AND OBJECTIVES: Systolic function and myocardial perfusion are evaluated before hospital discharge and can change during follow-up. The purpose of this study was to evaluate these parameters by gated-SPECT in the first year after acute myocardial infarction. PATIENTS AND METHOD: We studied 74 consecutive patients with a first uncomplicated acute myocardial infarction (49 infero-lateral and 25 anterior) by stress-rest 99mTc-tetrofosmin and rest-gated-SPECT before hospital discharge (6-8 days after admission) and one year after myocardial infarction. RESULTS: The ejection fraction (EF) increased > 5% in 51% of infero-lateral infarcts and 28% of non-revascularized anterior infarcts. EF increased significantly (48.4 8% to 54.6 8.7%; p < 0.0001, mean difference: 6.2; 95% IC, 2.8-9.5) and systolic volume decreased (51.3 19.2 ml to 44.3 19.4 ml; p = 0.001; mean diff.: 7.67; 95% IC, 1.5-13.8) in infero-lateral infarctions. The rest perfusion index in the necrotic region improved (2.3 0.57 to 2.17 0.58; p = 0.004; mean diff.: 0.18; 95% IC, 0.003-0.36) in infero-lateral infarcts and the ischemia index remained unchanged between the first and second studies. CONCLUSIONS: Left ventricular systolic function can change during the first year of evolution, a significant improvement being seen in infero-lateral infarctions. The ejection fraction increased > 5% in half of these patients, as opposed to only a quarter of anterior infarctions. This improvement was associated to increased myocardial perfusion at rest.     

Experimental study on myocardial salvage by coronary thrombolysis and mechanical recanalization

Salvage of the ischemic myocardium by coronary thrombolysis and mechanical recanalization (simulated angioplasty) was studied in a canine experimental model of acute myocardial infarction induced by coronary occlusive thrombus at the left anterior descending coronary artery. Forty-four open-chest dogs divided into three groups were studied. Group I (n = 15, control group) was observed for 6 hours following the onset of infarct. In group II (n = 14, thrombolysis group), thrombolysis was obtained by intravenous administration of urokinase 2 hours after the onset of infarct. In group III (n = 15, mechanical recanalization group), simulated angioplasty was performed 2 hours after infarct. Coronary reperfusion was continued for 4 hours in groups II and III. The areas of left ventricular risk and infarct were measured by double staining methods with Evans blue dye and triphenyl tetrazolium hydrochloride. There were no significant differences in control blood flow and risk area in the three groups. Myocardial infarct area/risk area was 65 +/- 3% in group I, 45 +/- 1% in group II, and 35 +/- 2% in group III (group I vs II, p less than 0.001; group II vs III, p less than 0.001). Restored coronary blood flow in the left anterior descending artery was 8 +/- 1 ml/min in group II and 14 +/- 1 ml/min in group III (p less than 0.001). The data suggest that coronary mechanical recanalization is more effective than thrombolysis in salvaging the ischemic myocardium in the early phase of myocardial infarction, most probably because coronary blood flow is better restored by mechanical recanalization.     

A prospective, randomized trial comparing combination half-dose tissue-type plasminogen activator and streptokinase with full-dose tissue-type plasminogen activator. Kentucky Acute Myocardial Infarction Trial (KAMIT) Group

BACKGROUND. The potential benefits of combination thrombolytic agents in the treatment of myocardial infarction remain uncertain. In a small pilot study, we demonstrated that combining half-dose tissue-type plasminogen activator (t-PA) with streptokinase (SK) achieved a high rate of infarct vessel patency and a low rate of reocclusion at half the cost of full-dose t-PA. METHODS AND RESULTS. We designed a prospective trial in which 216 patients were randomized within 6 hours of myocardial infarction to receive either the combination of half-dose (50 mg) t-PA with streptokinase (1.5 MU) during 1 hour or to the conventional dose of t-PA (100 mg) during 3 hours. Acute patency was determined by angiography at 90 minutes, and angioplasty was reserved for failed thrombolysis. Heparin and aspirin regimens were maintained until follow-up catheterization at day 7. Acute patency was significantly greater after t-PA/SK (79%) than with t-PA alone (64%, p less than 0.05). After angioplasty for failed thrombolysis, acute patency increased to 96% in both groups. Marked depletion of serum fibrinogen levels occurred after t-PA/SK compared with t-PA alone at 4 hours (37 +/- 36 versus 199 +/- 66 mg/dl, p less than 0.0001) and persisted 24 hours after therapy (153 +/- 66 versus 252 +/- 75 mg/dl, p less than 0.0001). Reocclusion (3% versus 10%, p = 0.06), reinfarction (0% versus 4%, p less than 0.05), and need for emergency bypass surgery (1% versus 6%, p = 0.05) tended to be less in the t-PA/SK group. Greater myocardial salvage was apparent in the t-PA/SK group as assessed by infarct zone function at day 7 (-1.9 SD/chord versus -2.3 SD/chord after t-PA alone, p less than 0.05). In-hospital mortality (6% versus 4%) and serious bleeding (12% versus 11%) were similar between the two groups. CONCLUSIONS. These results suggest that a less expensive regimen of half-dose t-PA with SK yields superior 90-minute patency and left ventricular function and a trend toward reduced reocclusion compared with the conventional dose of t-PA.     

Influence of vessel involvement and early streptokinase therapy on regional and global left ventricular function in acute myocardial infarction

150 consecutive patients with acute myocardial infarction received 750,000 units of intravenous streptokinase within four hours of pain onset. Angiography was performed on day 6, from which ejection fraction (EF), infarct-related ejection fraction (IREF), and non-infarct related ejection fraction (NREF) were calculated. 50% stenosis was considered to be significant. The streptokinase patients with patent infarct-related arteries who had no evidence of previous myocardial infarction were compared with 82 conventionally treated (without streptokinase) patients who had no evidence of previous myocardial infarction. Sub-group analysis based on vessel involvement, usage and timing of streptokinase was done. Streptokinase was associated with better left ventricular function in all sub-groups if given less than 2 hours after pain onset. In inferior myocardial infarction, streptokinase patients with single-vessel disease had normal EF (67 +/- 8), compared to significantly depressed EF in multi-vessel disease (56 +/- 12, p less than 0.05). This difference is accounted for more by the NREF than the IREF. In anterior infarction, patients with single-vessel disease did only slightly better than multi-vessel disease. In multi- and single-vessel anterior infarction, preservation of function by streptokinase appears to be due to the compensatory ability of the non-infarcted region as well as the residual function of the infarct-related region. region.     

Immediate or delayed angioplasty during the acute phase of myocardial infarction. Apropos of 118 cases

The results of immediate percutaneous transluminal coronary angioplasty (PTCA) (260 +/- 167 minutes after onset of pain and an average of 56 minutes after thrombolysis) and deferred PTCA (average 9.6 days, range 1 to 30 days after infarction) were compared in 118 consecutive patients with acute myocardial infarction. The overall primary success rate of PTCA was 82.2 per cent; it was higher in those patients undergoing deferred angioplasty (96% vs 78%; p less than 0.05). The primary success rate of immediate PTCA was related to the severity of the stenosis before dilatation: 75 per cent success in occluded compared to 84 per cent in suboccluded vessels (over 90% stenosis) and 100 per cent success in vessels with under 90 per cent stenosis. Eighty one per cent of failed angioplasties occurred in patients with occluded arteries, the majority being left anterior descending (LAD) arteries (71.4%). The incidence of restenosis was 13.4 per cent. This complication was diagnosed at coronary arteriography performed 40 days after PTCA in 1 case, 47 days after PTCA in another case and at the 6 month control in 11 cases. Reocclusion was observed in 21 patients (21.7% of immediate successes). The occlusion was diagnosed at the first control after an average of 8 days in 15 cases. The interval between the onset of pain and thrombolysis and dilatation was significantly longer in the group with reocclusion compared with patients without reocclusion (314 minutes vs 193 minutes for thrombolysis, p less than 0.01; and 356 minutes vs 204 minutes fort PTCA, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Early prediction of left ventricular function in streptokinase-treated acute myocardial infarction

We administered 750,000 units of intravenous streptokinase to 121 consecutive patients experiencing their first acute myocardial infarction within 4 h of pain onset. The following information was collected: hours between pain onset and streptokinase administration (TS), hours of pain after streptokinase administration (DP), initial and peak creatine phosphokinase levels (ICK and PCK), time to peak creatine phosphokinase, time to electrocardiographic ST segment resolution. Six days after the infarction, catheterization was performed to calculate ejection fraction, infarct-related regional ejection fraction, and dysfunction index. Data was analyzed using stepwise multiple regression. In patients experiencing anterior infarctions, the following equation was obtained predicting the ejection fraction (EF) with a correlation coefficient of 0.86: EF = 69 - 0.0050(PCK) - 3.7(TS) - 1.8(DP). In anterior infarctions the infarct-related ejection fraction and dysfunction index were similarly predictable. We were slightly less accurate in forecasting the outcome of inferior infarctions. The outcome of intravenous streptokinase therapy can be predicted early in the evolution of acute myocardial infarction using routinely available information.     

Carbon monoxide and ventricular fibrillation threshold in dogs with acute myocardial injury

In a blind, randomized study, the effect of breathing 100 p.p.m. of CO versus compressed, purified air for 2 hours on ventricular fibrillation threshold (VFT) was investigated in 21 dogs with acute myocardial injury. The mean arterial carboxyhemoglobin was 1.16 per cent in the air control period, 1.07 per cent after air, 1.08 per cent in the CO control period, and 6.34 per cent after CO. In comparison to air, CO increased the mean arterial carboxyhemoglobin (P less than 0.001). One dog developed spontaneous ventricular fibrillation 100 minutes after CO. Mean VFTs in the other 20 dogs were 12.8 +/- 6.8 milliamperes after CO, 11.2 +/- 6.0 milliamperes in the air control period, and 15.0 +/- 5.1 milliamperes after air. In comparison to air, CO decreased the VFT (P less than 0.001). These data show that breathing 100 p.p.m. of CO for 2 hours reduces the VFT in dogs with acute myocardial injury.