Usefulness of intracoronary isosorbide dinitrate in alleviating myocardial ischaemia during coronary balloon angioplasty.

The effect of intracoronary isosorbide dinitrate on provoked myocardial ischaemia during percutaneous transluminal coronary angioplasty (PTCA) was studied in 60 patients who had at least 1 mm electrocardiographic (ECG) ST segment deviation during a 70 s control balloon inflation period. Isosorbide dinitrate (dose 1 mg, 2 mg or 3 mg) or placebo (saline) was administered by slow intracoronary injection, and the ST segment changes recorded again during an identical dilatation period 2-4 min later. Following injection of isosorbide dinitrate, the severity of ST segment deviation decreased (1 mg -31 +/- 30%, P = 0.03; 2 mg -51 +/- 35%, P = 0.0001; 3 mg -36 +/- 32%, P = 0.002) during coronary balloon inflation, and the time until onset of 1 mm ST deviation was prolonged (1 mg +79 +/- 137%, P = 0.06; 2 mg +85 +/- 87%, P = 0.02; 3 mg +78 +/- 109%, P = 0.02). With the 3 mg dose, the time to maximum ECG change increased (+37 +/- 87%, P = 0.02). In the placebo group, there was a small decrease in the severity of ST segment deviation in patients receiving placebo (-23 +/- 32%, P = 0.03), but no change in the time to its onset or in the time to maximum ST deviation. Isosorbide dinitrate did not alter heart rate, systolic arterial pressure or the rate-pressure product at maximum ST segment change, implying that when isosorbide was administered by direct intracoronary injection, a direct cardiac effect was responsible for the major anti-ischaemic effect of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)     

Release of atrial natriuretic peptide in relation to metabolic changes during myocardial ischaemia induced by coronary angioplasty

The inter-relationships between ischaemia-induced metabolicchanges and atrial natriuretic peptide (ANP) release were studiedin 18 patients undergoing elective percutaneous transluminalcoronary angioplasty (PTC A). Transcardiac differences in ANP,lactate, pH, pCO₂ and O₂ saturation were analysed before andafter balloon inflation. The patients were divided into ischaemiaand non-ischaemia groups on the basis of the change in lactateextraction ratio during balloon inflation. The ischaemia group(patients with a decrease in lactate extraction ratio) showedan increase of 27±15 pg. ml^–1 in the transcardiacANP difference, whereas a decrease of 27±17pg.ml^–1occurred in the non-ischaemia group (no decrease in lactateextraction ratio). The change between the two patient groupswas statistically significant (P<0.05). Metabolic ‘pre-conditioning’was not observed in patients with successive dilatations, thereforedata from all the dilatations were combined and evaluated byregression analysis. A correlation coefficient of 0.40 (P<0.05)was obtained between the PTCA-induced changes in transcardiacANP and lactate differences. We conclude that transient myocardialischaemia induced by PTCA increases circulating ANP concentrationsin patients with signs of metabolic ischaemia, but not in thosewithout.     

Effect of pre-treatment with transdermal glyceryl trinitrate on myocardial ischaemia during coronary angioplasty.

OBJECTIVE: In the light of the reported inconsistent anti-ischaemic and antianginal effects of transdermal glyceryl trinitrate, its efficacy and influence on the effects of intracoronary glyceryl trinitrate were examined during coronary angioplasty, which provides a model of controlled, reversible ischaemia. DESIGN: Double blind, randomised study of the effect of transdermal and intracoronary glyceryl trinitrate on ischaemia during coronary angioplasty. PATIENTS: 40 patients with isolated severe stenosis of the left anterior descending coronary artery. INTERVENTIONS: Patients were randomised (double blind) to transdermal glyceryl trinitrate (10 mg per day) and placebo, starting four to six hours before angioplasty. After 4 one-minute balloon inflations intracoronary glyceryl trinitrate was injected (0.2 mg) and then 4 further one-minute inflations were performed. MAIN OUTCOME MEASURES: The time to angina and the time to > 0.2 mV ST shift on surface electrocardiogram (ECG) or intracoronary ECG during the individual inflations. RESULTS: These times did not significantly differ during initial inflations between transdermal glyceryl trinitrate (27 (11), 25 (9), and 19 (9) s, respectively) and placebo (34 (11), 30 (8), and 21 (7) s. After intracoronary glyceryl trinitrate, they were significantly prolonged compared with the initial values, without differences between patients with transdermal glyceryl trinitrate (37 (10), 30 (8), and 23 (8) s, respectively) or placebo (39 (15), 36 (11), and 28 (12) s). Ischaemic preconditioning was not seen. CONCLUSIONS: Transdermal glyceryl trinitrate (10 mg per day), unlike intracoronary glyceryl trinitrate, did not alleviate the myocardial ischaemia produced by balloon inflation during coronary angioplasty.     

Body surface mapping during percutaneous transluminal coronary angioplasty. QRS changes indicating regional myocardial conduction delay

Using a radiotransparent electrode array, body surface maps (BSMs) were constructed based on simultaneous recordings from 62 leads on the entire thorax before, during, and after balloon inflation during percutaneous transluminal coronary angioplasty (PTCA). Twenty-five patients were studied, and 30 angioplasties were performed; 20 patients had one-vessel disease, and five patients had two-vessel disease. In total, 15 dilations in the left anterior descending artery (LAD), seven in the right coronary artery (RCA), and eight in the left circumflex artery (LCx) were studied. For each patient, the BSM and the QRS integral map before, during, and after the inflation was compared by subtraction of recordings "during-minus-before" inflation and "before-minus-after" inflation. The subtraction was performed on the results of the QRS integral maps. The conclusions derived from the inspection of the BSMs and the difference maps show specific changes in the QRS complex during ischemia related to the corresponding ischemic segment in 21 of 25 patients in the three groups. An area of positive potentials remained present on the BSM during dilation, indicating a depolarization wave front. For the LAD group, positive potentials were seen on the anterior thorax and, for the RCA group, on the lower part of the thorax. By subtraction analysis, these changes were extracted and presented as difference maps. For the LCx group, the BSM revealed no changes in pattern but the difference map showed a difference vector pointing in a anteroposterior direction. A regional myocardial conduction delay was hypothesized as the most likely cause for the results.     

Coronary sinus pH during percutaneous transluminal coronary angioplasty: early development of acidosis during myocardial ischaemia in man.

Coronary sinus pH was measured continuously in eight patients undergoing angioplasty to the left anterior descending coronary artery. A catheter tip pH sensitive electrode with a response time of less than 300 ms and an output of greater than or equal to 57 mV/pH unit was placed high in the coronary sinus. Recordings were obtained during a total of 24 balloon occlusions of the left anterior descending coronary artery varying in duration from 5 to 45 s. Continuous 12 lead surface electrocardiograms were recorded. During or after balloon inflation of greater than or equal to 12 s (n = 4) there was no change in coronary sinus pH or the electrocardiogram. During balloon inflation of greater than or equal to 15 s (n = 20) coronary sinus pH was unaltered but between 4 and 6 s after balloon deflation coronary sinus pH fell transiently by between 0.010 and 0.120 pH units before returning to the control value within 65 s. Ischaemic changes were seen on the electrocardiogram during 15 balloon occlusions. In individual patients the peak fall in coronary sinus pH was related to the duration of occlusion of the left anterior descending coronary artery. A rise in coronary sinus pH (alkalosis) was never seen. In man acidosis occurs in the myocardium after short periods (greater than or equal to 12 s) of ischaemia. The fall of pH precedes ischaemic changes on the surface electrocardiogram and occurs concurrently with the earliest reported changes in contractile function.     

Associations between different status of myocardial ischemia and ischemiarelated negative or positive epicardial U-waves: Observations during coronary angioplasty

This study examined the relationships between the polarity of the U wave on intracoronary electrocardiogram (ECG) and the status of myocardial ischemia during angioplasty. The ECG features of ischemia-related U waves were also evaluated. Among 63 patients with intracoronary ECGs adequate for analysis of U waves, there were 26 patients showing a change of the U wave to a negative direction and 18 patients showing a change to a positive direction from baseline to coronary occlusion. Among these patients, 10 of the former showed a distinct change in polarity of the U wave from positive to negative (group A), and 7 of the latter patients showed the opposite change (group B). Patients in group B had a higher incidence of prior myocardial infarction (86% vs 30%; P < .05), presence of an abnormal Q wave on intracoronary ECG (71% vs 20%; P < .05), poor wall motion in the angioplasty-related area (100% vs 30%; P < .01), and lower left ventricular ejection fraction (55.7% +/-8.1% vs 66.6% +/- 4.5%; P < .01) than patients in group A. The remaining patients (other than groups A and B) showing U wave change in a negative (n = 16) or positive (n = 11) direction presented with similar features to those in groups A or B, respectively. The ECG features of several types of ischemia-related U wave were determined by analysis of intracoronary ECG obtained from the patients in groups A and B. In group A, the Bazett-corrected Q (positive U) interval measured at baseline (myocardial state; near normal) was significantly shorter than the Q-(negative U) interval measured during coronary occlusion (acute ischemia) (0.518 +/- 0.031 s vs 0.579 +/- 0.046 s; P < .01). In group B, the Q-(negative U) interval measured at baseline (chronic ischemia) was longer than the Q-(positive U) interval measured during angioplasty (acute-on-chronic ischemia) (0.582 +/- 0.034 s vs 0.501 +/- 0.027 s; P < .001). Thus, intracoronary ECG recorded during angioplasty in the present study revealed physiologic U wave, two types ("acute" and "chronic") of ischemia-related negative and one type ("pseudonormal") of ischemia-related positive U waves, each of which appeared in a different status of myocardial ischemia and possessed characteristic ECG features in its appearance.     

The value of the intracoronary electrogram for the early detection of myocardial ischaemia during coronary angioplasty.

The clinical value of intracoronary electrography for the detection of myocardia ischaemia was assessed during coronary angioplasty and compared to a standard technique of surface ECG monitoring. In 73 patients undergoing single lesion angioplasty, an intracoronary electrogram and four representative surface ECG leads were obtained. During angioplasty of the left anterior descending artery leads, I, V3, V5, V6 were recorded. For the circumflex artery leads I, aVL, aVF, V6, and for the right coronary artery leads II, III, aVF, V6 were monitored. Eight patients were excluded due to transient intraventricular conduction disturbances during balloon inflation; 65 patients remained for further analysis. Out of a total of 154 balloon inflations (35 in the circumflex, 71 in the left anterior descending and 48 in the right coronary artery), the percentage that produced a greater than or equal to 1 mm ST segment elevation, the time to the appearance of a greater than or equal to 1 mm ST segment elevation and the maximal ST segment elevation were recorded. During inflations in the circumflex artery, the respective values of these three parameters were 20%, 22.6 +/- 11.5 s and 0.37 +/- 0.80 mm in V6, the most sensitive surface lead, versus 70% (P less than 0.001), 14.4 +/- 9.6 s (P less than 0.01) and 5.82 +/- 6.35 mm (P less than 0.0001) on the intracoronary electrogram.(ABSTRACT TRUNCATED AT 250 WORDS)     

Coronary sinus pH during percutaneous transluminal coronary angioplasty: early development of acidosis during myocardial ischaemia in man

Coronary sinus pH was measured continuously in eight patients undergoing angioplasty to the left anterior descending coronary artery. A catheter tip pH sensitive electrode with a response time of less than 300 ms and an output of greater than or equal to 57 mV/pH unit was placed high in the coronary sinus. Recordings were obtained during a total of 24 balloon occlusions of the left anterior descending coronary artery varying in duration from 5 to 45 s. Continuous 12 lead surface electrocardiograms were recorded. During or after balloon inflation of greater than or equal to 12 s (n = 4) there was no change in coronary sinus pH or the electrocardiogram. During balloon inflation of greater than or equal to 15 s (n = 20) coronary sinus pH was unaltered but between 4 and 6 s after balloon deflation coronary sinus pH fell transiently by between 0.010 and 0.120 pH units before returning to the control value within 65 s. Ischaemic changes were seen on the electrocardiogram during 15 balloon occlusions. In individual patients the peak fall in coronary sinus pH was related to the duration of occlusion of the left anterior descending coronary artery. A rise in coronary sinus pH (alkalosis) was never seen. In man acidosis occurs in the myocardium after short periods (greater than or equal to 12 s) of ischaemia. The fall of pH precedes ischaemic changes on the surface electrocardiogram and occurs concurrently with the earliest reported changes in contractile function.     

Electrocardiographic changes resembling myocardial ischaemia in asymptomatic men with normal coronary arteriograms.

T wave and ST segment abnormalities in 20 asymptomatic men aged 18 to 55 were investigated because they were identical with myocardial ischaemic changes, and the professional livelihood of the subjects was jeopardised. Coronary arteriograms showed unobstructed arteries in all except one in whom a 50 per cent lesion of the left anterior descending artery was present. Left ventricular angiograms showed a normal contraction pattern, Ejection fractions were normal in 12 and increased in 8. Three characteristic electrocardiographic patterns were observed: flat or inverted T waves in leads II, III, aVF, and V4 to 6 designated type 1; deep T inversion particularly evident in leads V2 to 5 designated type 2, and minor ST segment depression in the inferior and lateral leads without T changes designated type 3. Characteristically, type 1 changes were temporarily suppressed by either beta-blockade or an overnight rest and were more abnormal in the standing position. Type 2 and 3 changes were relatively uninfluenced by these manoeuvres. Maximal treadmill exercise tests were positive in 6 and borderline or negative in 14. When repeated after oxprenolol all tests were negative. Echocardiograms showed asymmetric septal hypertrophy in 3 subjects (ratio of greater than 1.5 between ventricular septum and posterior left ventricular wall). After normalisation by an overnight rest, type 1 T wave abnormalities were reproduced by intravenous adrenaline infusion (0.024 to 0.18 microgram/kg/min) but not by noradrenaline or by adrenaline after prior administration of oxprenolol. When the T waves had remained deeply inverted before infusion despite rest (type 2) adrenaline infusion normalised them and again noradrenaline was without effect. This effect was also prevented by oxprenolol. Type 3 changes were uninfluenced by catecholamine infusion. Plasma catecholamine estimations suggest that catecholamine hypersecretion and hypersensitivity may both be relevant, particularly the latter. The apparent bimodal response of the ventricular myocardium to adrenaline infusion is not surprising since in vitro experiments suggest that reversal of T wave polarity in either direction may result from summation of changes in action potential duration in different parts of the heart. Such changes may be unimodal, that is both areas involved show lengthening or shortening of action potential duration, but by occurring at different rates may lead to a bimodal change in the differences in duration which generate the T wave.     

Electrocardiographic changes resembling myocardial ischaemia in asymptomatic men with normal coronary arteriograms.

T wave and ST segment abnormalities in 20 asymptomatic men aged 18 to 55 were investigated because they were identical with myocardial ischaemic changes, and the professional livelihood of the subjects was jeopardised. Coronary arteriograms showed unobstructed arteries in all except one in whom a 50 per cent lesion of the left anterior descending artery was present. Left ventricular angiograms showed a normal contraction pattern, Ejection fractions were normal in 12 and increased in 8. Three characteristic electrocardiographic patterns were observed: flat or inverted T waves in leads II, III, aVF, and V4 to 6 designated type 1; deep T inversion particularly evident in leads V2 to 5 designated type 2, and minor ST segment depression in the inferior and lateral leads without T changes designated type 3. Characteristically, type 1 changes were temporarily suppressed by either beta-blockade or an overnight rest and were more abnormal in the standing position. Type 2 and 3 changes were relatively uninfluenced by these manoeuvres. Maximal treadmill exercise tests were positive in 6 and borderline or negative in 14. When repeated after oxprenolol all tests were negative. Echocardiograms showed asymmetric septal hypertrophy in 3 subjects (ratio of greater than 1.5 between ventricular septum and posterior left ventricular wall). After normalisation by an overnight rest, type 1 T wave abnormalities were reproduced by intravenous adrenaline infusion (0.024 to 0.18 microgram/kg/min) but not by noradrenaline or by adrenaline after prior administration of oxprenolol. When the T waves had remained deeply inverted before infusion despite rest (type 2) adrenaline infusion normalised them and again noradrenaline was without effect. This effect was also prevented by oxprenolol. Type 3 changes were uninfluenced by catecholamine infusion. Plasma catecholamine estimations suggest that catecholamine hypersecretion and hypersensitivity may both be relevant, particularly the latter. The apparent bimodal response of the ventricular myocardium to adrenaline infusion is not surprising since in vitro experiments suggest that reversal of T wave polarity in either direction may result from summation of changes in action potential duration in different parts of the heart. Such changes may be unimodal, that is both areas involved show lengthening or shortening of action potential duration, but by occurring at different rates may lead to a bimodal change in the differences in duration which generate the T wave.     

A comparison of electrocardiographic changes during reperfusion of acute myocardial infarction by thrombolysis or percutaneous transluminal coronary angioplasty

BACKGROUND: Different electrocardiographic changes have been described during thrombolytic therapy for acute myocardial infarction to indicate successful reperfusion. The occluded coronary artery also can be reopened by percutaneous transluminal coronary angioplasty (PTCA). This study was performed to compare electrocardiographic changes during primary or rescue PTCA and thrombolytic therapy. The electrocardiographic changes were studied directly at the moment of reperfusion during PTCA. METHODS AND RESULTS: Continuous 12-lead electrocardiographic monitoring was performed in 110 patients with acute myocardial infarction undergoing a reperfusion intervention (thrombolytic therapy or primary or rescue PTCA) to assess electrocardiographic changes during reperfusion. Patency and Thrombolysis In Myocardial Infarction flow in the infarct-related artery were assessed by coronary angiography. During reperfusion of the infarct-related coronary artery, early signs of reperfusion were an increase of ST-segment deviation (30%), ST-segment normalization (70%), and terminal T-wave inversion (60%); only 11% of patients showed no ST-segment changes. Thrombolytic therapy was significantly more often accompanied by a transient increase in ST-segment deviation compared with primary PTCA. Accelerated idioventricular rhythm was documented in 51%, an increase in the number of ventricular premature complexes in 42%, nonsustained ventricular tachycardia in 7%, and bradycardia in 18% of all patients. CONCLUSIONS: This study confirms the occurrence of specific electrocardiographic changes at the time of reperfusion. The pattern of ST-segment change upon reperfusion relates to the type of treatment. Awareness of electrocardiographic changes at the moment of reperfusion will help to select patients for rescue PTCA and can be used to assess the effect of future pharmacologic interventions to limit reperfusion damage.     

ST segment changes in exercise body surface mapping after myocardial infarction in patients with isolated left anterior descending coronary artery disease

To investigate the clinical significance of exercise-induced ST segment elevation and ST segment depression after myocardial infarction (MI), we performed 87-lead ECG mapping after previous anterior infarction in 24 patients with isolated left anterior descending coronary artery disease before and 1.5 minutes after treadmill exercise. Thirteen patients showed ST segment elevation only, seven patients showed both ST segment elevation and depression, and four patients showed ST segment depression only. ST segment elevation most frequently occurred in the left anterior chest leads corresponding to the QS area, and ST segment depression developed in the left lower chest and left lower back leads. There was good correlation between the number of lead points showing ST segment elevation (nSTe) after exercise and the number of lead points showing QS waves (nQS) before exercise (r = 0.65). nSTe was also correlated with the asynergy index (r = 0.43). These findings suggest that ST segment elevation is mainly the result of aggravation of wall motion abnormalities of the infarcted myocardium. Body surface distribution of ST segment depression was similar to that in effort angina pectoris without MI. We conclude that exercise-induced ST segment depression in MI mainly reflects the ischemia of the surviving myocardium of small infarcts or the peripheral area of large infarcts.     

The changes in regional myocardial surface area during coronary occlusion and reperfusion

Summary For the analysis of regional myocardial function, the measurement of regional myocardial surface area (RMA) was performed on the epicardial surface of myocardial segment lengths in a direction parallel to the superficial myocardial fibers (SLa) and at right angles to the first (SLb). In eight anesthetized dogs with opened-chests, measurements were done during a 60 s left anterior descending coronary artery occlusion and reperfusion. In the ischemic region, coronary occlusion resulted in dyskinesis in RMA, and the reduction of it during the ejection phase (ERA) decreased significantly at 10 s (p<0.05) and thereafter (p<0.01). Regional myocardial work (EWA) from the pressure-area loops during the ejection phase also decreased significantly at 10 s (p<0.05) and thereafter (p<0.01). The end-diastolic RMA (EDRMA) increased significantly at 30 s (p<0.01) and thereafter (p<0.01). In the non-ischemic region, compensatory changes were shown, namely ERA, EWA and EDRMA, increased significantly during occlusion. After reperfusion, recovery to the control level was prompt, and only EDRMA remained the increased value after 30 s (p<0.01). Between SLa and SLb, characteristics differed from each other, which suggested that the directional differences of SLs should be considered when regional myocardial function is assessed from unidirectional SL. The changes in RMA reflect both changes of SLa and SLb during coronary occlusion and reperfusion, and were more marked than each SL. Thus, the usefulness of RMA to assess regional myocardial function was demonstrated during coronary occlusion and reperfusion.     

Hyperoxemic perfusion of the left anterior descending coronary artery after primary angioplasty in anterior ST-elevation myocardial infarction.

OBJECTIVES: To assess left ventricle function recovery, ST-segment changes, and enzyme kinetic in ST-elevation myocardial infarction patients treated with intracoronary hyperoxemic perfusion (IHP) after primary percutaneous coronary intervention and compare them with the results obtained in control patients. BACKGROUND: IHP has been shown to attenuate microvascular reperfusion injury, which may result in poor LV function recovery despite successful primary percutaneous coronary intervention. METHODS: Twenty seven anterior ST-elevation myocardial infarction patients treated < or = 12 hr after symptom onset by primary percutaneous coronary intervention were subjected to selective IHP into the left anterior descending coronary artery for 90 min. They were compared with 24 anterior ST-elevation myocardial infarction control patients matched in clinical and angiographic characteristics and treated with conventional primary percutaneous coronary intervention. Left ventricular function recovery was evaluated by serial 2D contrast echocardiography. RESULTS: Left anterior descending coronary artery recanalization was successful in all patients. After IHP (100% successful, duration 90 +/- 5.4 min), patients showed a 4.8 +/- 2.2 hr shorter time-to-peak creatine kinase release (P = 0.001), a shorter creatine kinase half-life period (23.4 +/- 8.9 hr vs. 30.5 +/- 5.8 hr, P = 0.006), and a higher rate of complete ST-segment resolution (78% vs. 42%, P = 0.01). A significant improvement of mean left ventricular ejection fraction (from (44 +/- 9)% to (55 +/- 11)%, P < 0.001) and wall motion score index (from 1.77 +/- 0.2 to 1.39 +/- 0.4, P < 0.001) was observed at 3 months in IHP patients only. CONCLUSION: After successful primary coronary intervention, IHP is associated with significant left ventricular function recovery when compared to conventional treatment. Enzyme kinetic and ST-segment changes suggest faster and more complete microvascular reperfusion and may explain the salutary effects of this new therapy on left ventricular function.     

Intracoronary electrocardiogram for early detection of myocardial viability during coronary angioplasty in acute myocardial infarction.

PURPOSE: The clinical value of the intracoronary electrocardiogram (ECG) for detecting myocardial viability in acute myocardial infarction was evaluated by thallium-201 scintigraphy and left ventriculogram at the chronic stage. METHODS: Intracoronary ECGs, recorded from the tip of a guidewire during emergency coronary angioplasty, were obtained in 65 patients with reperfused anterior myocardial infarction. Further ST segment elevation of greater than 0.2 mV detected during the balloon inflation was taken as significant. The left ventricular segmental shortening was measured from left ventriculograms recorded at acute and chronic stages. The infarct area was defined as viable when a thallium uptake of more than 50% was detected on thallium-201 myocardial scintigraphy at the chronic stage. RESULTS: During emergency coronary angioplasty, significant ST segment elevation was noted in 45 patients (Group A); however, the ST segment was not significantly elevated in the other 20 patients (Group B). The infarct area of 42 patients in Group A and three patients in Group B was viable on scintigraphy. Improvement left ventricular wall motion of the infarct area was observed in 39 of the 42 patients in Group A and the three patients in Group B. Therefore, intracoronary ECG can predict reversible dysfunction with excellent sensitivity (92.9%) and specificity (73.9%). CONCLUSIONS: The myocardium within an infarct area can be regarded as viable when a further ST segment elevation occurs on intracoronary ECG during emergency coronary angioplasty. It is useful, therefore, to monitor the intracoronary ECG during coronary angioplasty balloon inflation to assess the myocardial viability of the infarct area.     

Percutaneous transluminal coronary angioplasty, alone or in combination with urokinase therapy, during acute myocardial infarction

To investigate the effect of pre-treatment of a thrombus with a low dose of urokinase on establishing patency in a persistent infarct-related artery (IRA) during direct percutaneous coronary angioplasty (PTCA), the frequency of acute restenosis during direct PTCA, alone, or in combination with the intracoronary administration of urokinase, was examined in a consecutive nonrandomized series of patients with acute myocardial infarction (AMI). Two hundred and seventy-two successful PTCA patients (residual stenosis <50%) were divided into 2 groups: 88 patients received pre-treatment with intracoronary urokinase following PTCA (combination group); 184 received only direct PTCA without thrombolytic therapy (PTCA group). In the present study, after achievement of a residual stenosis of less than 50%, IRA was visualized every 15 min to assess the frequency of acute restenosis, which was defined as an acute progression of IRA with more than 75% restenosis after initially successful PTCA. In the patients with a large coronary thrombus, the frequency (times) of acute restenosis was significantly lower in the combination group than in the PTCA group (0.98+/-0.19 vs 2.92+/-0.32, p<0.0001). On the other hand, in the patients with a small coronary thrombus, the frequency of acute restenosis showed no difference in either group. The present study indicates that in patients with AMI, PTCA combined with pre-treatment of a low dose of urokinase is much more effective than PTCA alone, especially for those patients who have a large coronary thrombus.