Effectiveness of intravenous streptokinase on infarct size and left ventricular function in acute myocardial infarction. Prospective and randomized study

Within 3 h after the onset of symptoms of myocardial infarction, 64 patients were randomly assigned to receive either a 1-h intravenous infusion of 1,500,000 IU of streptokinase (SK) or a conventional therapy. Infarct size was estimated in CK gram equivalent (CKg) by measurement of CK-MB every 3 hours during a 48-h period. Enzymatic study revealed that myocardial infarction of the SK group was significantly smaller (61.4 +/- 45 vs. 89.4 +/- 56 CKg, p less than .05). Angiograms were performed at early stage and five weeks after myocardial infarction. At first coronary angiogram, the infarct-related vessel was open in 82% in the SK group versus 12% in controls. The SK group had higher global ejection fraction at second angiogram (57 +/- 11% vs. 49 +/- 11%, p less than .02), but differences in regional wall motion were not significant. By analysis according to patency or occlusion of infarct-related vessel, global and regional ejection fractions were significantly better at first and at second angiograms in all patients and in anterior infarctions with a patent infarct-related coronary artery. There was no significant difference for inferior infarction. We conclude that intravenous streptokinase infusion early after the onset of myocardial infarction reduces infarct size and improves left ventricular function, chiefly in anterior infarction. This benefit appears to be closely correlated to patency of infarct-related vessels.     

Bradycardia and hypotension following reperfusion with streptokinase (Bezold-Jarisch reflex): a sign of coronary thrombolysis and myocardial salvage

Acute myocardial infarction, particularly of the inferior wall, is frequently associated with bradycardia and hypotension. This study reports the occurrence of transient bradycardia hypotension (TBH) (Bezold-Jarisch reflex) following thrombolytic therapy with intravenous streptokinase. Of the 52 patients, 42 had successful reperfusion, and 12 of the latter developed reflex TBH. The Bezold-Jarisch reflex occurred in 10 of 24 patients with inferior wall acute myocardial infarction and in 2 of 28 patients with anterior wall infarction (p less than 0.05). The reflex was associated with significantly more non-Q wave infarctions (p less than 0.05) and also with reduction of left ventricular damage, as evidenced by a lower QRS score (4 +/- 3.8 vs 8.9 +/- 5.6, p less than 0.01) and a higher ejection fraction (61 +/- 13% vs 49 +/- 16%, p less than 0.05). Patients with inferior wall acute myocardial infarction were divided into those with TBH (10 patients) and those without TBH (14 patients). TBH was associated with a significantly higher infarct-related regional ejection fraction (60 +/- 19% vs 35 +/- 18%, p less than 0.05). The results of this study confirm previous findings that reperfusion of the inferoposterior myocardium is capable of stimulating reflex TBH. Furthermore, TBH is associated with patency of infarct-related coronary arteries and myocardial salvage.     

Prevalence and significance of residual flow to the infarct zone during the acute phase of myocardial infarction

Residual flow to the infarct zone was assessed by coronary angiography during the acute phase of myocardial infarction in 130 patients. In 36 patients, the infarct-related coronary artery was not completely obstructed, thereby providing residual anterograde flow to the infarct area (Group I). Complete obstruction of the infarct vessel with residual flow to the infarct zone by means of collateral circulation was observed in 56 patients (Group II). Complete obstruction of the infarct vessel without residual flow was seen in 38 patients (Group III). Ejection fraction during the acute phase of infarction was found to be significantly higher in Group I (55 +/- 13%) than in either Group II (48 +/- 13%) or Group III (50 +/- 10%) (p less than 0.05). Group II patients had a longer history of angina pectoris (14.2 +/- 21.4 months) than did Group III patients (0.7 +/- 3.1 months) (p less than 0.01). Patients in Group I and Group II were more likely to be taking antianginal medication (56 and 54%, respectively) than were the patients in Group III (16%) (p less than 0.01). Thirty-seven patients in whom reperfusion techniques were not employed had repeat angiography in the chronic phase of infarction, enabling assessment of spontaneous changes in left ventricular function and coronary morphology.(ABSTRACT TRUNCATED AT 250 WORDS)     

Utility and limitation of treadmill exercise echocardiography for detecting significant coronary stenosis in infarct-related arteries in patients with healed myocardial infarction.

This clinical study examines the diagnostic accuracy of exercise echocardiography for detecting significant coronary stenoses in infarct-related arteries in patients with healed myocardial infarction. Quantitative coronary angiography and exercise echocardiography using treadmill testing were performed within 2 weeks of each other in 123 patients with a prior myocardial infarction. Coronary lumen diameter stenosis > or =50% by quantitative coronary angiography and the lack of a hyperdynamic response on exercise echocardiography was considered significant. For detection of infarct-related coronary lesions, treadmill exercise echocardiography was highly sensitive (91%) but less specific (59%) than for detection of non-infarct-related artery lesions. The 2 groups of patients with large and small infarct sites had similar sensitivity for detection of residual stenosis of the infarct-related artery (88% vs 96%, p = NS); however, the specificity of the small infarct sites for this purpose was significantly higher than that of the large infarct sites (86% vs 33%, p < 0.01). When remote ischemia was detected on exercise echocardiography, the specificity of exercise echocardiography was significantly lower (33% vs 70%, p < 0.05) than when remote ischemia was not present. Thus, although there is high sensitivity, the specificity of treadmill exercise echocardiography for detecting infarct-related artery lesions is limited. However, high specificity is maintained when the infarct size is small and/or remote ischemia is not present.     

Impact of chronic patency of infarct-related coronary artery on prevalence of myocardial ischemia during the pharmacologic and exercise stress test

Background: Even late restoration of anterograde coronary flow may have beneficial effects on left ventricular function, electrophysiology, and survival in postinfarction patients. Hypothesis: The patency or occlusion of an infarct-related coronary artery in the chronic phase may also be associated with myocardial ischemia provoked by pharmacologic and physiologic stress tests. Methods: High-dose dipyridamole echocardiography test (DET) (up to 0.84 mg/kg over 10 min), exercise electrocardiography (EET), and coronary angiographic data in a group of 127 in-hospital patients who had survived an acute myocardial infarction were analyzed. Patients who had only angiographic evidence of infarct-related single artery disease (≥50% luminal diameter reduction) and no previous revascularization were enrolled in the study. DET and EET were performed (DET in all, EET in 118 patients) within 5 days before coronary angiography. Fifty-seven patients had total occluded infarct arteries (Group 1) with various degrees of collateral circulation (2.6±1.1 collateral score, by a 3 grading system), whereas the other 70 patients had patent infarct arteries (Group 2) with significant residual stenoses (82±13% diameter reduction). Results: The prevalence of rest angina or effort angina and topography of the infarct-related coronary artery did not differ between the two groups (all p = NS). There were more patients with Q wave in Group 1 than in Group 2 (72 vs. 57%, p = 0.08) compared with non-Q wave infarction (Group 1 = 28 vs. Group 2 = 43%, p = 0.08). Ischemia in the infarct-related artery territory detected by DET (defined as new wall motion dyssynergy or marked worsening of resting hypokinesia) was 61% in Group 1 and 41% in Group 2 (p = 0.025). EET was positive in 26 of 54 (48%) Group 1 and in 21 of 64 (33%) Group 2 patients (p = 0.09). Conclusions: Patients with occluded infarct-related arteries have a higher prevalence of ischemia during DET and EET regardless of the presence of collateral flow. These results suggest that the presence of partial anterograde flow in the prolonged period could have a favorable influence on prevalence of residual ischemia in these patients.     

Coronary perfusion during acute myocardial infarction with a combined therapy of coronary angioplasty and high-dose intravenous streptokinase

Two hundred and sixteen patients with acute myocardial infarction were treated with immediate infusion of high-dose (1.5 million units) intravenous streptokinase followed by emergency coronary angioplasty. The infarct lesion was crossed and dilated in 99% and persistent coronary perfusion after the procedure was achieved in 90% (including 3% with significant residual stenosis). Total in-hospital mortality was 12%. Multivariable analysis showed a higher hospital mortality with cardiogenic shock (41% vs 5% without shock), older age, lower left ventricular ejection fraction, and female sex. Final patency of the infarct-related vessel was determined by follow-up in-hospital cardiac catheterization. Coronary reocclusion occurred in 11% (symptomatic in 7%, treated with emergency angioplasty or bypass surgery; silent in 4%, treated medically). Of the surviving patients with successful initial establishment of infarct vessel patency, 94% were discharged from the hospital with an open infarct artery or a bypass graft to the infarct vessel. There was significant improvement in both ejection fraction (44% to 49%; p less than .0001) and regional wall motion in the infarct zone (-3.0 SD to -2.4 SD; p less than .0001) among patients with persistent coronary perfusion and insignificant residual stenosis at the time of the follow-up cardiac catheterization. Thus, a treatment strategy for acute myocardial infarction that includes immediate administration of streptokinase followed by emergency coronary angioplasty, and coronary bypass surgery when necessary, results in a high rate of early and sustained patency of the infarct-related vessel.     

Prognosis of culprit lesion PTCA in acute myocardial infarction for multi versus single vessel disease.

We studied 417 patients undergoing single vessel culprit lesion percutaneous transluminal coronary angioplasty (PTCA) for acute myocardial infarction to determine the impact of disease in other vessels. Group A (189 patients, 45%) had coronary artery disease (greater than or equal to 70% stenosis) in at least 1 additional vessel while Group B (228 patients, 55%) did not. The groups were similar in sex distribution (A = 75% male, B = 76%), number of lesions in the single culprit vessel dilated (1 lesion in 83% A, 80% B), and PTCA success (A = 92%, B-94%) (all p = NS). Group A patients were older (63 +/- 10 vs. 56 +/- 11 years) and had more prior myocardial infarctions (27% vs. 7%), and more prior coronary artery bypass grafting (15% vs. 0.4%) (all p less than .01). Group A patients were more likely to have repeat catheterization (48% vs. 32%, p less than .005) although restenosis of the infarct-related vessel was similar (A = 24%, B = 16%) (p = NS). Group A was more likely to need angioplasty in a 2nd vessel (23% vs. 8%) and to need coronary artery bypass grafting (20% vs. 8%) (both p less than .001). Cumulative mortality was higher in Group A at 1 month (10% vs. 5%), 1 year (11% vs. 6%), and long-term (13% vs. 7%). This difference appeared to be due to the impact of lower mean ejection fraction in Group A. Conclusion: Treatment of acute myocardial infarction by direct PTCA of the culprit lesion can be performed with a high likelihood of success in patients with or without multivessel coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of early high-dose streptokinase intravenously on left ventricular function in acute myocardial infarction

One hundred seven patients who recently had acute myocardial infarction were randomly assigned either to standard heparin therapy or to intravenous streptokinase within 5 hours after the onset of symptoms in 7 hospitals without catheterization facilities. In the third week, the patients were referred to a university hospital, where the patency rate of the infarct-related artery was studied by selective coronary arteriography and left ventricular function by radionuclide angiography. Fifty-five patients received heparin and 52 streptokinase within a mean period of 190 minutes after the onset of symptoms. Seven patients in the heparin group and 4 in the streptokinase group died in hospital. The patency rate of the infarct-related artery was identical in both groups (69% in the heparin group vs 68% in the streptokinase group). Left ventricular ejection fraction was not statistically different (0.44 +/- 0.13 in the heparin group vs 0.45 +/- 0.12 in the streptokinase group). Left ventricular ejection fraction was significantly higher in patients with a patent infarct-related artery than in patients with an obstructed infarct-related artery (0.49 +/- 0.12 vs 0.41 +/- 0.15, p less than 0.01). In patients with inferior wall infarction, left ventricular ejection fraction was identical (0.50 +/- 0.10 in the heparin group vs 0.52 +/- 0.09, in the streptokinase group). In patients with anterior wall infarction, left ventricular ejection fraction was significantly higher in the streptokinase group than in heparin group (0.40 +/- 0.10 vs 0.33 +/- 0.09, p less than 0.05). Analysis of regional wall motion revealed that improvement occurred in the lateral wall of the left ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Higher Gensini score of coronary arteries in acute inferior myocardial infarction with precordial ST-segment depression.

To investigate the significance of precordial ST-segment depression in acute inferior myocardial infarction, we compared the Gensini score of coronary artery stenosis between 2 groups of patients with and without precordial ST-segment depression. Group I consisted of 28 patients who showed ST-segment depression on admission (greater than or equal to 1 mm in V2-V6) and Group II (n = 16) those without ST-segment depression (less than 1 mm). The Gensini score of the coronary arteries (56 +/- 29 vs. 28 +/- 18; p less than 0.001), the partial score of the infarction-related artery (29 +/- 16 vs. 17 +/- 11; p less than 0.01) and of the infarction-nonrelated artery (27 +/- 24 vs. 11 +/- 12; p less than 0.02) were significantly higher in Group I than in Group II. The Killip score (greater than or equal to II) (34% vs. 6%; p less than 0.05), frequency of arrhythmias (75% vs. 38%; p less than 0.02) and peak CK value (3,676 +/- 2,290 vs. 1,818 +/- 1,153 IU/L; p less than 0.005) were higher in Group I than in Group II. Four patients in Group I died following admission, while no patient died in Group II (N.S.). Autopsy findings from the 4 Group I patients revealed fresh extensive inferior infarction and healed diffuse subendocardial infarction which could not be predicted from electrocardiograms. All patients who survived the acute stage performed treadmill exercise testing and 22 patients underwent exercise thallium-201 single photon emission computer tomography (SPECT). On treadmill exercise test, there was no significant difference between the 2 groups in the frequency of angina pectoris and ST-segment depression. On SPECT, the perfusion defect area under 55% of maximum uptake at the redistribution phase was 45.8 +/- 19.6 cm2 in Group I (n = 14) and 34.7 +/- 21.3 cm2 in Group II (n = 8; N.S.). In conclusion, precordial ST-segment depression in acute inferior myocardial infarction suggested advanced atherosclerosis in both the infarction-related and nonrelated coronary arteries, indicating a larger infarct size.     

Early reperfusion therapy improves left ventricular function after acute inferior myocardial infarction associated with right coronary artery disease

Quantitative global and regional ventriculographic analysis was performed acutely and 1 week later in 46 patients undergoing reperfusion procedures within 6 hours of acute inferior myocardial infarction due to right coronary artery disease. While serial improvement in global left ventricular ejection fraction was not demonstrated for the group, infarct zone regional wall motion did improve (-2.7 +/- 0.9 vs -2.3 +/- 1.4 SD/chord, p less than 0.007). Serial improvement in global ejection fraction was demonstrated in the subgroup of patients treated within 2 hours of symptom onset (55 +/- 10 vs 62 +/- 10%; n = 5; p less than 0.03). Infarct zone regional wall motion improved serially only in the subgroup of patients treated within 3 hours of symptom onset (-2.4 +/- 1.1 vs -1.3 +/- 1.7 SD/chord; n = 11; p less than 0.007). Patients with initially patent arteries had a higher ejection fraction on follow-up catheterization than did those with initially occluded vessels (61 +/- 11 vs 55 +/- 7%; p less than 0.02), and patients with patent arteries at follow-up had a higher ejection fraction than did those whose arteries were occluded (60 +/- 9 vs 48 +/- 4%; p less than 0.0001). We conclude that significant improvement in global and regional left ventricular function in patients with inferior myocardial infarction is possible when reperfusion therapy is begun early or when arterial patency is achieved.     

Development of collateral circulation after acute myocardial infarction: its role in preserving left ventricular function

The present study evaluated the effects of coronary collateral circulation developing after acute myocardial infarction on global and regional left ventricular function during the chronic stage. The study group consisted of 16 patients with initial myocardial infarction having total occlusion of the proximal left anterior descending coronary artery. To eliminate the effects of collateral circulation existing at the onset of infarction, patients with pre-infarction angina were excluded from this study. The patients were categorized in two groups depending on the extent of their collateral circulation (collateral index: CI 0-3): group A--patients with significant collateral circulation (CI = 2 or 3) to the infarct-related coronary artery; group B--patients without significant collateral circulation (CI = 0 or 1). Their heart rate, left ventricular peak systolic and end-diastolic pressures and cardiac index were similar in the two groups. The left ventricular end-systolic volume index in the group B was significantly greater than that in the group A (60 +/- 21 ml/m2 vs 34 +/- 9 ml/m2, p less than 0.05). Left ventricular ejection fraction in the group A was significantly greater than that of the group B (55 +/- 9% vs 39 +/- 15%, p less than 0.05), and a significant difference was observed in the percentage of segment shortening in the infarct area between the groups A and B (10.8 +/- 9.2% vs -0.2 +/- 5.4%, p less than 0.01). It was concluded that coronary collateral circulation which develops after acute myocardial infarction exerts beneficial effects on global and regional left ventricular function during the chronic stage.     

The prevalence and clinical significance of residual myocardial ischemia 2 weeks after uncomplicated non-Q wave infarction: a prospective natural history study

Despite having smaller infarct size and better left ventricular function, patients with non-Q wave myocardial infarction (NQMI) appear to have an unexpectedly high long-term mortality that is ultimately comparable to that of patients with Q-wave myocardial infarction (QMI). Patients with NQMI may lose their initial prognostic advantage because there is more viable tissue in the perfusion zone of the infarct-related vessel, rendering myocardium more prone to reinfarction. We tested this hypothesis in a prospective study of 241 consecutive patients 65 years of age or younger with acute uncomplicated myocardial infarction confirmed by creatine kinase levels (MB fraction). All patients received customary care and none underwent thrombolytic therapy or emergency angioplasty. Predischarge coronary angiography, radionuclide ventriculography, 24 hr Holter monitoring, and quantitative thallium-201 (201T1) scintigraphy during treadmill exercise were performed 10 +/- 3 days after infarction. Infarcts were designated as QMI (n = 154) or NQMI (n = 87) by accepted criteria applied to serial electrocardiograms obtained on days 1, 2, 3, and 10. The baseline Norris coronary prognostic index, angiographic jeopardy scores, and prevalence of Lown grade ventricular arrhythmias were similar between groups despite evidence for less necrosis with NQMI vs QMI, reflected by lower peak creatine kinase levels (520 vs 1334 IU/liter; p = .0001, 4 hr sampling), higher resting left ventricular ejection fraction (53% vs 46%; p = .0001), fewer akinetic or dyskinetic segments (1.2 vs 2.4; p = .0001), and fewer persistent 201Tl defects in the infarct zone (0.9 vs 1.9; p = .0001). Patients with NQMI also had more patent infarct-related vessels (54% vs 25%; p less than .0001) and a shorter time from onset of infarction to peak creatine kinase level (16.9 vs 22.5 hr; p = .0001). Importantly, the prevalence and extent of quantitatively determined 201Tl redistribution within the infarct zone on exercise scintigraphy was greater in patients with NQMI vs those with QMI (60% vs 36%, p = .007; and 0.98 vs 0.53 myocardial segments, p = .0003); when the two groups were stratified on the basis of the infarct-related vessel, subset analysis revealed the same findings. During 30 months median follow-up, cardiac mortality was low, 8.4% in the QMI group and 9.2% in the NQMI group (p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)     

Coronary flow after successful angioplasty in patients with acute myocardial infarction: comparison between coronary flow reserve by nicorandil and papaverine

In order to evaluate coronary flow response to 2 different vasodilators, nicorandil and papaverine, in patients with myocardial infarction, we measured coronary flow reserve using a Doppler guide wire in infarct-related and non infarct-related arteries. The study group consisted of 28 patients with first acute myocardial infarction 3 weeks after successful coronary angioplasty within 6 hr after symptom onset. Twelve patients with atypical chest pain served as the control group. Coronary flow reserve induced by intracoronary papaverine(12 mg) was lower in infarct-related arteries than in non infarct-related arteries, but there were no differences in coronary flow reserve induced by intracoronary nicorandil(1 mg) between infarct-related and non infarct-related arteries. Coronary flow reserve induced by nicorandil was lower than that by papaverine in non infarct-related arteries and the control group. However, there were no differences between coronary flow reserve induced by nicorandil and papaverine in infarct-related arteries. Vasodilatory response induced by nicorandil was relatively preserved in infarct-related arteries compared with papaverine. These results suggest that impairment of coronary microvascular response in infarct myocardium varies in the different sites acted on by different vasodilator agents.     

Myocardial creatinine kinase liberation and left ventricular function in myocardial infarct with and without collateral blood supply

In 24 patients (aged 52 years) with angiographically proven acute first myocardial infarction and isolated occlusion of the infarct-related vessel, serial measurements of creatine kinase (CK) activity were performed. Peak CK levels (CKmax), time-to-peak activity (tmax), infarct size, and cumulative CK were calculated from the serum curve by a computer program. No reperfusion interventions were performed. In accordance with the angiographic results 3-5 weeks after infarction, patients were divided into two groups: 11 patients demonstrated a proximal occlusion of one major coronary artery with retrograde contrast filling by non-compromised collaterals; in 14 patients no collateral filling of the distal vessel segment was visible. The contralateral coronary arteries and corresponding LV wall segments were normal. Localization of the infarction and infarct related vessel were not significantly different between both groups. In patients with collaterals, ejection fraction was significantly higher (63.1 vs. 45.5%; p less than 0.0005) and LV-enddiastolic volume (109.9 vs. 130.1 ml/m2) and enddiastolic pressure (10.0 vs. 14.1 mm Hg, p = n.s.) were lower. CKmax, tmax, infarct size, and cumulative CK activity were significantly reduced in patients with collaterals compared to non-collateralized occlusions. Four patients with, but none without collaterals reached tmax within 12 h. In ten patients without and four with collaterals, tmax was reached after 14 h. The initial slope of the normalized serum CK curves was significantly different among both groups. A significant (p less than 0.005) linear correlation between ejection fraction and tmax, infarct size, CKmax, and cumulative CK was found for all patients (r = 0.76-0.53).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Angiographic coronary morphology in postinfarction angina

To investigate the pathophysiologic relevance of angiographically irregular coronary stenoses in postinfarction angina (PIA), we analyzed the clinical course and coronary angiograms of 73 patients studied within 30 days of infarction. Coronary lesions were classified as smooth or irregular. Thirty-six patients had PIA (Group 1) and 37 had an uncomplicated course (Group 2). Irregular lesion(s) in patent infarct-related arteries were found in 77% of Group 1 vs. 24% of Group 2 patients (P less than 0.005). Irregular lesion(s) in any coronary artery were found in 58% of Group 1 versus 19% of Group 2 patients (P less than 0.002). Other univariate predictors of PIA included older age, hypertension, angina before myocardial infarct, lower peak creatine kinase, three-vessel disease, and higher modified Gensini score. Multivariate analysis ranked lesion irregularity as the strongest predictor of PIA. Our data suggests that ruptured atherosclerotic plaques may be important in the pathogenesis of PIA. It is possible that lesion irregularity is associated with an active process and/or a residual thrombus, which may be responsible for postinfarction angina.     

Angiographic progression of coronary artery disease and the development of myocardial infarction

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions greater than or equal to 50% to infarction. This retrospective study suggests that myocardial infarction frequently develops from previously nonsevere lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Resolution of ST-segment elevation after streptokinase therapy in anterior versus inferior wall myocardial infarction

BACKGROUND: Resolution of ST-segment elevation is the best bedside predictor of myocardial reperfusion. HYPOTHESIS: This study was conducted to examine the resolution of ST-segment elevation after streptokinase therapy in anterior versus inferior acute myocardial infarction (MI) and to corroborate it with echocardiographic and coronary angiographic data. METHODS: The study population consisted of 70 patients, 35 each in the anterior and inferior MI groups. The electrocardiograms (ECGs) were recorded before, on completion of, and on Days 1 and 2 post streptokinase therapy. The resolution of ST segment determined from post-streptokinase ECGs was compared between the two groups and correlated with echocardiographic and coronary angiographic data. RESULTS: On completion of and on Day 1 post streptokinase therapy, ST-segment resolution in both groups was not significantly different. On Day 2 post streptokinase therapy, resolution of the ST segment per lead was significantly lower in anterior than that in inferior MI (61 +/- 21% anterior vs. 77 +/- 21% inferior, p 0.003). The number of patients with akinesis of infarct-related ventricular wall was significantly higher (17 anterior vs. 7 inferior, p 0.02), and left ventricular ejection fraction was significantly lower in anterior MI (39 +/- 7% anterior vs. 48 +/- 8% inferior, p < 0.01). There was no significant difference in coronary angiographic data. One patient in each group demonstrated normal coronary arteries. CONCLUSIONS: The resolution of ST-segment elevation on the completion of and on Day 1 post streptokinase therapy was comparable between anterior and inferior MI. The significantly less frequent resolution of ST-segment elevation in anterior MI on Day 2 post streptokinase could be due to more akinesis, larger infarct size, and worse systolic function rather than due to failure to open the infarct-related vessel.     

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.     

Effect of infarct location on myocardial salvage assessed by technetium-99m isonitrile.

To investigate the influence of infarct location on myocardial salvage, technetium-99m isonitrile was injected into 43 patients with a first myocardial infarction before early reperfusion therapy. Primary coronary angioplasty was performed in 22 patients and successful intravenous thrombolytic therapy was given to 15 patients, both within 6 h of the onset of chest pain. Patency of the infarct-related artery was confirmed by angiography in all 37 patients. In the remaining six patients (three with and three without early thrombolytic therapy) the infarct-related artery remained occluded. Single photon emission computed tomography was performed within 6 h of the administration of technetium-99m isonitrile and repeated at the time of hospital discharge. Radionuclide ejection fraction at discharge was significantly lower for patients with anterior infarction (0.41 +/- 0.12) than for those with inferior infarction (0.56 +/- 0.09, p less than 0.001). Early perfusion defect size, a measure of myocardium at risk, was greater in patients with anterior than in those with inferior infarction (52 +/- 9% vs. 18 +/- 10% of the left ventricle, p = 0.0001) as was final defect size (30 +/- 20% vs. 9 +/- 8%, p less than 0.01). The change in myocardial perfusion, an estimate of myocardial salvage, was also greater in patients with anterior infarction (24 +/- 16% vs. 10 +/- 7%, p less than 0.01). However, the proportion of jeopardized myocardium salvaged (salvage index) was not significantly different between patients with anterior or inferior infarction (0.49 +/- 0.34 vs. 0.59 +/- 0.35, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)