Intracoronary Thrombolysis Research Articles

First month course of left ventricular asynergy after intracoronary thrombolysis in acute myocardial infarction. A longitudinal echocardiographic study.

Can intracoronary thrombolytic therapy (ITT) reduce the infarct size and improve regional and global left ventricular function and if so how long after recanalization does this improvement develop? 42 patients were treated with ITT, of whom 25 showed successful recanalization (group A) and 17 had persistent occlusion or reocclusion (group B). Both groups were examined five times during the first month after infarction with two-dimensional echocardiography. The 'asynergy index' improved in group A by 45% of initial pretreatment values, compared with no significant change in group B (P less than 0.005). The 'asynergy extent' improved in group A by 35%, while in group B again no change was observed (P less than 0.01). This improvement occurred slowly, significant differences being achieved by the 10th day. Entire normalization of left ventricular wall motion was observed in 5 patients (20%) from group A and in no patient from group B. We conclude that successful recanalization of the occluded coronary artery by ITT improves left ventricular wall motion in 80% of patients, with entire normalization of local function in 20% of cases. The improvement occurs slowly during the first 10 days.

Scintigraphic evidence that the right ventricular myocardium tolerates ischaemia better than the left ventricular myocardium.

To study the incidence of right ventricular infarction and the effect of intracoronary thrombolysis on the ischaemic right ventricular myocardium, we performed intracoronary myocardial thallium scintigraphy in 18 patients with complete occlusion of the right coronary artery who underwent intracoronary thrombolysis. In 15 of these patients, intracoronary thallium-201 and technetium-99 m pyrophosphate scintigrams were performed simultaneously. All 18 patients had a right ventricular thallium defect before thrombolysis, and all had new thallium uptake after thrombolysis. 17 out of 18 patients had a left ventricular thallium defect before thrombolysis, but only 10 of them showed new thallium uptake after thrombolysis. 14 out of 15 patients had a left ventricular technetium-99 m pyrophosphate spot after thrombolysis and some diffuse pyrophosphate accumulation in the area of the right ventricle. In one patient pyrophosphate accumulation was found only in the area of the right ventricle. Thus, right ventricular thallium defects were detected by intracoronary thallium scintigraphy in the majority of patients with inferior acute myocardial infarction due to right coronary artery occlusion. Right ventricular thallium defects were always reversible in contrast to left ventricular thallium defects in the same patients, suggesting that right ventricular myocardium tolerates ischaemia better than left ventricular myocardium.

Time from onset of symptoms to thrombolytic therapy: A major determinant of myocardial salvage in patients with acute transmural infarction

To determine whether myocardial salvage after successful intracoronary or intravenous thrombolysis is time dependent, the relation between left ventricular wall motion and the time to treatment was studied in 69 patients admitted less than 3 hours after onset of acute transmural myocardial infarction (42 patients with reperfusion by intracoronary streptokinase, 27 by intravenous urokinase). A similar significant relation between the time to treatment and the severity of regional hypokinesia at follow-up was found in the intracoronary and intravenous groups. To better define this relation, particularly during the early phase of infarction, the groups were combined. In patients in whom thrombolytic treatment was initiated within 2 hours after symptom onset, wall motion at follow-up was within 2 standard deviations of the normal mean in 82% (14 of 17 patients). If treatment was started 2 to 5 hours after symptom onset, the probability of improved wall motion decreased to 46% (24 of 52 patients, p less than 0.025). The time/wall motion relation appeared to be independent of infarct location, angiographically visible collateral vessels and the presence of subtotal coronary artery occlusion. The severity of hypokinesia at follow-up study correlated with the magnitude of peak serum creatine kinase (r = -0.71), indicating that thrombolytic therapy initiated within 2 hours after the onset of symptoms improves regional left ventricular function and reduces infarct size more than later therapy does.

Relation of effectiveness of intracoronary thrombolysis in acute myocardial infarction to systemic thrombolytic state

Twenty-nine patients received intracoronary thrombolytic therapy for acute myocardial infarction 3.5 ± 1.4 hours (mean ± standard deviation) after the onset of pain. Ten patients received urokinase (UK) and 19 patients received streptokinase (SK). Laboratory variables of the coagulation system were measured before and immediately after therapy. When comparing patients in whom coronary artery recanalization occurred vs those in whom the artery remained occluded, those in whom recanalization was achieved had greater alterations in fibrinogen, prothrombin time, activated partial thromboplastin time, fibrin/fibrinogen degradation products and plasminogen by thrombolytic therapy than did those in whom recanalization was not achieved (p < 0.05 for all variables). Euglobulin lysis time showed a similar but nonsignificant trend (p = 0.114). Patients who received SK showed markedly greater alterations in coagulation parameters than did patients treated with UK (p < 0.05 for 5 of 6 variables measured) and had a much higher incidence of successful thrombolysis (74% for SK, 20% for UK). These data indicate that the development of a systemic fibrinolytic state contributes to success when using intracoronary thrombolytic agents in acute myocardial infarction. Rather than being considered an adverse effect of therapy, a systemic lytic state may serve as a reasonable clinical goal in attempting to produce thrombolysis.

Kinetics of serum creatine kinase and creatine kinase-MB after intracoronary thrombolysis.

The kinetics of the activity of total creatine kinase (CK) and creatine phosphokinase isoenzyme muscle-brain were investigated in 48 patients with acute myocardial infarction after successful intracoronary thrombolysis, and compared to the enzyme activities in 17 patients in whom thrombolysis failed. CK activity peaked significantly earlier after a successful thrombolysis than after an unsuccessful attempt: in patients with successful thrombolysis, CKmax = 10.5 +/- 3.7 h and in patients with an unsuccessful attempt, CKmax = 19.3 +/- 5.9 h; p less than or equal to 0.05. The area under the activity time curve after successful thrombolysis was significantly smaller than after unsuccessful thrombolysis: in patients with successful thrombolysis, CK area = 25,255 U/l per day and in patients with an unsuccessful attempt, CK area = 32,602 U/l per day; p = 0.015. There was a negative correlation between the area under the CK serum curve after successful thrombolysis, and the change of regional wall motion at the site of the acute infarct (p less than or equal to 0.05). From the smaller area under the CK curve in patients after successful thrombolysis, and the significant negative correlation of this measurement with regional left ventricular wall motion, we conclude that myocardial salvage after intracoronary thrombolysis can be assessed by serial CK measurements.

Importance of coronary collaterals for restoration of left ventricular function after intracoronary thrombolysis

In an evaluation of the role of coronary collaterals in the early period of acute myocardial infarction (AMI), 30 patients with acute total coronary occlusion treated with intracoronary thrombolysis 2 to 8 hours after the onset of symptoms were studied. Only 13 patients with well-developed collaterals in the early period of AMI and successful thrombolysis showed improvement of global and regional ejection fraction (EF) from the acute phase to the chronic phase (global EF from 50% to 71%, p < 0.001; regional EF from 25.4% to 49.2%, p < 0.001). In patients with no or less well-developed collaterals and successful thrombolysis, global and regional EF were similar to those in patients in whom thrombolysis was unsuccessful. Among the 19 patients with successful thrombolysis, there was no significant correlation between the duration of ischemia and the improvement of regional EF (r = −0.03, difference not significant). These data suggest that the extent of coronary collateral vessels in the early period of AMI is an important determinant of restoration of left ventricular function after intracoronary thrombolysis.

Scintigraphic evidence of the “No reflow” phenomenon in human beings after coronary thrombolysis

To assess whether the absence of new thallium-201 uptake after successful intracoronary thrombolysis reflects a disturbance of myocardial cell function or lack of capillary reperfusion, dual isotope scintigraphic studies with thallium-201 and technetium-99m micro-albumin aggregates were performed in 16 patients with acute anterior myocardial infarction. Intracoronary thallium-201 and technetium-99m scintigraphy performed before intracoronary thrombolysis in 12 of the 16 patients resulted in identical thallium-201 and technetium-99m defect sizes. Immediately after intracoronary thrombolysis, thallium-201 and technetium-99m scintigraphy was repeated in 11 of the 12 patients. In 4 of the 11, the initial thallium and technetium scintigraphic defects were significantly reduced, and in 6 of the 11, they were only slightly reduced; there was no difference in the size of the residual defect as assessed with both radionuclides in all 10 of the 11 patients. In the eleventh patient, there was a significant reduction of the initial technetium-99m scintigraphic defect but no change in the size of the thallium-201 defect. In four other patients, scintigrams were obtained only after intracoronary thrombolysis; these revealed no difference in thallium-201 and technetium-99m defect size. In seven of eight patients restudied 2 to 4 weeks after intracoronary thrombolysis, thallium-201 and technetium-99m defect sizes were identical with those immediately after intracoronary thrombolysis; in the eighth patient there was no difference in thallium-201 and technetium-99m defect size, although such a difference had been present immediately after intracoronary thrombolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Sequential intervention procedures after intracoronary thrombolysis; balloon dilatation, bypass surgery, and medical treatment

After successful intracoronary thrombolysis of an acute myocardial infarction in 145 patients subsequent intervention procedures were evaluated. In 48 of 62 patients (43%), percutaneous transluminal coronary angioplasty was performed successfully (success rate 77%), 41 patients (28%) were operated on and 56 patients (39%) were treated only medically. During the hospital phase in the angioplasty group, 4 reinfarctions were noted and 3 repeat angioplasties were required, while 41 of the 48 successfully treated patients (85.4%) remained clinically stable. In the surgical group, one cardiac failure occurred, while 40 patients (97.6%) were without cardiac event. In the medical group, 5 patients died (8.9%), 8 patients (14.3%) had a reinfarction, and 76.8% were clinically stable. During the follow-up period in the surgical group of 6 months 37 patients (90.2%) were clinically stable, all in functional classes I and II. In the angioplasty group 33 patients were stable (68.8%), and in the medical group 26 patients were stable (46.6%). In the whole group of 145 patients the hospital mortality together with that in the 6 months follow-up period was 9.7% with a reinfarction rate of 22.8%. After successful thrombolysis, the underlying coronary artery disease with its mostly severe stenoses poses a high risk of reinfarctions, recurrent angina, and flow obstructions. Bypass surgery or angioplasty may diminish these risks and improve myocardial perfusion and survival rate in carefully selected patients.

Emergency coronary artery bypass surgery after intracoronary thrombolysis for evolving myocardial infarction.

Sixteen patients underwent emergency coronary artery bypass surgery immediately after intracoronary streptokinase infusion for acute evolving myocardial infarction. Of these, 11 patients had 70% residual stenosis in the recanalised vessel, and in five thrombolysis was unsuccessful. There were no hospital deaths. All the patients sustained myocardial necrosis, the peak activity of creatine phosphokinase correlating with the time to reperfusion. Chest tube drainage (mean 960 ml) was significantly higher than for control patients but did not correlate with the total dosage of streptokinase. No patients had further myocardial infarction or developed recurrent angina. Selected patients may benefit from coronary bypass surgery after intracoronary streptokinase infusion. If necessary this may be performed immediately with low mortality and morbidity.

Thrombolysis in early transmural myocardial infarction. Feasibility and efficacy.

PreviewIn patients experiencing transmural infarction, early reperfusion of the infarct zone offers the best hope of preserving myocardial function. Dr Vetrovec reviews methods of recanalization and details a procedure—intracoronary thrombolysis—that has received much attention and is widely applied, alone or with angioplasty. Intravenous use of streptokinase is also discussed.

The Role of Intracoronary Thrombolysis and Percutaneous Transluminal Coronary Angioplasty in Evolving Myocardial Infarction

Early reperfusion and interruption of the evolution of myocardial ischemia to necrosis can dramatically reduce the extent of myocardial damage and favorably influence the outcome of acute myocardial infarction. Intracoronary thrombolysis and percutaneous transluminal coronary angioplasty, alone or in combination, are an effective method of nonsurgical revascularization in selected patients. Potential applications of these methods, their advantages and disadvantages, and current available experience are discussed.

Selective intracoronary thrombolysis in the coronary care unit without cineangiography.

Selective coronary artery visualization was performed in the CCU by means of a movable fluoroscopy device in 96 patients with suspected myocardial infarction within 6 hours after onset of symptoms. Intracoronary streptokinase (SK) was administered in a total dosage of 200 000 to 400 000 U within 30-60 min to 69 patients with complete (N = 57) or subtotal obstruction (N = 12) of the infarct-related vessel. Recanalization was achieved in 39 of the 57 patients (68%) with initially complete occlusion. Three of the 39 successfully treated patients died (7.7%) versus 8 of 33 subjects (24%) with persistent complete obstruction (chi-square 3.21, not significant). Selective cineangiography subsequently performed in 8 patients and postmortem examination of 12 subjects who had died, showed that all haemodynamically significant lesions had been recognized by the examination in the CCU with one exception. It is concluded that intracoronary thrombolysis performed in the CCU, by means of a standard mobile fluoroscopy equipment is effective, safe, inexpensive and may be started virtually without delay after admission.

Effects of intracoronary thrombolysis on infarct size and left ventricular function in patients with anterior myocardial infarction--enzymatic, electrocardiographic, radionuclide and hemodynamic evaluations.

The influence of the duration of ischemia on infarct size and left ventricular function (LV) was assessed in 30 patients with a first anterior myocardial infarction (MI) and intracoronary thrombolysis (ICTL) on admission. The occlusion time of the left anterior descending coronary artery (LAD) was 4 hours or less in 11 patients (group I), 4-10 hours in 11 (group II) and 10 hours or more in eight (group III). Serial measurements of serum creatine kinase-MB were carried out during the acute phase. Four weeks after the procedure, electrocardiographic pathological Q waves on 34-lead precordial mapping were scored, viable left ventricular myocardial volume and the ratio of infarcted to total left ventricular myocardial volume was estimated by myocardial emission computed tomography (ECT) with thallium-201. In the acute phase enzymatic estimation of infarct size showed a significant difference between group I and the other two groups but not between groups II and III; there were no significant differences in the degree of left ventricular asynergy among the three groups. In the chronic phase infarct sizes evaluated by both Q wave mapping and ECT were smaller in group I than those in group II, which were smaller than those in group III; there were significant differences in the degree of LV asynergy among the three groups (group I less than II less than III). LV function was nearly normal in group I, moderately impaired in group II, but severely depressed in group III 4 weeks later. The present study indicates that infarct size extends and LV function deteriorates with the duration of occlusion of the LAD and that not only early (less than or equal to 4 hours) but also later (4-10 hours) reperfusion is beneficial to prevent the extension of MI and deterioration of LV function in patients with anterior MI.

Effects of intracoronary thrombolysis therapy on left ventricular function after acute myocardial infarction.

To treat the acute phase of myocardial infarction, nitroglycerin and urokinase were injected directly into the infarct-related coronary artery. Left ventricular ejection fraction and regional ejection changes were significantly preserved in the chronic phase, compared with conventional therapy in patients with obstruction at the same site. Comparing left ventricular function in the acute and chronic phases, left ventricular ejection fraction, regional ejection changes and left ventricular end-diastolic pressure were significantly improved in the chronic phase in patients with reperfusion within 6 hours. On the other hand, in patients who had no reperfusion in either the acute or chronic phase, left ventricular ejection fraction deteriorated in the chronic phase. Even in patients with reperfusion in the acute phase, reocclusion later meant a worse left ventricular ejection fraction in the chronic phase. These results suggest that intracoronary thrombolysis with urokinase within 6 hours gives a good chance of recovery from myocardial damage in patients with myocardial infarction.

急性心筋こうそく症に対するウロキナーゼによる冠動脈内血せん溶解療法時の線溶活性について

急性心筋こうそく症に対するウロキナーゼによる冠動脈内血せん溶解療法時の線溶活性について

Combined medical and mechanical recanalization in acute myocardial infarction.

A technique of combined medical and mechanical recanalization was employed in 96 patients with acute transmural myocardial infarction. The mean time between onset of symptoms and admission to hospital was 170 +/- 65 min (X +/- SD). After 10 +/- 16 min, 250,000 U streptokinase was administered intravenously for 20 min. Intracoronary thrombolysis was commenced within 38 +/- 14 min. First coronary angiograms demonstrated reperfusion, an open vessel in 25/96 patients (26%). In 15/71 patients (21%) reperfusion occurred during thrombolysis therapy, before mechanical recanalization could be performed. Recanalization was achieved mechanically in 37/71 patients (52%) with occluded coronary vessels. In 8/71 patients (11%) mechanical recanalization failed but the vessel opened during thrombolysis. In 12/96 patients (12%), the coronary vessel remained occluded. Thus, reperfusion could be achieved in 88% of the patients. Reperfusion rate was 76% in the first 38 patients and 95% subsequently. After reperfusion, coronary thrombi were found in 25/96 patients (26%) but dissolved during thrombolysis in 16/25 patients (64%). Peripheral coronary embolism was observed in 3/25 patients (12%). For the whole group, reocclusion occurred in 8/84 patients (10%). By combined medical and mechanical recanalization, the recanalization rate could be increased with low reocclusion rate. Trends showed an improvement in regional and global left ventricular function in patients with anterior myocardial infarction.

A successful case of intracoronary thrombolysis with total occlusion of left main coronary artery

A successful case of intracoronary thrombolysis with total occlusion of left main coronary artery

Indications for and limitations of coronary thrombolysis.

Experimental studies in dogs with coronary thrombi induced by copper wire confirmed the optimal method of intracoronary thrombolysis, and showed that a high-dose, brief intravenous infusion of urokinase can lead to recanalization. The thrombolytic effects of intracoronary thrombolysin at a rate of 50 IU/kg over 10 minutes are similar to the effects of intracoronary urokinase at a rate 500 IU/kg over 20 minutes. Overall reperfusion rates of 83-86% have been achieved. These results indicate that the thrombolytic effect of thrombolysin is 20 times stronger than that of urokinase. The effect of a brief intravenous infusion of urokinase was less than that of intracoronary urokinase. The reperfusion rate in the same experimental model was 40%. Later, a clinical trial of intracoronary urokinase was performed in 47 patients with acute myocardial infarction who were admitted within 12 hours of the onset of symptoms. In 25 of 33 (75.8%) patients with complete occlusion, selective or ostial infusion of urokinase 500 IU/kg over 20 minutes was successful. When given intravenously, recanalization was achieved in 11 of 15 (73%) patients with complete occlusion who were admitted within 6 hours. Both reperfusion rates were similar except for dosage and the duration of infusion.

Applications of anticardiac myosin monoclonal antibodies in the diagnosis of heart disease.

We have developed anticardiac myosin antibodies, especially monoclonal antibodies, for helping in the diagnosis of heart disease. Our investigations were divided into three research projects. We visualized the distribution of myosin isozymes in human atrial and ventricular myocardium by an immunofluorescence staining method using monoclonal antibodies specific for individual human cardiac myosin isozymes. We also revealed the redistribution of these cardiac myosin isozymes in an overloaded condition. The isozymic pattern of cardiac myosin was changed from the atrial type to the ventricular type in the overloaded atrium. This isozymic redistribution can be considered as physiological adaptive mechanism to meet increased cardiac work during overload. We developed a new method of imaging for myocardial infarction by single photon emission tomography using labelled monoclonal antibody specific for cardiac myosin heavy chain. Specific localization of the labelled antibody was demonstrated in the infarcted area and no accumulation of radioactivity was shown in the bone matrix as observed in 99mTc pyrophosphate images. We developed a sensitive radioimmunoassay of cardiac myosin light chain I (LCI) and demonstrated that peak serum levels of LCI in the patients with acute myocardial infarction correlated well with the left ventricular ejection fraction. Furthermore, LCI release from the infarcted myocardium was not affected by coronary reperfusion due to intracoronary thrombolysis. Thus, serial determinations of serum LCI better quantify the extent of myocardial damage even after coronary reperfusion in acute myocardial infarction.

Prevention of myocardial infarction by very early treatment with intracoronary streptokinase. Some clinical observations.

ASERIES of recent studies indicate that the occluded coronary artery can be recanalized in 60 to 85 per cent of cases of acute myocardial infarction if intracoronary streptokinase is infused within six hours of the onset of chest pain.1 2 3 4 This rate of recanalization is far higher than the rate found to occur spontaneously.5 , 6 Although it has been claimed that intracoronary thrombolysis can reduce myocardial damage in treated groups as compared with controls, this has not been consistently confirmed by controlled studies.7 , 8 In individual patients the extent to which myocardial necrosis is prevented by successful thrombolysis is difficult to assess because . . .