Correlation of angiographic findings and right (V1 to V3) versus left (V4 to V6) precordial ST-segment depression in inferior wall acute myocardial infarction

This study assessed whether differences in the underlying mechanisms for various patterns of precordial ST-segment depression with inferior acute myocardial infarction (AMI) are associated with poorer prognoses. We studied 1,155 patients with inferior AMI who underwent thrombolysis in the Global Utilization of Streptokinase and TPA for Occluded arteries (GUSTO-I) angiographic substudy: those without precordial ST depression (n = 412; 35.7%), those with maximum ST depression in leads V1 to V3 (n = 547; 47.4%), and those with maximum ST depression in leads V4 to V6 (n = 196; 17.0%) on admission electrocardiogram. We compared the infarct-related artery, presence of left anterior descending or multivessel coronary artery disease, and left ventricular function among groups. Patients with maximum ST depression in leads V4 to V6 more often had 3-vessel disease (26.0%) than those without precordial ST depression (13.5%) or those with ST depression in leads V1 to V3 (15.7%; p = 0.002), and they had a lower ejection fraction (median 54% vs 60% and 55%, respectively; p <0.001). Patients with maximum ST depression in leads V1 to V3 less often had AMIs due to proximal right coronary artery obstruction (23.9%) than patients without precordial ST depression (35.2%) or those with ST depression in leads V4 to V6 (40.0%; p = 0.001) and had larger AMIs as estimated by peak creatine kinase. Different patterns of precordial ST depression are associated with distinctive coronary anatomy. ST depression in leads V4 to V6, but not V1 to V3, confers a greater likelihood of multivessel coronary artery disease.     

Inferior ST segment depression during acute anterior myocardial infarction: clinical and angiographic correlations

This study was performed to determine whether inferior ST segment depression during early stages of acute transmural anterior myocardial infarction identifies patients with multivessel coronary artery disease and additional inferior ischemia. Coronary and left ventricular angiography were performed within 3.4 months in 33 patients with acute transmural anterior infarction. Initial electrocardiograms, 2 to 5 hours after onset of chest pain, revealed significant ST segment depression (greater than or equal to 0.1 mV) in at least two of leads II, III and a VF in 15 patients (45%) (group B); in 18 patients (group A) this finding was absent. Compared with group A, patients in group B had greater anterior ST elevation (1.2 versus 0.7 mV, p less than 0.025); higher serum peak creatine kinase (2,475 versus 1,147 IU/liter, p less than 0.005); higher Killip scores (2.1 versus 1.3, p less than 0.001); more in-hospital complications (60 versus 17%, p less than 0.05); lower mean left ventricular ejection fraction (34 versus 55%, p less than 0.001); more frequent regional left ventricular dysfunction in anterolateral (91 versus 44%, p less than 0.05), posterolateral (36 versus 0%, p less than 0.05) and inferior (100 versus 6%, p less than 0.005) regions; greater wall motion abnormality scores (10.0 versus 5.5, p less than 0.005); higher frequency of concomitant left circumflex or right coronary artery disease, or both (80 versus 28%, p less than 0.01); more frequent postinfarction angina (100 versus 39%, p less than 0.001) and lower New York Heart Association functional classification scores (1.7 versus 2.4, p less than 0.05) at 6 month follow-up. The time course of inferior ST depression differed from that of anterior ST elevation. Thus, inferior ST depression was maximal in the first 48 hours and decreased (p less than 0.05) thereafter. In contrast, ST elevation in leads V1 to V6 and I appeared to decrease (p = NS) between days 4 and 7. However, inferior ST depression "mirrored" ST elevation in lead aVL, which also decreased (p less than 0.05) after 48 hours. Thus, inferior ST depression during anterior infarction is associated with more extensive infarction, greater morbidity and higher frequency of multivessel coronary disease. Such inferior ST depression might reflect not only "reciprocal change," but also ischemia in adjacent lateral and remote inferior regions.     

Predictive Value of Admission Electrocardiogram For Multivessel Disease in Acute Anterior and Anterior‐Inferior Myocardial Infarction

Background: Our aim was to investigate the correlation between admission ECG and coronary angiography findings in terms of predicting the culprit vessel responsible for the infarct or multivessel disease in acute anterior or anterior‐inferior myocardial infarction (AMI). Methods: We investigated 101 patients with a diagnosis of anterior AMI with or without ST‐segment elevation or ST‐segment depression in at least two leads in Dll, III, aVF. The patients were classified as those with vessel involvement in the left anterior descending (LAD) coronary artery and patients with multivessel disease. Vessel involvement in LAD + circumflex artery (Cx) or LAD + right coronary artery (RCA) or LAD + Cx + RCA were considered as multivessel disease. Thus, (a) anterior AMI patients with reciprocal changes in inferior leads, (b) anterior AMI patients with inferior elevations, (c) all anterior AMI patients according to the ST‐segment changes in the inferior region were analyzed according to the presence of LAD or multivesssel involvement. Results: Presence of ST‐segment depression in aVL and V6 was significantly correlated with the presence of multivessel disease in anterior AMI patients with reciprocal changes in the inferior leads (P = 0.005 and P = 0.003, respectively). No statistically significant difference between the leads were detected in terms of ST‐segment elevation in predicting vessel involvement in the two groups of anterior AMI patients with inferior elevations. When all the patients with anterior AMI were analyzed, the presence of ST‐segment depression in leads aVL, V4, V5 and V6 were significantly associated with the presence of multivessel disease (P = 0.035, P = 0.010, P = 0.011, P = 0.001, respectively). Conclusions: The presence of ST‐segment depression in anterolateral leads in the admission ECG of anterior AMI patients with reciprocal changes in inferior leads was associated with multivessel disease.     

Dipyridamole-induced ST segment depression during thallium-201 imaging in patients with coronary artery disease: angiographic and hemodynamic determinants

To examine the angiographic and hemodynamic determinants of dipyridamole-induced ST segment depression in patients with coronary artery disease, 41 patients with angiographically documented coronary disease who underwent dipyridamole-thallium-201 myocardial scintigraphy were studied. Dipyridamole-induced ST depression occurred in 14 (34%) of the 41 patients. Stepwise multivariate logistic regression was performed to compare the predictive value of angiographic findings (good coronary collateral vessels, jeopardized collateral vessels, multivessel disease), hemodynamic changes (changes in heart rate, systolic pressure, diastolic pressure and rate-pressure product), thallium-201 results (perfusion defect, thallium-201 redistribution) and demographic data (age, gender, medications). Only the presence of good coronary collateral vessels (p less than 0.02) and increases in rate-pressure product after dipyridamole infusion (p less than 0.02) were significant multivariate predictors of dipyridamole-induced ST depression. Good collateral vessels were more common in the group with ST depression (11 [79%] of 14) than they were in the group without ST depression (6 [22%] of 27; p less than 0.001). Rate-pressure product increased 2,835 +/- 1,648 beats/min.mm Hg in the group with ST depression compared with 1,179 +/- 1,417 beats/min.mm Hg in patients without ST depression (p less than 0.005). In conclusion, dipyridamole-induced ST segment depression in patients with coronary artery disease appears to be related to 1) the presence of good coronary collateral vessels, which may act by facilitating "coronary steal", and 2) increases in rate-pressure product, reflecting increased myocardial oxygen demand. These observations may explain the lack of prognostic value of dipyridamole-induced ST segment depression described in previous reports.     

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.     

Correlation of coronary arteriography after acute myocardial infarction with predischarge limited exercise test response

This study of post-acute myocardial infarction (AMI) patients compared the extent and distribution of coronary narrowings and left ventricular dysfunction in 45 patients who had greater than or equal to 1 mm ST-segment depression on a predischarge low-level exercise test (positive-result group) with those found in 78 patients who had less than 1 mm ST depression (negative-result group). Cardiac catheterization was done 50 +/- 20 days (mean + standard deviation) after AMI. Patients with positive responses more often had multivessel coronary artery disease (80 vs 47%, p = 0.001) and a greater than or equal to 75% narrowing in the left anterior descending (LAD) (87 vs 62%, p = 0.003) and left circumflex (71 vs 37%, p = 0.001) arteries, as well as in the proximal LAD segment before the first septal branch (58 vs 29%, p = 0.002). Among patients with positive responses 93% had normal or hypokinetic wall motion in the vascular territory of a severely diseased coronary artery (viable but potentially ischemic myocardium) while 63% of the negative-result group had these findings (p = 0.001). No difference in ejection fraction could be identified between the 2 groups (54 +/- 15% vs 54 +/- 16%). Prior studies of AMI patients have shown that ST-segment depression on a predischarge low-level exercise test will identify patients at higher risk of subsequent cardiac death. Our observations have identified differences in cardiac angiographic findings between patients with positive and negative responses to this test that may explain this difference in outcome.     

Significance of ST segment depression in the precordial leads during the acute phase of inferior myocardial infarction

Reciprocal changes of the ST segment in the acute phase of inferior myocardial infarction are common but their significance remain controversial. We studied this problem by comparing the ECG on admission of 83 patients with acute inferior myocardial infarction, with the clinical outcome and haemodynamic and angiographic data obtained on average 3 weeks after the onset of symptoms. Fifty nine patients (Group I) had ST depression greater than or equal to 1 mm in at least one of the leads V1 to V4; 24 patients (Group II) had no ST depression in this territory. The patients in Group I were older (59.6 +/- 6.4 vs 54 +/- 5.3 years, p less than 0.01), had higher total CPK (1 835 +/- 940 vs 875 +/- 305, p less than 0.01) and MB fractions (269 +/- 102 vs 95 +/- 35), more complications during the hospital period (80%, mainly haemodynamic vs 38%, p less than 0.01) and more severe left ventricular dysfunction: ejection fraction 52.2 +/- 6% vs 59.2 +/- 7%, p less than 0.05; cardiac index 2.75 +/- 0.4 l/min/m2 vs 3.25 +/- 0.3 l/min/m2, p less than 0.005). There was no difference in left ventricular wall motion between the groups on biplane angiography. However, coronary angiography showed left coronary disease to be more common in Group I (84%) than in Group II (37%), p less than 0.005. Left anterior descending and left circumflex disease was equally common. Patients with persistent ST depression after 48 hours had lower ejection fractions than those in whom it regressed within 48 hours.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrically induced ventricular arrhythmias in acute myocardial infarction treated with thrombolytic agents

Ninety-two patients underwent programmed ventricular stimulation 12 +/- 3 days after acute myocardial infarction (AMI) treated with thrombolytic agents (streptokinase, recombinant tissue plasminogen activator, or both). Cardiac catheterization was performed in all patients on admission to hospital and was repeated in 97% of them 13 +/- 5 days later. Sustained ventricular arrhythmias--either tachycardia (VT) or fibrillation--were induced in 20 (22%) patients, with nonsustained VT induced in another 12 (13%). Multivariate analysis was used to identify predictors of induction of sustained VT, with short right ventricular effective refractory period (p = 0.0061), site of AMI (inferior or posterior, p = 0.008), infarct-related artery (right or circumflex coronary artery, p = 0.018), multivessel coronary artery disease (p = 0.043) and male sex (p = 0.028) being significant predictors of sustained VT. Neither successful reperfusion, time to reperfusion, nor residual stenosis in the infarct-related artery was significant. All patients in whom VT was induced were treated with electrophysiologically guided antiarrhythmic therapy. Cardiac mortality after hospital discharge was 1% over 30 +/- 16 months.     

Detection of Multivessel Disease Post Myocardial Infarction Using an Exercise‐Induced QRS Score

Objective: The aim of this study was to investigate the ability of Athens QRS score values to detect stenoses in other coronary arteries than the obstructed ones (which caused the myocardial infarction [MI]) in patients with a history of MI. Methods: We studied 125 patients (93 males and 32 females, mean age 54 ± 7 years [range 45–68 years]) with a history of MI (46 patients with anterior MI, 54 patients with inferior MI, 25 patients with lateral MI). All patients underwent treadmill exercise testing and coronary arteriography. Results: Athens QRS score values were inversely related to the extent of CAD: ?0.5 ± 0.3 mm for patients with 1‐VD (obstructed vessel), ?3.4 ± 2.2 mm for patients with 2‐VD (obstructed vessel and stenosis in another vessel), and ?5 ± 1.8 mm for patients with 3‐VD (obstructed vessel and stenoses in two more vessels). The ROC curves for the detection of multivessel disease showed that the area under the curve for QRS score values < ?3 mm is significantly higher than the curve for ST‐segment depression ≥1 mm (0.948 vs 0.792, P < 0.001). Conclusions: Values of the Athens QRS score less than ?3 may distinguish single‐ from multivessel coronary artery disease in patients with a history of MI.     

Pathophysiology and prognostic significance of Holter-detected ST segment depression after myocardial infarction. The Tissue Plasminogen Activator: Toronto (TPAT) Study Group.

OBJECTIVES: We performed Holter monitoring on days 4 and 7 after acute myocardial infarction in 109 patients to assess whether ST segment shift would identify those with more severe coronary artery disease, left ventricular dysfunction and unfavorable prognosis. BACKGROUND. Silent myocardial ischemia is a frequent and prognostically significant event after acute myocardial infarction. However, the specific pathophysiologic mechanisms and the impact of thrombolytic therapy are uncertain. METHODS. In addition to Holter monitoring, patients underwent exercise testing, radionuclide angiography on days 1 and 9 and quantitative coronary angiography on day 9. RESULTS. Thirty-five patients (32%) had ST segment depression and had similar recombinant tissue-type plasminogen activator (rt-PA) treatment assignment and a reduced cross-sectional area of the infarct-related artery (0.59 +/- 0.57 vs. 1.04 +/- 1.26 mm2, p < 0.05). Global left ventricular function improved from day 1 to day 9 in patients without (4% +/- 11%, p < 0.001) but not in those with (0% +/- 7%) ST segment depression. In-hospital event rates were similar; however, follow-up 18 +/- 11 months after hospital discharge revealed a greater frequency of death and recurrent myocardial infarction in patients with compared with those without ST segment depression (27% vs. 6%, p = 0.03). CONCLUSIONS. After acute myocardial infarction, approximately one third of patients have ST segment depression on Holter monitoring, independent of the use of thrombolytic therapy. The unfavorable prognosis observed in these patients may be related to greater lumen obstruction in the infarct-related artery and lack of improvement in left ventricular function.     

ST segment shift in unstable angina: pathophysiology and association with coronary anatomy and hospital outcome

The significance of ST segment shift with respect to coronary anatomy and hospital outcome was evaluated in 135 patients with unstable angina. ST shift was evident in 44% of patients on admission electrocardiogram (ECG) and in 66% on Holter monitor ECG. During hospitalization, 7% of patients had myocardial infarction, 4% died and 34% had urgent coronary revascularization. By comparing patients with and without ST shift on admission ECG, an unfavorable outcome was found in 55% versus 25% (p less than 0.005), multivessel disease in 77% versus 63% (p less than 0.05) and left main coronary artery stenosis in 22% versus 7% (p less than 0.025). When patients with and without ST shift on Holter monitor ECG were compared, an unfavorable outcome was found in 48% versus 20% (p less than 0.005), multivessel disease in 76% versus 54% (p less than 0.01) and left main coronary stenosis in 18% versus 4% (p less than 0.05). The duration of ST shift was also greater in patients with 1) unfavorable outcome (129 +/- 136 versus 52 +/- 111 min, p less than 0.01); 2) multivessel disease (98 +/- 129 versus 36 +/- 90 min, p less than 0.01); and 3) left main stenosis (150 +/- 147 versus 67 +/- 114 min, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

急性前壁心肌梗死并下壁导联ST段压低与冠状动脉病变的关系

目的：观察急性前壁心肌梗死下壁导联ＳＴ段压低与冠状动脉病变的关系。方法：对６６例急性前壁心肌梗死患者均常规行冠状动脉造影术,根据常规心电图下壁导联ＳＴ段压低＞１ｍｍ分为ＳＴ段压低组（４８例）与ＳＴ段正常组（１８例）,比较分析心电图与冠状动脉造影之间的关系。结果：急性前壁心肌梗死患者２７．３％有下壁导联ＳＴ段压低,ＳＴ段压低组中冠状动脉病变支数与正常组无显著性差异（Ｐ＞０．０５）,７３．２％为左前降支（ＬＡＤ）近端病变,显著高于ＳＴ段正常组（４５．８％）。ＳＴ段压低组５５．６％伴有心电图ＳＴＩ,ａＶＬ抬高,显著高于ＳＴ段正常组（４．２％）（Ｐ＜０．０１）。结论：急性前壁心肌梗死并下壁导联ＳＴ段压低与冠状动脉病变支数无关,而与ＬＡＤ近端病变有关,可能反映高侧壁心肌缺血时的心电图对应性改变。     

Factors that determine the direction and magnitude of precordial ST-segment deviations during inferior wall acute myocardial infarction

Sixty-one patients with inferior acute myocardial infarction (AMI) and no evidence of prior AMI were studied to determine which factors influence the magnitude of precordial ST-segment depression. In the total study group, there was a significant but weak correlation between the magnitude of precordial ST-segment depression and the magnitude of inferior ST-segment elevation (r = -0.46, p less than 0.001). In the 29 patients with evidence of concomitant right ventricular (RV) involvement, precordial ST-segment depression was significantly smaller both in absolute terms (-1.3 +/- 1.8 vs -2.8 +/- 1.9 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -0.2 +/- 1.0 vs -1.1 +/- 0.5, p less than 0.01), whereas in the 15 patients with lateral ST-segment elevation (greater than or equal to 1 mm in lead V6), precordial ST-segment depression was significantly greater both in absolute terms (-3.5 +/- 2.3 vs -1.6 +/- 1.7 mm, p less than 0.01) and relative to the magnitude of inferior ST-segment elevation (ratio of -1.1 +/- 0.8 vs -0.5 +/- 0.9, p less than 0.02). Consistent with these findings, the correlation between the magnitudes of precordial and inferior ST-segment deviations was considerably improved when only the 24 patients with neither evidence of RV involvement nor lateral ST-segment elevation were analyzed (r = 0.89, p less than 0.001, n = 24). These data suggest that in patients with inferior AMI, there is a reciprocal relation between precordial and inferior ST-segment deviations, which is distorted by concomitant RV involvement and by concomitant lateral left ventricular wall involvement.     

Reliability of resolution of ST-segment elevation after coronary reperfusion in predicting myocardial salvage in anterior wall acute myocardial infarction

Resolution of ST-segment elevation (ST resolution) after reperfusion therapy has been shown to correlate with improved left ventricular (LV) function in patients with acute myocardial infarction (AMI). However, not all patients with ST resolution have preserved LV function. We evaluated the clinical significance of ST resolution in 129 patients with anterior wall AMI who underwent successful coronary recanalization within 6 hours after symptom onset by studying the relation to myocardial blush grade, another angiographic marker of myocardial reperfusion. A reduction of > or =50% in ST-segment elevation after recanalization was defined as ST resolution. Ninety-eight patients had ST resolution and 31 patients did not. Patients with ST resolution were subdivided into 2 groups according to myocardial blush grade after recanalization: 67 patients with blush grade 2 or 3, and 31 with blush grade 0 or 1. The QRS score after recanalization was higher (5.9 +/- 1.9 vs 3.4 +/- 2.0, p <0.01) and predischarge LV ejection fraction was lower (39 +/- 8% vs 57 +/- 9%, p <0.01) in patients with blush grade 0 or 1 than in those with blush grade 2 or 3. However, the QRS score after recanalization and the predischarge LV ejection fraction were similar in patients who had ST resolution with blush grade 0 or 1 and in those without ST resolution. Our findings suggest that ST resolution after recanalization does not consistently predict myocardial salvage in patients with anterior AMI.     

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.     

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.     

Effect of preinfarction angina pectoris on ST-segment resolution after primary coronary angioplasty for acute myocardial infarction

The presence of preinfarction angina has been shown to exert a favorable effect on left ventricular function after acute myocardial infarction (AMI). Whether or not preinfarction angina is beneficial for myocardial tissue reperfusion, however, remains to be determined. We sought to evaluate the influence of preinfarction angina on resolution of ST-segment elevation, which could be affected by microcirculatory damage after recanalization therapy. We studied 96 patients with a first AMI in whom Thrombolysis In Myocardial Infarction (TIMI)-3 flow in the infarct-related artery was established by primary angioplasty. Percent reduction in the sum of ST elevation from baseline to 1 hour after angioplasty (percent delta summation operator ST) was examined. Poor ST resolution, defined as percent delta summation operator ST <50%, was observed in 25 patients, who had a worse clinical outcome, larger infarct size, and poorer left ventricular function. On multivariate analysis, the absence of preinfarction angina, as well as anterior wall infarction, were major independent predictors of poor ST resolution, whereas age, sex, coronary risk factors, ischemic time, Killip class on admission, multivessel disease, initial TIMI flow grade, and extent of collaterals were not significant. Patients with preinfarction angina had a greater degree of ST-segment resolution than those without angina (71 +/- 21% vs 49 +/- 43%, p = 0.02). Additional ST elevation after reperfusion was noted exclusively in patients without preinfarction angina (p = 0.02). Preinfarction angina is associated with a greater degree of ST-segment resolution in patients with TIMI-3 flow after primary angioplasty, suggesting a protective effect of preinfarction angina against microcirculatory damage after reperfusion.     

Aerobic responses to low level exercise testing following an acute myocardial infarction

Thirty-four patients who had recently sustained an acute myocardial infarction performed low-level exercise testing with analysis of expired gas 7.1 +/- 2.6 days after the event. They were classified as finishers (F) and nonfinishers (NF) of the low-level protocol. The ejection fraction in the NF was 39 +/- 14% vs 56 +/- 17% in the F (p less than 0.01), and the NF had 2.6 +/- 0.8 vessels stenosed vs 1.8 +/- 0.9 vessels stenosed in the F (p less than .05). Ten normal subjects also performed the exercise test. At the same workload, patients with recent myocardial infarction had significantly lower oxygen consumption (NF less than F), significantly higher minute ventilation (NF greater than F), ventilatory equivalent for oxygen (NF greater than F), and higher respiratory exchange ratio (NF greater than F) than did normal subjects. The heart rate responses were higher in the post infarction patients than in normal subjects. The oxygen pulse was significantly lower in the cardiac patients compared to normals. These findings suggest that during the early recovery phase from an acute myocardial infarction, patients, particularly the NF, utilize less oxygen at submaximal work loads than do normal subjects. This suggests that in these patients part of the energy requirements for exercise are met anaerobically. This could be due to abnormal extraction of oxygen by the working muscles or as a result of poor delivery of oxygen due to abnormal left ventricular function.     

Abnormalities of endocardial activation pattern in patients with previous healed myocardial infarction and ventricular tachycardia

Endocardial catheter mapping was performed in 27 patients with anterior wall acute myocardial infarction (AMI) and in 10 patients with inferior wall AMI. All patients had a history of ventricular tachycardia. Left ventricular breakthrough occurred at 10 +/- 4 ms after the QRS complex in inferior AMI and 11 +/- 7 ms after the QRS complex in anterior AMI. Total electrical activity recorded during sinus rhythm was 164 +/- 46 ms in inferior and 144 +/- 28 ms in anterior AMI (p = 0.05). Nine of the 10 patients with inferior AMI had complete activation of the anterior wall within the initial one-half of the QRS complex, compared with only 15 of the 27 patients with anterior AMI (p = 0.05). All 10 patients with inferior AMI had activation of the ventricular septum within the initial half of the QRS complex compared with only 13 of 27 with anterior AMI (p less than 0.005). None of the patients with inferior AMI had activation of the inferoposterior base within the initial one-half of the QRS complex, compared with 21 of 27 patients with anterior AMI (p less than 0.001). Complete activation of the anterior wall occurred at 33 +/- 15 ms in inferior and 58 +/- 30 ms in anterior AMI (p less than 0.005). Complete activation of the septum occurred at 38 +/- 12 ms in inferior and 63 +/- 28 ms in anterior AMI (p less than 0.005). Complete activation of the inferoposterior base occurred at 100 +/- 38 ms in inferior and 50 +/- 21 ms in anterior AMI (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Dipyridamole echocardiography evaluation of acute inferior myocardial infarction with concomitant anterior ST segment depression

The significance of anterior ST segment depression in inferioracute myocardial infarction (AMI) remains controversial. Theaim of this study was to relate precordial ST segment depressionto the topography of residual myocardial ischaemia, with myocardialmapping of the asynergic area and coronary anatomy. Twenty-fivepatients with first inferior AMI (15 patients with anteriorST segment depression: group A and 10 patients without anteriorST segment shift: group B), all underwent: (1) electrocardiographicevaluation on admission to the Coronary Care Unit and at 24h intervals thereafter; (2) 2D-echocardiographic study within3 h of CCU admission: (3) dipyridamole echocardiographic test(DET) (doses of dipyridamole up to 0.84 mg.kg^–1 i.v. over10 min) 4 days after AMI; (4) coronary arteriography within14 days from AMI. To assess regional left ventricular wall motion,a 16 segment model was used and a wall motion score index (WMSI)was derived. The results of DET were correlated to the anatomyof the infarct-related vessel. Compared to group B, group Apatients showed a significantly greater maximal ST segment elevationin inferior limb leads (lead III: 3.9±1.9 mm vs 2.2±1.1mm, P<0.05; aVF: 3.5±13 mm vs 1.7±0.8 mm, P<0.001).Group A patients showed greater WMSI (1.35±0.22 vs 117±0.12,P<0.05), with more frequent postero-lateral wall involvement(72% vs 20%, P<0.05). No patient of either group showed asynergyof the anterior, anterolateral or anteroseptal segments. Nodifferences in the distribution of coronary artery disease wereobserved. Left anterior descending coronary artery disease waspresent in only three patients (20%) in group A and in one patientin group B. DET was positive in eight patients (53%) in groupA and in three (30%) in group B (P = statistically not significant).In all patients DET induced new wall motion abnormalities locatedin the territory of the infarct-related artery. None of thepatients developed new wall motion abnormalities remote fromthe infarct zone or adjacent to the infarct zone, but locatedin different vascular regions. In conclusion, anterior ST segmentdepression in inferior A MI appears to indicate a more extensivearea of asynergy, with frequent involvement of the posterolateralwall. The topography of DET-induced residual myocardial ischaemiadoes not support the hypothesis of concomitant anterior ischaemia.