Presence of angina pectoris before acute myocardial infarction and degree of residual stenosis after coronary thrombolysis

This study tested the hypothesis that the degree of residual stenosis after coronary thrombolysis reflected that of original stenosis presented by symptom of angina before acute myocardial infarction (AMI). The relation between the presence of angina before AMI and the degree of residual stenosis after coronary thrombolysis was observed in 57 patients with successful coronary thrombolysis for AMI. Patients with significant coronary artery stenoses other than the artery responsible for AMI were excluded from this study. In 22 patients with chronic angina for 2 weeks or longer before AMI, 14 patients had a residual stenosis of 75% or more and 8 patients had a residual stenosis of less than 75%. In 35 patients with angina for less than 2 weeks or not at all before AMI, 9 patients had a residual stenosis of 75% or more, and 26 patients had a residual stenosis of less than 75% (p less than 0.01). In the course of progression of coronary artery disease, some patients had AMI without severe underlying stenosis and others with severe underlying stenosis. Patients with chronic angina before AMI might tend to have AMI with acute occlusion superimposed on the severe organic stenosis. Patients without chronic angina before AMI would be more at risk for AMI caused by acute occlusion without underlying severe stenosis.     

Assessment of residual coronary arterial stenosis after thrombolytic therapy during acute myocardial infarction

Maximal myocardial salvage appears to be related to the severity of residual coronary arterial stenosis after thrombolysis. The degree of residual infarct vessel stenosis was assessed in 119 consecutive patients with patent arteries who received streptokinase during acute myocardial infarction. After administration of streptokinase, 99 of 119 patients (83%) had a residual stenosis 70% or more in diameter. Assuming that a residual diameter stenosis of at least 70% is flow limiting, the feasibility for percutaneous transluminal coronary angioplasty (PTCA) was determined by the following criteria: length less than 10 mm, no significant distal narrowing or left main stenosis, and an adequate-sized distal artery. In 81 of 99 patients (82%), arterial anatomy was suitable for PTCA. Thus, after therapy with streptokinase for acute myocardial infarction, most patients have a significant infarct arterial residual stenosis and are candidates for PTCA.     

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.     

Frequency of complications of cardiopulmonary resuscitation after thrombolysis during acute myocardial infarction.

Prolonged external cardiac massage is often regarded as a contraindication for thrombolytic therapy because of the risk of fatal hemorrhage. The influence of cardiopulmonary resuscitation on complications of thrombolytic bleeding was assessed analyzing data of all patients with myocardial infarction admitted to our clinic during the 10-year period between 1978 and 1987. From the total of 2,147 patients with acute myocardial infarction, 590 received thrombolytic therapy (intracoronary in 229, intravenous in 400). Of these, 43 patients underwent prolonged cardiopulmonary resuscitation and received thrombolysis within a time interval of less than 24 hours. In 21 patients, resuscitation was performed within a short period of time (5 minutes to 20 hours) after thrombolysis (10 intracoronary, 10 intravenous, 1 intravenous + intracoronary) had been initiated; 9 of these patients survived (43%). In the other 22 patients, thrombolytic therapy was initiated during ongoing resuscitation (n = 6: intravenous in 5, intravenous + intracoronary in 1) or in the early phase (10 to 120 minutes) after successful resuscitation (n = 16: intracoronary in 10, intravenous in 4, intravenous + intracoronary in 2). From this group, 14 patients survived (in-hospital mortality 36%). The mean duration of cardiopulmonary resuscitation was 36 +/- 32 minutes (range 4 to 120). Autopsy studies were performed in 16 of 20 decreased patients. Bleeding complications occurred in 8 of 43 patients. No case of bleeding was directly related to cardiocompression despite the often traumatic procedure with rib fractures verified in 17 patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Angina preceding myocardial infarction and residual coronary narrowing after intracoronary thrombolysis

Thirty-six consecutive patients with evolving acute myocardial infarction underwent emergent coronary angiography and intracoronary thrombolysis with urokinase. Nineteen of the patients had had angina before the infarction (group A), whereas the infarction was unheralded in the remaining 17 (group B). Thirty-two vessels (88%) were patent at follow-up angiography performed after 3 to 4 weeks, and the residual stenosis was 87% +/- 14% in group A and 47% +/- 25% in group B (p less than 0.001). Coronary spasm was provoked by ergonovine maleate in four of 12 patients in group A (33%) and in three patients in group B (18%). Coronary revascularization was undertaken in nine patients in group A and three in group B. These results indicate that patients with angina preceding acute myocardial infarction are more likely to have significant stenosis even at the late follow-up stage and to have a more urgent need for subsequent coronary revascularization. It also seems apparent that thromboembolism in most patients and coronary spasm in a few patients without significant coronary narrowing play significant causal roles in the onset of acute myocardial infarction.     

Changes in ventricular function and coronary stenosis after successful intravenous thrombolysis in acute myocardial infarction

Temporal changes in residual stenosis in the infarct-related coronary artery and ventricular function were studied in 30 consecutive patients with an acute myocardial infarction who received rapid, high dose intravenous infusions of streptokinase within 4 h of pain onset. Patients were studied 6 days and 3.9 +/- 1.3 months after the acute episode. Inferior infarction, early thrombolysis (less than 1.5 h after pain onset) and adequate reperfusion (less than 75% residual stenosis in the infarct-related coronary artery) were associated with smaller left ventricular infarcts, smaller ventricular volumes and better ventricular function. Residual stenosis tended to increase with time and in 6 patients the artery closed completely (1 with an overt clinical episode). Ventricular function and volumes improved progressively in patients with good initial function and less residual stenosis in the infarct-related coronary artery.     

Access-site complications after rescue percutaneous coronary intervention during thrombolysis for acute myocardial infarction

Aggressive antithrombotic medical therapy may increase the rate of access-site complications after percutaneous coronary intervention. Frequently, emergency coronary interventions have to be performed in a situation when thrombolysis therapy was administered as the first-line therapeutic approach in acute myocardial infarction but failed to achieve stable conditions.We analyzed the rate of femoral bleeding complications after emergency coronary intervention in 76 consecutive patients with unsuccessful thrombolysis in acute myocardial infarction. All invasive procedures were performed in a time period no longer than eight hours after thrombolysis was administered. Additional antithrombotic therapy with heparin and glycoprotein IIb/IIIa-inhibitors was given during intervention in 100% and 38.2% of patients, respectively. In three patients (3.9%) femoral hematomas without therapeutic consequences were documented; one patient (1.3%) developed a hematoma requiring blood transfusion. A pseudoaneurysm, fistula or surgical vascular intervention did not occur.Coronary interventional procedures in rescue situations can be performed with excellent safety with respect to access-site bleeding complications even under conditions of ongoing thrombolysis therapy and aggressive antithrombotic medical regimens.     

Late angiographic follow-up after successful coronary arterial thrombolysis and angioplasty during acute myocardial infarction

Emergency percutaneous transluminal coronary angioplasty (PTCA) is accepted as an important reperfusion intervention for acute myocardial infarction (AMI). Although its primary success rate is well documented, the frequency of restenosis after this procedure is unclear. The frequency of restenosis was determined in patients undergoing emergency PTCA at least 6 months after PTCA was performed during AMI. Of 66 consecutive patients undergoing emergency PTCA, 25 had a second, elective catheterization at an average of 22 months after AMI and 6 underwent repeat catheterization because of recurrent chest pain. Restenosis of the PTCA site was found in 10 of the 31 patients (32%) restudied. Also, 14 (45%) of these 31 patients showed progression of narrowing in the non-infarct-related coronary arteries. In summary, patients in whom AMI is treated by PTCA are at risk for restenosis and for progressive narrowing of the non-infarct artery.     

Improved prognosis after coronary thrombolysis with urokinase in acute myocardial infarction

The effectiveness of coronary thrombolysis with urokinase (UK) on short- and long-term outcome after acute myocardial infarction was studied by comparison of 120 patients treated with UK and 124 with conventional therapy followed up for a period of 20 months. UK was administered to patients within 6 hours of the onset of chest pain, by the intracoronary route (20,000 U/min, at a mean dose of 698,000 U) in 46 patients, intravenously (960,000 to 1,920,000 U in 15 or 30 min, at a mean dose of 1,293,000 U) in 56 patients and by the combined route (at a mean dose of 2,333,000 U) in 18 patients. Complete occlusion or 99% stenosis with severe delay of the contrast medium was found in 72.5% and recanalization by UK was achieved in 68.0%. Cumulative mortality rate was significantly reduced in the UK group (9.2% vs. 29.0%). Cardiac death from recurrent MI was also significantly reduced (2.5% vs. 10.5%). The reduction in mortality rate was demonstrated even in older patients as well as in those cases graded as severe according to the Killip and Forrester classifications. Thus, it is concluded that coronary thrombolysis with UK therapy improves the prognosis of acute myocardial infarction.     

急性心肌梗死时尿激酶溶栓加即刻准备的冠状动脉内支架置入术

目的：探讨急性心肌梗死（AMI）时尿激酶溶栓加即刻血管造影，TIMIⅡ级或以下时进行冠状动脉内支架置入术（支架术）的安全性。方法：选择1999年1月至2001年12月AMI（发病6h以内）患25例，常规应用尿激酶（商品名：天普洛欣）150万U0.5h内静脉滴注，其中6例无创指标未见再通，25例患90min后即刻血管造影，其中13例TIMIⅡ级或以下进行冠状动脉内支架置入术。结果：13例TIMIⅡ级或以下均成功进行冠状动脉内支架置入术，术后冠脉血流均达到TIMIⅡ级，未见需要输血的严重出血并发症。结论：AMI时尿激酶溶栓加即刻准备的支架术安全、疗效好。     

Massive hemorrhagic myocardial infarction after coronary thrombolysis

A 53-year-old man with occlusion of the proximal left anterior descending coronary artery received intravenous tissue plasminogen activator, and reperfusion was achieved within four and a half hours from the onset of chest pain. Recurrence of electrocardiographic ST segment elevation without attendant chest pain heralded reocclusion in the first hour after thrombolysis, which was successfully treated. After a stable course, post-infarction refractory cardiogenic shock developed on day 4, and autopsy demonstrated a massive (more than 100 cm2) hemorrhagic infarct. Several features of this case underscore the potential of coronary thrombolysis to cause significant reperfusion injury.     

Bleeding after thrombolysis in acute myocardial infarction

232 consecutive patients with acute myocardial infarction weretreated either with 2 x 10⁶ IU urokinase as an intravenous bolusinjection, or 250000 IU streptokinase intracoronary, or 60 mgrecombinant tissue-type plasminogen activator (rt-PA) over 90min. All patients enrolled had chest pain for more than 30 minand less than 3 h before admission and a typical electrocardiogram.Contra-indications to thrombolytic treatment were absent. Allbleeding complications occurring within 24 h after admissionwere assumed to be due to thrombolytic therapy. Bleeding complicationsoccurred in 14 patients (6.5%). Only seven patients receiveda blood transfusion (3%). No correlation was evident betweenprevious hypertension, diabetes mellitus, smoking, sex, age,fibrinogen level before and 24 h after thrombolytic therapyand bleeding complications. The risk of bleeding was not significantlydifferent between the different thrombolytic regimens despitemarked differences in the fall of the fibrinogen level. Thedecrease of fibrinogen following thrombolytic therapy did notinfluence the patency rate of the infarct vessel. Thrombolytictherapy in acute myocardial infarction is a safe treatment evenamong patients advanced in years and with medically controlledhypertension and diabetes mellitus, irrespective of the kindof thrombolytic treatment.     

Percutaneous coronary interventions in patients with acute myocardial infarction after unsuccessful thrombolysis

In 176 patients with acute myocardial infarction admitted to N.V. Sklifosofsky institute of urgent aid in 2003-20007 we compared efficacy of 3 strategies of treatment after unsuccessful thrombolytic therapy (TLT): percutaneous coronary intervention (PCI) during first 24 hours (n = 30), PCI on days 2 or 3 (n = 38); conservative treatment (n = 108). The data obtained show that it is expedient to consider absence of 50% reduction of STAsegment elevations in 90 min after start of TLT as indication to urgent late PCI when possibilities for immediate intervention after unsuccessful thrombolysis are lacking. Alternative reperfusion is the only type of effective treatment of patients with failed pharmacological reperfusion. Necessity to perform PCI during first 12 hours after unsuccessful TLT does not exclude possibility of its later fulfillment in acute period of myocardial infarction. Efficacy of the latter is comparable with success rate of rescue PCI. The use of both invasive strategies has allowed to lessen rate of complications and prevent lethal outcomes. Success of late urgent interventions in acute period of infarction after failed thrombolysis opens possibilities for their active use in patients transferred from other hospitals.     

急性心肌梗塞静脉溶栓后冠状动脉造影早期和晚期的改变

目的研究急性心肌梗塞（ALMI）静脉溶栓后冠状动脉的解剖特点及其演变。方法100例AMI病人应用尿激酶和链激酶溶栓后”分钟行早期的冠状动脉造影（CAG）。3～4周后再次行晚期的CAG。结果100例AMI溶栓成功60例，失败40例，再通率％％。CAG提示有残留血栓的84例（84％），其中有40例（48％）为冠状动脉完全阻塞。溶栓再通病人经3～4周后再次CAG发现，8例狭窄加重，10例狭窄减轻。结论AMI是由突然冠状动脉血栓性闭塞所致并可用溶栓剂或机械的方法使闭塞的冠状动脉再通。溶栓通常不能使血栓完全溶解，使用PTCA已被建议为改善严重残留狭窄病变的重要疗法。     

Macroscopic hemorrhagic infarction following selective coronary thrombolysis in acute myocardial infarction

Macroscopic hemorrhagic infarction was studied in 14 autopsied hearts with selective coronary thrombolysis (SCT) after acute myocardial infarction (AMI). In all patients urokinase, 240,000 - 720,000 units, had been selectively injected into ischemia-related coronary artery at 2 - 7 hours after the onset of AMI. The degree of stenosis after SCT was 90 - 99% in 13 patients and 100% in one patient. According to the duration of illness at death, the 14 patients were classified into 3 stages; stage I: 4 - 9 hours; stage II: 15 hours to 11 days; stage III: 19 days to 12 months. Three hearts in stage I had no macroscopic hemorrhage. In stage II, marked and diffuse hemorrhage in the infarct area was macroscopically evident in 6 of 7 hearts. In a stage II patient, extravasation of contrast medium into the myocardium was found at 3 hours after the onset of AMI. In stage III, 4 hearts had massive fibrosis or granulation in the left ventricular wall without macroscopic hemorrhage. Cardiac rupture was seen in 4 of 10 patients from stages I and II. It is concluded that macroscopic bleeding appears in most patients with AMI treated with coronary thrombolysis. In the majority of cases, the hemorrhage increases gradually after SCT and becomes macroscopically definite approximately 15 hours after the onset of AMI. Rarely, massive bleeding appears earlier. Hemorrhagic infarction is replaced by massive fibrosis after approximately 2 weeks.     

Significance of a negative exercise thallium test in the presence of a critical residual stenosis after thrombolysis for acute myocardial infarction

BACKGROUND. After thrombolytic therapy for acute myocardial infarction, increasing emphasis is placed on early submaximal exercise testing, with further intervention advocated only for demonstrable ischemia. Although significant residual coronary artery lesions after successful thrombolysis are common, many patients paradoxically have no corresponding provokable ischemia. METHODS AND RESULTS. The relation between significant postthrombolytic residual coronary artery disease and a negative early, submaximal exercise thallium-201 tomogram was studied among 101 consecutive patients with uncomplicated myocardial infarction and at least 70% residual stenosis of the infarct artery. A negative test occurred in 49 (48.5%) patients with a mean 88% residual infarct artery stenosis. Further characteristics of the group were as follows: mean time to treatment was 3.1 hours; mean age was 54 +/- 10 years; 80% were male; 47% had anterior infarction; 39% had multivessel disease; mean left ventricular ejection fraction was 53 +/- 14%; and mean peak creatine kinase level was 3,820 +/- 3,123 IU/ml. A similar group of 52 (51.5%) patients, treated within 3.3 hours from symptom onset, with a mean postthrombolysis stenosis of 90%, had a positive exercise test. Characteristics of this group were as follows: age was 58 +/- 10 years; 92% were male; 56% had anterior infarction; 40% had multivessel disease; and mean left ventricular ejection fraction was 54 +/- 15%. The peak creatine kinase level associated with the infarction, however, was lower: 2,605 +/- 1,805 IU/ml (p = 0.04). There was no difference in performance at exercise testing with respect to peak systolic pressure, peak heart rate, or time tolerated on the treadmill between the two groups. By multivariate logistic regression, only peak creatine kinase level predicted a negative stress result in the presence of a significant residual stenosis (odds ratio, 4.2; 95% confidence interval, 1.1-16.3). CONCLUSIONS. The explanation for the relatively frequent finding of a negative early stress 201Tl tomogram after apparently successful reperfusion appears to be more extensive myocardial necrosis and not delay in therapy or inadequate exercise performance.     

Recurrent ischemia after thrombolysis for acute myocardial infarction

BACKGROUND: Reliable predictors have yet to be found for recurrent ischemia after thrombolysis for acute myocardial infarction (AMI), nor do we know whether early angiography can herald recurrent ischemia. This study sought to investigate the relationship between recurrent ischemia and cardiac procedures after thrombolysis for AMI. METHODS: The Global Utilization of Streptokinase and Tissue Plasminogen Activator for Occluded Coronary Arteries (GUSTO-I) trial prospectively studied recurrent ischemia, which was defined as the presence of angina and changes in hemodynamics or the electrocardiogram. Cox regression analysis was used to identify predictors of recurrent ischemia. Other variables examined included time to coronary angiography and revascularization. RESULTS: Of 21,772 US GUSTO-I patients, 6313 (29%) had recurrent ischemia before discharge. Women (hazard ratio [HR] 1.25, 95% confidence interval [CI] 1.17-1.33) and patients with hypercholesterolemia (HR 1.14, 95% CI 1.07-1.22) or prior angina (HR 1.40, 95% CI 1.32-1.49) had a higher likelihood of recurrent ischemia. Current smoking and hours to thrombolysis were inversely related to recurrent ischemia (HR 0.86, 95% CI 0.81-0.92, HR 0.97, 95% CI 0.95- 0.99, respectively). Patients who underwent angiography before recurrent ischemia had a marginally increased risk of ischemia within 12 hours after angiography (HR 1.2, 95% CI 1.1-1.4); ultimately, they had a considerably lower risk 1 week after angiography than did patients without angiography (HR 0.57, 95% CI 0.45-0.72). CONCLUSIONS: Female sex, hypercholesterolemia, prior angina, and nonsmoking status weakly predict recurrent ischemia. Early coronary angiography reduces recurrent ischemia, probably because high-risk patients are identified and revascularized.