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.     

Value of percutaneous transluminal coronary angioplasty after unsuccessful intravenous streptokinase therapy in acute myocardial infarction

The effect of sequential high-dose intravenous streptokinase (SK) (1.5 million units) followed by emergency percutaneous transluminal coronary angioplasty (PTCA) on preserving left ventricular function was assessed prospectively in 34 patients with acute myocardial infarction (AMI). Intravenous SK therapy was initiated 2.6 +/- 1.3 hours (mean +/- standard deviation) after the onset of chest pain. Urgent coronary angiography showed persistent total occlusion in 13 patients, significant diameter stenosis (70 to 99%) in 18 patients and a widely patent artery (less than 50% stenosis) in 3 patients. Emergency PTCA was performed in 29 patients 5.0 +/- 2.1 hours after symptom onset. Successful recanalization was achieved in 33 of the 34 patients (97%) treated with sequential therapy. Repeat contrast ventriculograms recorded 7 to 10 days after intervention in 23 patients showed that the left ventricular ejection fraction increased from 53 +/- 12% to 59 +/- 13% (area-length method, p less than 0.002). Regional wall motion of the infarcted segments improved from -2.7 +/- 1.1 to -1.5 +/- 1.7 SD/chord (centerline method, p less than 0.003). In the subgroup of patients with an occluded artery on initial angiography (group A, n = 10), both global left ventricular ejection fraction (49 +/- 12% vs 59 +/- 12%, p less than 0.002) and regional wall motion (-3.2 +/- 1.0 vs -1.9 +/- 1.7 SD/chord, p less than 0.002) improved significantly. In contrast, no significant improvement was seen in patients with a patent artery on initial angiography (n = 13). Thus, sequential intravenous SK and emergency PTCA is efficacious in achieving coronary reperfusion and in improving both global and regional left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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

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

Evaluation of functional myocardial recovery after emergency revascularization by intracoronary fibrinolysis in the acute infarct period

An angiographic study was carried out to evaluate myocardial recovery in 50 patients who had undergone coronary angiography in the first six hours of myocardial infarction with the object of attempting emergency revascularisation by a selective intracoronary infusion of streptokinase. Left ventriculography performed before initial coronary arteriography and 2 to 10 weeks later was compared. The ejection fractions and two indices obtained by quantitative analysis of regional contractility, the surface (SHK) and extent (EHK) of the ischemic zones were calculated. The patients were divided into two groups according to results: Group I, 25 patients with patent arteries at the second control, and Group II, 25 patients not revascularised or with a reobstructed artery at the second angiographic control. In Group I, the ejection fraction remained stable (47 +/- 11 p. 100 to 48 = 10 p. 100 N.S.) but SHK (13 +/- 6 cm2 to 10 +/- 5 cm2, p less than 0,01) and EHK in percentage of ventricular circumference (48 +/- 12 p. 100 to 42 +/- 11 p. 100, p less than 0,05) fell significantly. In Group II, the ejection fraction fell (55 +/- 9 p. 100 to 44 +/- 11 p. 100, p less than 0,001) whilst SHK (7 +/- 4 cm2 to 11 +/- 5 cm2, p less than 0,001) and EHK (34 +/- 11 p. 100 to 43 +/- 14 p. 100, p less than 0,001) increased significantly. These results show that revascularisation may result in significant functional myocardial recovery and, consequently, that some ischemic myocardium can be salvaged in these patients.     

Factors that predict improvement in left ventricular ejection fraction after coronary angioplasty for acute myocardial infarction

Acute and follow-up angiograms were analyzed in 75 patients with acute myocardial infarction treated with emergency coronary angioplasty to determine factors that might predict improvement in left ventricular ejection fraction. Ejection fraction improved 8.4 +/- 8.2% in 60 patients who maintained patent infarct vessels at follow-up angiography, compared with -4.1 +/- 6.0% in 15 patients who developed reocclusion (p less than .001). In patients with patent infarct vessels, univariate analysis revealed the following significant predictors of improvement in ejection fraction: initial ejection fraction (r = -.38, p less than .003) subtotal vs total stenosis (12.9 +/- 9.3% vs 6.9 +/- 7.3%, p less than .02), infarct vessel (left anterior descending 11.0 +/- 8.4%, right 6.8 +/- 6.4%, circumflex 2.6 +/- 7.5%, p less than .02), and time to follow-up study (less than or equal to 15 days vs greater than 15 days) (4.8 +/- 5.8% vs 9.8 +/- 8.6%, p less than .03). Reperfusion time (less than or equal to 2 hr vs greater than 2 hr) predicted improvement when subtotal stenoses and stuttering infarctions were excluded (10.6 +/- 7.0% vs 4.9 +/- 6.9, p less than .03). Multivariate analysis showed initial ejection fraction and subtotal vs total stenosis to be independent predictors. Patients with anterior infarctions, low initial ejection fractions, and subtotal stenoses or reperfusion times less than or equal to 2 hr are likely to benefit most from coronary angioplasty for acute myocardial infarction.     

Myocardial infarction with minimal coronary atherosclerosis in the era of thrombolytic reperfusion. The Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study Group

The incidence of minimal residual atherosclerotic coronary obstruction after successful intravenous thrombolytic therapy was evaluated in 799 patients with acute myocardial infarction. Minimal residual coronary obstruction (less than or equal to 50%) was observed on selective coronary angiography performed 90 min after initiation of thrombolytic therapy in 43 patients (5.5%). In 42 other patients (5.4%), a greater than 50% but less than 100% residual stenosis noted at 90 min demonstrated further resolution of obstruction to less than 50% at an angiographic follow-up study 7 to 10 days later. Patients with minimal residual coronary obstruction were significantly younger (52 +/- 10.7 versus 56.7 +/- 10 years; p = 0.002) and had less multivessel coronary disease (p less than 0.001), better initial left ventricular ejection fraction (54 +/- 12% versus 50.2 +/- 11.4%; p = 0.006) and a lower in-hospital mortality rate (1% versus 7%; p = 0.04) than did patients who had a significant (greater than 50%) residual coronary obstruction after intravenous thrombolysis. Long-term follow-up study of patients with a minimal coronary lesion (average 1.5 +/- 0.6 years) and those with significant residual stenosis (average 1.6 +/- 0.7 years) demonstrated that the incidence of death (2.4% in patients with minimal stenosis versus 3.5% in those with significant stenosis) and recurrent myocardial infarction (5% each) were similar in both groups. New strategies are needed to prevent coronary rethrombosis in patients with minimal atherosclerosis after thrombolytic therapy for acute myocardial infarction.     

Clinical and angiographic follow-up after coronary recanalization during acute myocardial infarction

Coronary angiography followed by percutaneous transluminal coronary angioplasty and/or intracoronary streptokinase infusion was performed in 50 patients 288 +/- 162 min after the onset of symptoms of acute myocardial infarction. Subocclusion of the infarct-related vessel was found in 5 patients, all of whom had angioplasty of the residual stenosis. Recanalization was achieved in 37 patients (success rate 82%). There was no procedure-related death. One patient died 4 days after the intervention. Control coronary angiography 5 +/- 2 months after the procedure in 35 of 42 patients with recanalization documented recurrence of stenosis or reocclusion in 8 (23%). Comparison of preintervention and control angiograms in 33 patients showed an increase in left ventricular ejection fraction from 55 +/- 8 to 61 +/- 13%, p less than 0.001, in patients with collaterals to the infarct-related vessel and/or recanalization within 180 min after the onset of pain, and from 55 +/- 9 to 59 +/- 8%, nonsignificant, in patients with recanalization later than 180 min and without collaterals. At follow-up 7 +/- 4 months after the procedure, 1 patient had died and 36 (86%) were asymptomatic. Good long-term results can be achieved at a reasonable risk by coronary angioplasty with or without thrombolysis in evolving myocardial infarction. Left ventricular function is better preserved in patients with collaterals and/or early recanalization.     

Impact of late coronary artery reperfusion on left ventricular function one month after acute myocardial infarction (results from the ISAM study)

To evaluate the impact of late reperfusion of an infarct-related coronary artery on left ventricular (LV) function in the month after myocardial infarction, findings from 368 patients in the Intravenous Streptokinase in Myocardial Infarction study are presented. All patients had a late peaking in the creatine kinase-MB serum time-activity curve, suggesting absence of early reperfusion. Contrast angiography was performed 1 month after the acute event. The infarct-related coronary artery was patent in 74 of 116 (64%) streptokinase-treated patients and 141 of 252 (56%) patients treated with anticoagulant therapy (placebo group). In all baseline variables, including the actually developed enzymatic and electrocardiographic infarct sizes, there were no differences between the patent- or occluded-artery groups. A patent infarct artery 1 month after infarction was associated with significantly better LV function regardless of the vessel involved and whether or not patients had been treated with streptokinase. Ejection fraction in patients with patent versus occluded artery was 56 +/- 13 versus 50 +/- 14 (p less than 0.0005). Most benefit was noted in patients in whom the proximal left anterior descending coronary artery was affected: ejection fraction was 52 +/- 14 versus 36 +/- 12% (p less than 0.0005). Our data confirm that restoration of adequate flow through an infarct-related coronary artery beyond the time window for actual salvage of ischemic myocardium has a definite beneficial effect on LV function.     

Improvement in three-month angiographic outcome suggested after primary angioplasty for acute myocardial infarction (Zwolle trial) compared with successful thrombolysis (APRICOT trial). Antithrombotics in the Prevention of Reocclusion In COronary Thrombolysis.

It has been shown that primary percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction results in higher patency rates than thrombolytic therapy. However, no data are available on differences in long-term angiographic outcome after successful primary PTCA compared with successful thrombolysis. Therefore, we compared angiographic data of the Antithrombotics in the Prevention of Reocclusion In COronary Thrombolysis (APRICOT) trial and the Zwolle primary PTCA trial. In the APRICOT trial 248 patients underwent coronary angiography at a mean of 24 hours after thrombolysis and had a patent infarct-related vessel (Thrombolysis In Myocardial Infarction-3 trial flow) when entering the study. Reocclusion rates were assessed at a second angiography after 3 months. In the Zwolle trial 136 patients had a successful primary PTCA. At 3 months 131 patients underwent a second angiography. Quantitative coronary angiography showed a significant lower mean diameter stenosis of the infarct-related vessel after primary PTCA (27 +/- 12% vs 57 +/-12%; p = 0.00001). At 3 months this difference was sustained (35 +/- 22% vs 63 +/- 26%; p = 0.00001). After thrombolysis the reocclusion rate at 3 months was 29% compared with 5% after primary PTCA (p = 0.0001). Results show that compared with successful thrombolytic therapy, primary PTCA for acute myocardial infarction results in an improved infarct-related vessel status not only short term but also long term, with a low reocclusion rate.     

Association of patency of the infarct-related coronary artery with plasma levels of plasminogen activator inhibitor activity in acute myocardial infarction.

To examine the fibrinolytic capacity in patients with acute myocardial infarction (AMI), baseline levels of plasma plasminogen activator inhibitor (PAI) activity and tissue-type plasminogen activator (t-PA) antigen were measured in 47 patients with Q-wave AMI who underwent emergent coronary angiography 3.0 +/- 0.2 hours after the symptom onset. They received intracoronary injection of urokinase if their infarct-related arteries were occluded. They were classified into 3 groups according to the patency of the infarct-related artery before and after thrombolytic therapy: the patent group (13 patients), the recanalized group (23 patients) and the occluded group (11 patients). The mean level of plasma PAI activity (IU/ml) was higher in patients with AMI as a whole than in the control group (12.8 +/- 1.6 vs 5.4 +/- 0.5, p less than 0.01). The level was lower in the patent group (3.0 +/- 1.1) and higher in the recanalized (18.6 +/- 2.2) and occluded (10.8 +/- 2.5) groups than in the control group (each p less than 0.01). The level was lower in the occluded than in the recanalized group (p less than 0.01) and 62% of the patients in the occluded group had levels within range of the control group. The mean level of plasma t-PA antigen (ng/ml) was higher in patients with AMI as a whole than in the control group (10.3 +/- 0.8 vs 5.8 +/- 0.3, p less than 0.01). There was no difference in the level among the 3 groups with AMI.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Dipyridamole echocardiography test. A new tool for detecting jeopardized myocardium after thrombolytic therapy

BACKGROUND. We wished to assess whether dipyridamole echocardiography test (DET) can detect jeopardized myocardium after thrombolytic therapy. METHODS AND RESULTS. Seventy-six consecutive patients with a first acute myocardial infarction (AMI) were treated with 2 million IU urokinase i.v. within 4 hours of the onset of AMI and underwent high-dose (as much as 0.84 mg/kg over 10 minutes) DET 8-10 days after AMI. The results were correlated to the anatomy of the infarct-related vessel (IRV). In patients with positive DET, we evaluated the wall motion score index (WMSI; a semiquantitative integrated estimation of extent and severity of the stress-induced dyssynergy). WMSI was derived by summation of individual segment scores divided by the number of interpreted segments. In a 13-segment model, each segment was assigned a score ranging from 1 (normal) to 4 (dyskinetic). Fifty-three patients had positive results on DET. Of these, 42 had dipyridamole-induced new wall motion abnormalities (WMAs) confined to the infarct zone or adjacent segments. In these patients, mean WMSI increased from 1.46 +/- 0.26 (at resting conditions) to 1.73 +/- 0.35 (at peak dipyridamole) (p less than 0.01), whereas no significant change was detected in negative patients (1.6 +/- 0.34 versus 1.57 +/- 0.34, p = NS). Coronary angiography showed a patent IRV (TIMI grade 2 or 3) in 53 patients and no or minimal reperfusion (TIMI grade 0 or 1) in 23 patients. A patent IRV with critical residual stenosis was found in 35 of 42 patients with dipyridamole-induced WMAs in the infarct zone and in 18 of 34 patients without WMAs (p less than 0.05). Among the 23 patients with occluded IRVs, nine had collateral flow to the distal vessel; six of these had a positive DET. Thus, the sensitivity and specificity for identifying a critically stenotic but patent IRV or the presence of a collateral-dependent zone were 66% and 93%, respectively. In a subset of nine patients with a positive DET in the infarct zone or adjacent segments, DET and a control coronary angiography were repeated 1-3 months after an angiographically successful (residual stenosis, 50% or less) coronary angioplasty in the IRV. The repeat DET was negative in eight patients (all with patent IRV at control angiography) and again positive in one patient, who showed restenosis at angiography. The WMSI, at resting conditions was similar before and after angioplasty, whereas it differed significantly at peak dipyridamole (1.7 +/- 0.2 versus 1.4 +/- 0.2, p less than 0.01). CONCLUSIONS. DET can identify the anatomy of the IRV, and dipyridamole-induced WMAs within the infarct zone detect regions with jeopardized myocardium that may benefit from intervention.     

The course of residual stenosis after intracoronary thrombolysis

Clinical outcome after coronary thrombolysis are strictly related to the residual stenosis. However, the natural history of this lesion is largely unknown. To assess this topic we evaluated 25 patients who had coronary recanalization by urokinase in acute myocardial infarction. Serial coronary angiograms were taken immediately after fibrinolytic therapy, before hospital discharge and 1 year later. Angiographically detected coronary reocclusion and/or new ischemic events were exclusion criteria. Angiographic analysis was performed at a five-fold magnification. The followings were specifically evaluated: a) vessel contours at the site of the residual stenosis; b) luminal diameter reduction; c) presence of intraluminal filling defects. Results: the vessel narrowing progressively improved from the acute phase (percent of stenosis 92 +/- 7) to the hospital discharge (82 +/- 8%, p less than .01) and to 1 year follow-up (76 +/- 11%, p less than .001 vs hospital discharge). Moreover, the residual stenosis appears to be "complicated" in early period (irregular contours with superimposed thrombus), but become regular and "uncomplicated" at follow-up examination (smooth contours, hourglass configuration, no intraluminal filling defects). In conclusion: a) the residual coronary stenosis is a dynamic process and may improve at follow-up examination; b) a practical approach to the management of the residual stenosis must take in account the natural history of the lesion to give a correct indication for coronary surgery or PTCA.     

Comparative effects of intracoronary fibrinolysis and conventional treatment of myocardial infarction

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

Effects of percutaneous transluminal coronary angioplasty: intracoronary thrombolysis with urokinase in acute myocardial infarction

Coronary angiography and percutaneous transluminal coronary angioplasty (PTCA) were performed in 32 patients with evolving acute myocardial infarction. Of the 25 patients with complete occlusion of an infarct-related coronary artery, in 18 (72%) the occluded vessel was successfully opened by an intracoronary infusion of urokinase. With a small dose of urokinase the successful recanalization was achieved in only 25%; with a larger dose it was achieved in 94%. After PTCA, all patients received glucose-insulin-potassium solution for 76 hours. Repeat angiography 42 days later showed a patent coronary artery in 12 (group A) of 18 patients with successful PTCA. In group A, left ventricular ejection fraction increased from 51 +/- 13% to 72 +/- 10% (p less than 0.01) and regional wall shortening from 4.5 +/- 9.5% to 29 +/- 19% (p less than 0.01). In contrast, these variables did not change significantly in patients with unsuccessful PTCA or late reocclusion of an infarct-related vessel (group B). These data suggest that successful PTCA with sustained patency of an infarct-related coronary artery has a beneficial effect on the salvage of the jeopardized myocardium, and glucose-insulin-potassium therapy may enhance the beneficial effect of PTCA.     

Frequency of low-grade residual coronary stenosis after thrombolysis during acute myocardial infarction

The clinical, angiographic and demographic characteristics of 42 patients with low-grade (less than 50%) residual stenosis at the infarct lesion after thrombolysis for acute myocardial infarction (MI) were assessed. The study group (group I) represented 21% of 198 consecutive patients receiving thrombolytic therapy over a 59-month period. Data on the 156 remaining patients were pooled for comparison (group II). Group I patients were predominantly men (86%) who were cigarette smokers (81%). Group II patients were predominantly men (75%, p greater than 0.10) but were significantly older (52 +/- 12 vs 56 +/- 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (greater than 50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (greater than 50% diameter stenosis) residual vessel disease was 0.6 +/- 1.0 for group I and 1.9 +/- 0.9 for group II (p less than 0.001). In group I, average residual infarct lesion diameter stenosis was 36 +/- 7% in the right anterior oblique and 34 +/- 8% in the left anterior oblique views. Thirty-nine group I patients were discharged with medical therapy and 100% follow-up was obtained over a mean interval of 18 +/- 17 months. Fifteen patients experienced chest pain after acute MI accounting for 17 discrete events. Fifty-nine percent of group I had a benign course on follow-up. Eight events were classified as unstable angina, 4 as acute MI and 5 as atypical angina. Documented coronary vasospasm occurred in 3.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Significance of exercise induced ST elevation in patient without a history of previous myocardial infarct

Between 1980 and 1995, we observed twenty-five patients (22 males, 3 females) at the mean age of 50.6 +/- 13 years, without previous myocardial infarction who presented exercise induced ST elevation on a bicycle stress test. METHODS: Significant ST elevation was defined as a > or = 1 mm change present in > or = 1 lead measured 0.08 sec after the J point and in 3 consecutive beats. All patients have undergone coronary angiography in the days following the exercise test. RESULTS: Most of patients (56%) presented a history of typical angina that was either purely exertional (8 pts) or also occurred at rest (6 pts). Others (36%) had non typical angina or no angina (8%); 78% of pts were smokers. Sixteen patients (group I) had ST elevation during exercise (exercise duration: 7.6 +/- 4 min; peak heart rate: 135.5 +/- 29 batt/min; ST = 3.5 +/- 1.5 mm) and nine (group II) during the recovery phase (exercise duration 16.3 +/- 1.6 min; p < 0.05; peak heart rate 168 +/- 22 batt/min; p < 0.05; ST: 5.8 +/- 3 mm; p < 0.05). In group I, 1 patient had no vessel disease, 12 had one vessel disease, 3 had multivessel disease with 6 cases of hypersevere coronary stenose (> 90%). In group II, 4 patients had normal coronary arteries, there was one vessel coronary artery disease in 4 patients and multivessel in one subject, without hypersevere coronary stenosis. Correlation between anatomic location of stenosis and electrocardiographic ST elevation was excellent, particularly in case of single vessel disease (100%). All patients underwent one or more new exercise tests after therapeutic intervention (surgery n = 3; angioplasty n = 7; medical treatment n = 15), only 2 patients had persistent exercise induced ST elevation. During follow-up (5 +/- 3 years), 3 patients died (2 cardiac deaths) and 3 had recurrent angina controlled by new treatment. CONCLUSION: Exercise-induced ST elevation is a rare phenomenon in patients without prior myocardial infarction. When occurring purely during exercise, coronary lesions are frequent and often servere, in the other hand ST elevation of the recovery phase is frequently associate with normal arteries or less severe lesions. In most cases, revascularisation or medical therapy can abolish clinical and electrocardiographic abnormalities.     

Recurrence of stenosis after first and repeat coronary angioplasty. Clinical and angiographic follow-up

The incidence of restenosis after initially successful first coronary angioplasty and the long-term effectiveness of repeat angioplasty for recurrence were examined on the basis of data on 282 consecutive patients with successful angioplasty. Primary success of first coronary angioplasty was obtained in 86% of patients and major complications (death, acute myocardial infarction and emergency coronary bypass surgery) occurred in 5% of patients. Control coronary angiography 10 +/- 6 months after successful angioplasty in 195 patients documented recurrence of stenosis in 33%. Repeat angioplasty was attempted in 52 patients with a primary success of 92%. One patient sustained an acute infarction as a complication of the procedure (2%). Control coronary angiography 7 +/- 4 months after a successful second procedure in 28 patients documented a second recurrence of stenosis in 39%. Recurrence rates after first and second coronary angioplasty were comparable (33 vs 39%, ns) but, for lesions of the left anterior descending coronary artery, recurrence was observed more frequently after second than after first angioplasty (47 vs 31%, p less than 0.05). Restenosis after second angioplasty, but not after first, was more frequent in women than in men. Patients with second recurrence were older than those with continuing angiographic success (59 +/- 8 vs 50 +/- 12 years, p less than 0.05). Recurrence was treated by a third coronary angioplasty in 5 patients, with success in all. Clinical follow-up 8 +/- 6 months after the last successful procedure was available for all 43 patients with repeat angioplasty who did not cross over to coronary surgery.(ABSTRACT TRUNCATED AT 250 WORDS)