Heparin and infarct coronary artery patency after streptokinase in acute myocardial infarction

Anticoagulant therapy is frequently used after thrombolytic agents in the treatment of acute myocardial infarction (AMI) although it is unclear that such therapy will prevent subsequent infarct vessel reocclusion. The role of duration of heparin therapy in maintaining infarct artery patency was studied retrospectively in 53 consecutive AMI patients who received streptokinase therapy and underwent coronary angiography acutely and at 14 +/- 1 days. Of the 39 patients with initial infarct vessel patency, patency at follow-up angiography was observed in 100% (22 of 22) of those who received greater than or equal to 4 days of intravenous heparin but in only 59% (10 of 17) of those patients who received less than 4 days of heparin (p less than 0.05). Of the 14 patients not initially recanalized after streptokinase, patent infarct-related arteries at follow-up angiography were found in 3 of 8 (38%) treated with greater than or equal to 4 days of heparin therapy but in none of the 6 patients treated for less than 4 days (difference not significant). No significant difference in hemorrhagic complications was noted between the short- and long-term heparin treatment groups. Thus, greater than or equal to 4 days of intravenous heparin therapy after successful streptokinase therapy in AMI is more effective in maintaining short-term infarct vessel patency than a shorter duration of therapy and it may maintain the short-term patency of the infarct vessel in those patients who later spontaneously recanalize.     

Coronary thrombolysis after intracoronary and intravenous administration of streptokinase to myocardial infarct patients

Coronary thrombolysis by intracoronary and intravenous streptokinase (SK) is reported in myocardial infarction patients. Forty-two patients were examined within the first 6 hours of infarction: they were subjected to coronary-angiography on admission and 24 hours later, and their plasma fibrinogen levels were measured repeatedly for 2 days. SK administration was intracoronary in 24 patients and intravenous in 18. Rapid intravenous SK injection was not inferior to intracoronary administration in terms of efficiency. Although coronary reperfusion takes a somewhat longer time in cases of intravenous SK treatment, its technical simplicity and relative safety, as well as the fact that it can be started early suggest that it is a promising method of treatment for myocardial infarction.     

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

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

Behavior of arterial pressure during administration of intravenous streptokinase, in patients with acute myocardial infarct

OBJECTIVE: To evaluate the effect on blood pressure (BP) of intravenous (IV) streptokinase (SK) in patients (PTS) with acute myocardial infarction (AMI). DESIGN: Retrospective study with analysis of BP registers ten minutes before and during SK infusion. SETTING: PTS admitted to the Coronary Care Unit (CCU) of Santo António Hospital, Oporto. PATIENTS: Thirty-eight male PTS, average ages of 54, ranging from 38 to 67, AMI confirmed, and criteria to thrombolytic therapy. One patient was excluded on account of persistent hypotension since admission. MATERIAL AND METHODS: IV infusion of 1,500,000 U of SK over 60 minutes, preceded by 200 mg IV of prednisolone. BP and heart rate (HR) were evaluated with a Datascope Accutorr 1A set. The lowest value of the systolic BP (SBP) recorded ten minutes before SK infusion was considered the baseline value. We valued the reduction of SBP above 15%, defining its fall as the difference between the baseline value and the minimum value of SBP recorded during the infusion. Hypotension was defined to SBP values below 90 mmHg. MAIN RESULTS: The SBP fall was 40.4 +/- 22.1 mmHg (range 9 to 102), having been recorded the minimum value at 22.9 +/- 10.9 minutes. It was accompanied by diastolic BP (DBP) fall of 30.6 +/- 18.9 mmHg (range -2 to 76) and by a HR increasing from 76.2 +/- 13.7 beats/min. to 80.8 +/- 14.1 beats/min. (p less than 0.01). In 86% of the PTS this fall was transient, lasting 8.9 +/- 6.3 minutes, and was corrected by slowing or stopping the infusion for a few minutes and placing the patient in Trendelenburg position. Two PTS needed sympaticomimetic amines because of persistent BP reduction despite the previous measures. 92% of the PTS had a SBP fall higher than 15% in relation to the baseline value. The SBP was kept over 90 mmHg in 20 PTS (54%); hypotension was recorded in the remaining 14 PTS (38%), and in 10 (27%) of these the SBP fell below 80 mmHg. We couldn't prove that the infarction location and the extension of the ischemic lesion had influenced this BP fall. CONCLUSION: The BP reduction during treatment with high doses of SK deserves some attention because, although transient and easily reversible, it is frequent and sometimes significative. It demands then careful monitoring in order to avoid the hypoperfusion to the ischemic myocardium, that could jeopardize the potential benefits of reperfusion in the reduction of infarction area, the main objective of the thrombolytic treatment.     

Usefulness of residual plasma fibrinogen after intravenous streptokinase for predicting delay or failure of reperfusion in acute myocardial infarction

The relation between the level of residual plasma fibrinogen and coronary artery reperfusion after 750,000 IU of intravenous (i.v.) streptokinase (SK) was examined in 76 patients with acute myocardial infarction. Both the frequency and rapidity of reperfusion were greater in the 53 patients in whom the residual fibrinogen level was 50 mg/dl or less (low fibrinogen) than in the 23 patients in whom it was more than 50 mg/dl (high fibrinogen). Reperfusion occurred in all 53 patients in the low-fibrinogen group, compared with only 15 patients in the high-fibrinogen group (p less than 0.001). The interval from initiation of SK to clinical signs of reperfusion was 50 +/- 34 minutes in the low-fibrinogen group and 110 +/- 54 minutes in the high-fibrinogen group (p less than 0.001). A high fibrinogen level occurred in 58% of patients who weighed more than 85 kg and in 25% of patients who weighed 85 kg or less (p less than 0.05). No patient who weighed 60 kg or less had a high fibrinogen level. The high-fibrinogen group also had a greater incidence of a high anti-SK antibody titer: 8 of 13 patients (62%) tested, compared with none of the 8 patients tested in the low-fibrinogen group (p less than 0.01). Our data indicate that a high residual fibrinogen level after administration of i.v. SK identifies patients in whom SK is relatively ineffective, probably because of inadequate dosage of inactivation of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation of spontaneous reperfusion in ST-elevation myocardial infarction to more distal coronary culprit narrowings

Spontaneous reperfusion (SR) of the infarct-related artery may occur in patients with ST-segment-elevation myocardial infarctions (STEMIs). Limited data are available on the angiographic characteristics of these patients. The objective of this study was to determine if there are differences in the distance of the culprit lesion from the coronary ostium in patients with STEMIs with and without SR. Patients who presented with acute STEMIs<12 hours after pain onset and who underwent coronary angiography were entered into the study. Measurement of the distance from the coronary ostium to the culprit lesion was performed. A total of 469 patients with STEMIs were included in the study, of whom 77 met criteria for SR (significant relief of chest pain associated with >or=50% resolution of ST-segment elevation on follow-up electrocardiography) and 392 did not. A highly significant difference was seen in ostial to culprit lesion distance, with the culprit lesions in the SR group being more distal than those in the non-SR group (45+/-22 vs 39+/-20 mm, p<0.009). In conclusion, the findings of this study demonstrate that the location of the culprit lesion in patients with STEMIs who undergo SR is more distal in the involved artery than in patients with STEMIs who do not undergo SR.     

Prediction of infarct coronary artery recanalization after intravenous thrombolytic therapy

Clinical assessment of patients with evolving acute myocardial infarction may suggest recanalization of the infarct coronary artery if chest pain, electrocardiographic ST-segment elevation and reperfusion arrhythmia are diminished. These 3 criteria, however, have not been correlated with immediate coronary angiography. Determination of which patients will achieve myocardial reperfusion after intravenous fibrinolytic therapy would allow for appropriate triage; those in whom it fails may be considered for mechanical or surgical recanalization. Fifty-six patients were studied: 28 received intravenous streptokinase and 28 intravenous recombinant tissue-type plasminogen activator. None of these clinical criteria, considered separately, was predictive of infarct artery recanalization status. Using the presence or absence of all 3 criteria, the specificity and predictive value increased to 100%. However, only 9% of patients in the series had all 3 criteria present (all had a patent infarct artery) and 34% had no criteria present (all had an occluded vessel). Noninvasive clinical markers are simple and practical, but only concordance of all 3 major criteria, when present, accurately predicts results of thrombolytic therapy.     

Electrocardiographic signs of coronary reperfusion in patients with myocardial infarct

ST changes were assessed in records from electrocardiographic leads I, II, III, V as well as monitoring leads in 109 patients with myocardial infarction on thrombolytic and/or heparin treatment conducted under angiographic control. In patients with coronary reperfusion, achieved by thrombolytic treatment within 8 hours of the onset of infarction, ST displacement diminished more than twofold by the third hour of treatment in records from leads I, II, III and V, there was a rapid ST fall in monitoring leads that started within 90 min after the onset of thrombolytic therapy and went on for not more than 60 min at a maximum rate; ST reached its baseline (mean ST level over the last 6 hours of 24-hour monitoring) in records from the monitoring leads within 7 hours after the onset of thrombolytic therapy. These signs of coronary reperfusion are suggestive of the recovery of coronary flow by means of thrombolytic therapy within 8 hours of the onset of myocardial infarction.     

静脉溶栓未再通急性心肌梗死病人的临床分析

目的　观察静脉溶栓治疗未再通与未溶栓急性心肌梗死 (AMI)病人的异同。方法　从我院收治的 AMI病人中随机选择出溶栓未通病人 38例 ,未溶栓病人 36例 ,,比较其严重心律失常及 AMI后心绞痛发生率、死亡率、心肌酶 (CK- MB)水平、Q波加深程度、ST段回落程度及左心室射血分数 (L VEF)。结果　严重心律失常发生率 (17/38;2 6 / 36 )、CK- MB(5 6 .43± 42 .93u/ L;75 .78± 2 7.2 3u/ L)及 Q 波加深程度 (0 .2 47± 0 .330 m V;0 .44 2± 0 .32 8m V)在溶栓未通组显著低于未溶栓组 ,其余指标两组间未达统计学差异。结论　即使经静脉法溶栓治疗未获再通 ,恶性心律失常发生率、心肌酶水平及 Q波加深程度也低于未溶栓组。因而更应积极采用静脉溶栓法治疗 AMI     

Fibrinolysis and hemorrhage after streptokinase in acute myocardial infarct

The purpose of this study is to analyze the relationship between occurrence of hemorrhagic complications, kinetic of fibrinogen degradation-regeneration and the changes of prothrombin time (PT), partial thromboplastin time (PTT), after intravenous administration of Streptokinase (SK), 1.500.000 U., in acute myocardial infarction. 45 selected patients with acute myocardial infarction had pretreatment analysis and serial post-SK measurement of fibrinogen levels, PT, PTT (for 48 hours). Basal fibrinogen levels were 3.2 g/l and displayed significant depression for 18 hours (0.30-0.46 g/l) and normalization after 30 hours from SK infusion. Similar behaviour showed PT and PTT. Minor bleeding was identified in 25 patients. In bleeders mean fibrinogen levels, PT, PTT before and maximum changes after SK were not significantly different compared with non bleeders. We conclude that SK infusion produces important and prolonged changes of fibrinogen levels, PT, PTT; hemorrhagic risk is not related, however, to the extent of lytic state, but probably to pre-existent vascular derangement, predisposing to bleeding complications during fibrinolytic therapy. Therefore we believe to be prudent to delay the infusion of heparin for 12-18 hours after SK administration, when fibrinogen levels are beginning to increase.     

Importance of the early intravenous administration of streptokinase in acute myocardial infarct

To evaluate the importance of early initiation of fibrinolytic therapy with intravenous streptokinase (IVSK), we studied 34 consecutive patients, within less than six hours of the onset of acute myocardial infarction, who were treated with 1.5 million units of intravenous streptokinase. All the patients had coronary angiograms in the first seventy two hours. We correlated the angiograms with the time of onset of the IVSK. The patients were divided into 3 groups: Group num. 1: From zero to two hours (twelve patients); Group num. 2: From two to four hours (13 patients); and Group num. 3: From four to six hours (nine patients). We had angiographic reperfusion in twenty-four patients (70.2%) P less than 0.05. We observed reopening in the patients of group num. 1 (83.3%); in group 2, nine patients (69%) and in group num. 3, five patients, (55.5%), with statistical significance only in group num. 1 (p less than 0.05). We also demonstrated the utility of the electrocardiographic and enzymatic criteria to predict reperfusion. No mortality was related to the procedure. We concluded that a higher percentage of reperfusion is obtained the sooner intravenous streptokinase therapy is initiated.     

Evaluation of clinical heart insufficiency in patients with acute myocardial infarct treated with intravenous streptokinase

We assessed the incidence of clinical heart failure in patients with acute myocardial infarction admitted to a coronary care unit and treated with intravenous streptokinase. We compared 2 groups of patients: 1) treated group: patients with acute myocardial infarction admitted to the unit in the last 3 years and treated with intravenous streptokinase, following a protocol established previously. 2) Control group: patients with the same characteristics and selection criteria as for the treated group, admitted to the unit during the previous 2 years and conventionally treated, without thrombolytic therapy. We assessed, in both groups, the incidence of heart failure at the time of admission, at discharge and the total incidence in the unit, following the Killip and Kimball criteria. The total incidence of heart failure was higher in the control group than in the treated group (43.8 vs 19.1%, p less than 0.001). This difference was even greater when the comparison was made with the reperfused patients (43.8% vs 18%, p less than 0.001). Heart failure incidence at the time the patients were discharged from de unit was also higher in the control group (21.2% vs 4.3%, p less than 0.001). When we considered severe heart failure (III-IV Killip Group) we also observed a significant difference between both groups. In conclusion, the incidence and the severity of clinical heart failure were lower in patients treated with streptokinase than in those treated conventionally.     

Rapid myoglobin analysis to assess coronary artery reperfusion after acute myocardial infarction

Background: Coronary artery reperfusion significantly improves outcome in patients with acute myocardial infarction. A noninvasive method for assessing reperfusion in the early stage of infarction should be helpful in patient management. Hypothesis:We sought to assess whether release pattern of myoglobin is helpful in identifying patients with and without reperfusion following thrombolytic therapy for myocardial infarction. Methods: Myoglobin was measured before thrombolysis, half hourly for 4 h, then every 2 h for 10 h. Myoglobin was analyzed using a ward-based “rapid” and automated analyzer that yielded quantitative results within 10 min of blood collection. Results: In the 15 patients with coronary reperfusion, the time from thrombolysis to peak myoglobin levels (mean ± SD, 2.4 ± 1.5 h) was significantly lower than in nonreperfused patients (5.1 ± 2.9, p < 0.01). As an indicator for reperfusion, a doubling of myoglobin 1 h after streptokinase achieved a sensitivity of 80%, a specificity of 80%, and a predictive accuracy of 80%. Conclusions: The difference in myoglobin release kinetics is useful in identifying patients without coronary reperfusion and should aid in their management.     

Do different doses of intravenous streptokinase alter the frequency of coronary reperfusion in acute myocardial infarction?

This study assessed the relative efficacy of 3 doses of intravenous streptokinase in causing hypofibrinogenemia and coronary reperfusion in patients with acute myocardial infarction. Accordingly, 56 patients (50 men and 6 women, ages 58 +/- 10 years [mean +/- standard deviation]) with evolving acute myocardial infarction and chest pain less than or equal to 5 hours in duration were assigned to receive varying doses of streptokinase. Twenty were administered 500,000 units during 145 minutes, 18 were given 750,000 units during 30 minutes and 18 received 1.5 million units in 60 minutes of streptokinase. Serum creatine kinase was measured on admission and 6, 12, 18 and 24 hours after the initiation of streptokinase. The time intervals from onset of pain to peak creatine kinase and from streptokinase administration to peak creatine kinase were used to determine the occurrence of reperfusion. The plasma fibrinogen concentration was measured 30, 60, 90 and 120 minutes after the initiation of streptokinase. For the 3 groups, the time from onset of pain to peak creatine kinase was less than 17 hours and the time from streptokinase to peak creatine kinase was 6 or 12 hours in 15 (75%), 16 (89%) and 12 patients (67%), respectively (differences not significant). The plasma fibrinogen concentration decreased to 45 +/- 34 mg/dl, 19 +/- 14 mg/dl and 29 +/- 43 mg/dl, respectively, during the 2 hours after streptokinase was begun (p less than 0.05 for the first versus the second and third values).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of residual coronary stenosis on myocardial salvage after reperfusion in dogs

In order to study the effects of residual stenosis on myocardial salvage, we created 99% coronary stenosis with or without contrast washout delay at reperfusion in six groups of dogs. In Group A (n = 8), the artery was occluded for 1h before being fully reperfused. In Group B (n = 9), the artery was occluded for 1h, then subjected to 6h of 99% stenosis without contrast washout delay. In Group C (n = 8), the artery was occluded for 1h, followed by 1 week of 99% stenosis without contrast washout delay. In Group D (n = 10), again the artery was occluded for 1h, then subjected to 6h of 99% stenosis with contrast washout delay. In Group E (n = 8), the artery was occluded for 7h, then fully reperfused for 1 week. Finally, in Group F (n = 8), the occlusion lasted for a full week. All dogs were sacrificed 1 week after occlusion. In Group A, myocardial creatine phosphokinase activity (CK) in the inner layer was 43.8 +/- 12.5% that of non-infarcted myocardium. Myocardial CK in Group B (46.5 +/- 7.4%) was little different but in Group C it dropped to 26.6 +/- 8.4%, suggesting that 99% residual stenosis is not deleterious if it is continued for 6h or less but that it will result in considerable depletion of myocardial CK, it is is sustained for 1 week. In Group D, myocardial CK dropped markedly to 11.3 +/- 3.7%, little different from that for either Group E (13.3 +/- 2.6%) or Group F (9.3 +/- 3.3%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Lack of relation between imaging and physiology in ostial coronary artery narrowings

This study compared ostial lesion angiographic severity with physiologic assessment and showed that, for diameter narrowings >70%, fractional flow reserves were >0.75 in 20 of 25 lesions and >0.75 in 30 of 30 lesions with <70% diameter narrowings. Using fractional flow reserve in all ostial narrowings > or =70% may prevent patients from undergoing unnecessary interventions.     

The influence of reperfusion on infarct size after experimental coronary artery occlusion

Summary Reperfusion following various intervals of coronary occlusion has produced conflicting results: increase in infarct size, especially with hemorrhage into the tissue, was reported as well as salvage of ischemic myocardium. To examine the problem and for the validation of our own method for infarct size measurement, which depends to a certain degree on reperfusion, we occluded two coronary arteries of the same heart in each of 12 open-chest dogs. One artery was reperfused, the other not. Comparable conditions for both occlusions were warranted by selection of small-to-medium sized arteries of equal size and by maintaining of constant MVO₂.Reperfused and non-reperfused myocardium did not differ with regard to infarct size, neither after a three-hour nor after a six-hour occlusion. Reperfusion always led to hemorrhagic infarction when performed after six-hour occlusion, while nonreperfused infarctions showed no hemorrhage. Hemorrhagic infarcts were not larger as compared to the non-hemorrhagic infarct in the same heart.

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Der Einfluß der Reperfusion auf die Infarktgröße nach experimentellem Koronarverschluß

Zusammenfassung Über die Wirkung einer Reperfusion nach unterschiedlich langem Koronargefäßverschluß liegen einander widersprechende Ergebnisse vor: Rettung ischämischen Myokards einerseits und Vergrößerung des Infarkts andererseits, besonders im Zusammenhang mit hämorrhagischer Infarzierung. Zur Abklärung dieser Frage und zur Bewertung unserer eigenen Methode der Infarktgrößenbestimmung, die z. T. auf einer Reperfusion beruht, wurden an 12 Hunden 2 Koronargefäße des jeweils selben Herzens okkludiert. Ein Gefäßgebiet wurde reperfundiert, das andere nicht. Durch die Auswahl zweier klein- bis mittelgroßer Arterien mit vergleichbarem Perfusionsgebiet und durch Aufrechterhaltung eines konstanten MVO₂ waren die Bedingungen beider Okklusionsperioden vergleichbar.Die Infarktgröße von reperfundiertem und nichtreperfundiertem Myokard war identisch-sowohl nach drei wie nach sechs Stunden Okklusionsdauer. Reperfusion nach sechsstündiger Okklusion war immer mit hämorrhagischer Infarzierung verknüpft, während nichtreperfundierte Infarkte hämorrhagiefrei blieben. Jedoch unterschieden sich hämorrhagische und nichthämorrhagische Infarkte aus einem Herzen nicht in ihrer Ausdehnung.

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